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<dc:date>2010-02-07T03:36+06:00
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<description><![CDATA[ Join Group of 2  This is an excellent opportunity for a BE/BC Gastroenterologist to join 2 others as an expansion to this very busy practice.  The group has a very loyal referral base that is sending ]]></description>
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<title>Great Location :: Maryland :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_maryland/page_3.html</link>
<description><![CDATA[Premier single specialty group of Gastroenterologists seeks additional GI for a growing and well-established practice. Physician to practice in new community practice/office location in area with existing ]]></description>
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<title>Great Location :: Massachusetts :: Intelligent Placement Solutions, Inc</title>
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<description><![CDATA[Need BC candidate with MA license to start in the next 3-4 months.  Offering $400K with $100K sign on bonus.We invite team oriented, motivated physicians to a hospital employed position.  We offer an ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_maryland/page_4.html">
<title>Great Location :: Maryland :: Intelligent Placement Solutions, Inc</title>
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<description><![CDATA[Looking for a conscientious GI to join a solo gastroenterologist in the DC area.   Endoscopy center close to office.  Call 1:3.  Offering $250K plus production bonus.  2 year partnership track.  Call ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_north_carolina/page_6.html">
<title>Great Location :: North Carolina :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_north_carolina/page_6.html</link>
<description><![CDATA[Incredible opportunity!  Multi Specialty practice looking to add a third GI.  Partnership avaiable.  Looking for a general GI.  This is a very family oriented town.  You will enjoy a comfortable lifestyle ]]></description>
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<title>Great Location :: West Virginia :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_west_virginia/page_1.html</link>
<description><![CDATA[Get in on the ground level replacing a GI who is leaving.  You can be employed or join a large multi-specialty group, call is 10 days/month.  ERCP training is a requisite for this job.  Comprehensive ]]></description>
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<title>Great Location :: North Carolina :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_north_carolina/page_7.html</link>
<description><![CDATA[Great opportunity to join a solo gastroenterologist.  Progressive growing community in Eastern NC. Hour from Raleigh and 1 1/2 hour from coast.  Excellent place to live and raise a family.  Three universities ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_florida/page_8.html">
<title>Great Location :: Florida :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_florida/page_8.html</link>
<description><![CDATA[Join a 2 person single specialty practice.  The surgical center is ownd by multiple physicians.  Buy in is an option.  Call is 1:4  Less that 10% of  patients come from the hospitals.  This is a two year ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_virginia/page_2.html">
<title>Great Location :: Virginia :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_virginia/page_2.html</link>
<description><![CDATA[Currently recruiting for a BE/BC Gastroenterologist Physician. Option to begin new practice or work with existing group in town. This is a Hospital Employed Position.  Generous Sign-On Bonus and Relocation ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_georgia/page_5.html">
<title>Great Location :: Georgia :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_georgia/page_5.html</link>
<description><![CDATA[Looking for 2010 candidates.  Join a well-established, single specialty; GI practice with steady growth for over 25 years. There is a strong referral base.  The Endoscopy Center is physician owned and ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_virginia/page_3.html">
<title>Great Location :: Virginia :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_virginia/page_3.html</link>
<description><![CDATA[Join a single specialty practice with a great group of GI's.  They are looking for a energetic, aggressive physician.  Good communication skills needed.  Little managed care.  Partnership track available. ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_texas/page_3.html">
<title>Great Location :: Texas :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_texas/page_3.html</link>
<description><![CDATA[Multi specialty group of 18 primary care providers and 1 surgeon is looking for a GI to join their group.  The group employment salary will be around the low $400,000 vicinity on a net income guarantee ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_michigan/page_1.html">
<title>Not Disclosed :: Michigan :: Locum Medical Group</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_michigan/page_1.html</link>
<description><![CDATA[A practice located in central Michigan is looking for a board certified or board eligible Gastroenterologist. The incoming physician will have excellent clinical and technical skills with experience in ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_texas/page_6.html">
<title>Not Disclosed :: Texas :: Locum Medical Group</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_texas/page_6.html</link>
<description><![CDATA[A Board Certified or Board Eligible Gastroenterologist is needed to join a multi-specialty group northeast of Dallas. You would start as an employee and grow to a partner. Time will be split between office ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_arizona/page_2.html">
<title>NorthWest :: Arizona :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_arizona/page_2.html</link>
<description><![CDATA[Seeking a Gastroenterologist(ERCP/liver disease)physician to be employed in hospital-owned clinic. Physicians in the community will provide coverage. Almost 100% procedures are currently being performed ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_north_carolina/page_1.html">
<title>SouthEast :: North Carolina :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_north_carolina/page_1.html</link>
<description><![CDATA[Join solo Gastroenterologist.  Hospital offering income gaurentee.  Practice owns their endoscopy center but also do endoscopies at hospital.  Looking for a general GI.      Hospital provides area residents ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_colorado/page_2.html">
<title>Central :: Colorado :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_colorado/page_2.html</link>
<description><![CDATA[Ten year old practice looking to add another GI ASAP.  ERCP is a must.  Partnership offered w/competitive salary.  Two years to partnership.  Cover two hospitals and  two offices and have 2 N.P's.  Own ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_north_carolina/page_8.html">
<title>North :: North Carolina :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_north_carolina/page_8.html</link>
<description><![CDATA[Solo opportunity with income guarentee in the beautiful foothills of the Blue Ridge Mountaitns..  There is another GI in town.  No shared call at this time. State of the art hospital- GI equipment  Not ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_south_carolina/page_8.html">
<title>South :: South Carolina :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_south_carolina/page_8.html</link>
<description><![CDATA[Physician to join a practice with full support of the hospital. Great opportunity with the support of the medical community to work with hospital in building an inpatient/outpatient practice. Interested ]]></description>
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<item rdf:about="http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_pennsylvania/page_18.html">
<title>East :: Pennsylvania :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/perma_gastroenterology_jobs_in_pennsylvania/page_18.html</link>
<description><![CDATA[This is an excellent full time opportunity for a Board Certified/Board Eligible Gastroenterologist. This busy, well-respected 3 physician practice is located on the campus of a  teaching hospital.  Need ]]></description>
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<title>Ketoprofen, peginterferon 2a and ribavirin for genotype 1 chronic hepatitis C: a phase II study.</title>
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<title>Education-based approach to addressing non-evidence-based practice in preventing NSAID-associated gastrointestinal complications.</title>
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<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20014464&#x26;dopt=Abstract">
<title>Neoadjuvant chemoradiotherapy for resectable esophageal carcinoma: a meta-analysis.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20014464&#x26;dopt=Abstract</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117246&#x26;dopt=Abstract">
<title>Editor, Clinical Gastroenterology &#x26; Hepatology.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117246&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        Editor, Clinical Gastroenterology &amp; Hepatology.
        Clin Gastroenterol Hepatol. 2010 Jan 28;
        Authors:  Maltz C
        
        PMID: 20117246 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117245&#x26;dopt=Abstract">
<title>Level of Fellowship Training Increases Adenoma Detection Rates.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117245&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        Level of Fellowship Training Increases Adenoma Detection Rates.
        Clin Gastroenterol Hepatol. 2010 Jan 28;
        Authors:  Peters SL, Hasan AG, Jacobson NB, Austin GL
        BACKGROUND &amp; AIMS:: The adenoma detection rate (ADR) is critical to the success of colonoscopy for colorectal cancer screening. The effects of involving gastroenterology fellows in screening colonoscopies are uncertain. We assessed the effects of gastroenterology fellow participation on ADR and whether outcomes vary with year of fellowship training. METHODS:: We performed a retrospective review of all average-risk screening colonoscopies performed from April 2005 to April 2007 at the University of Colorado Hospital. A gastroenterology attending physician alone performed 2895 colonoscopies; 699 were performed by a gastroenterology fellow supervised by an attending physician. Statistical analyses of polyp, adenoma, and advanced adenoma (or cancer) detection were performed using logistic regression. RESULTS:: The ADR was significantly higher (odds ratio [OR]=1.32, 95% CI: 1.10-1.59) among colonoscopies that included a gastroenterology fellow compared to those performed by only a gastroenterology attending physician. Similarly, the polyp detection rate was higher (OR=1.28, 95% CI: 1.08-1.52) among colonoscopies involving a gastroenterology fellow. There was no difference in the detection of advanced adenomas or cancers (OR=1.05, 95% CI: 0.77-1.44) among colonoscopies involving a gastroenterology fellow. The ADR differed greatly by year of training. Compared to colonoscopies performed by an attending gastroenterologist alone, the ADR increased with each year of training: OR=0.89 (95% CI: 0.66-1.22) for first-year fellows; OR=1.31 (95% CI: 0.89-1.93) for second-year fellows; and OR=1.70 (95% CI: 1.33-2.17) for third-year fellows. CONCLUSION:: Involvement of fellows in screening colonoscopies increases the ADR, primarily because of the increased ADR in procedures involving third-year gastroenterology fellows.
        PMID: 20117245 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117244&#x26;dopt=Abstract">
<title>Continuous Therapy With Certolizumab Pegol Maintains Remission of Patients With Crohn&#x27;s Disease for up to 18 Months.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117244&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        Continuous Therapy With Certolizumab Pegol Maintains Remission of Patients With Crohn's Disease for up to 18 Months.
        Clin Gastroenterol Hepatol. 2010 Jan 28;
        Authors:  Lichtenstein GR, Thomsen OO, Schreiber S, Lawrance IC, Hanauer SB, Bloomfield R, Sandborn WJ,  
        BACKGROUND &amp; AIMS:: The safety and efficacy of maintenance therapy with the anti-tumor necrosis factor antibody fragment certolizumab pegol has not been reported beyond 6 months. We assessed the long-term efficacy, safety, and immunogenicity of continuous vs interrupted maintenance therapy with subcutaneous certolizumab pegol in patients with Crohn's disease. METHODS:: Patients who responded to induction therapy at week 6 of the PRECiSE 2 trial were randomly assigned to groups given certolizumab pegol (continuous) or placebo (drug-interruption) during weeks 6-26. Patients who completed PRECiSE 2 were eligible to enter PRECiSE 3, an ongoing, open-label extension trial where patients have received certolizumab pegol (400 mg) every 4 weeks for 54 weeks to date (total of 80 weeks). Disease activity was measured by the Harvey-Bradshaw Index. PRECiSE 3 is the first prospective trial in which patients received continuous or interrupted anti-TNF-alpha therapy &gt;12 months and were not offered the option to increase their dose. RESULTS:: Harvey-Bradshaw Index responses at week 26 for the continuous and drug-interruption groups were 56.3% and 37.6%, respectively; corresponding remission rates were 47.9% and 32.4%, respectively. Of patients responding at week 26, response rates at week 80 in the continuous and drug-interruption groups were 66.1% and 63.3%, respectively; among patients in remission at week 26, week 80 remission rates were 62.1% and 63.2%, respectively. More patients in the drug-interruption group developed antibodies against certolizumab pegol (and had lower plasma concentrations of certolizumab pegol) than the continuously treated group. CONCLUSIONS:: Certolizumab pegol effectively maintains remission of Crohn's disease for up to 18 months. Continuous therapy is more effective than interrupted therapy.
        PMID: 20117244 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117243&#x26;dopt=Abstract">
<title>Success of self-administered home fecal transplantation for chronic Clostridium difficile infection.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117243&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        Success of self-administered home fecal transplantation for chronic Clostridium difficile infection.
        Clin Gastroenterol Hepatol. 2010 Jan 28;
        Authors:  Silverman MS, Davis I, Pillai DR
        Clostridium difficile infection (CDI) can relapse in patients with significant comorbidities. A subset of these patients becomes dependent on oral vancomycin therapy for prolonged periods with only temporary clinical improvement. These patients incur significant morbidity from recurrent diarrhea and financial costs from chronic antibiotic therapy. We sought to investigate whether self- or family-administered fecal transplantation could be used to definitively treat refractory CDI. We report a case series (n=7) where 100% clinical success was achieved in treating these individuals with up to 14 months follow up.
        PMID: 20117243 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117242&#x26;dopt=Abstract">
<title>Langerhans cell histiocytosis of the stomach mimicking early gastric cancer.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117242&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        Langerhans cell histiocytosis of the stomach mimicking early gastric cancer.
        Clin Gastroenterol Hepatol. 2010 Jan 28;
        Authors:  Nozaki Y, Oshiro H, Nakajima A
        
        PMID: 20117242 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117241&#x26;dopt=Abstract">
<title>High risk ulcer bleeding: when is second look endoscopy recommended?</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117241&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        High risk ulcer bleeding: when is second look endoscopy recommended?
        Clin Gastroenterol Hepatol. 2010 Jan 28;
        Authors:  Chiu PW, Sung JJ
        
        PMID: 20117241 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117240&#x26;dopt=Abstract">
<title>What are the risks of general surgical abdominal operations in patients with cirrhosis?</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117240&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        What are the risks of general surgical abdominal operations in patients with cirrhosis?
        Clin Gastroenterol Hepatol. 2010 Jan 28;
        Authors:  Henderson JM
        
        PMID: 20117240 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117239&#x26;dopt=Abstract">
<title>Diaphragm-like stricture of the small intestine related to cytomegalovirus infection.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=20117239&#x26;dopt=Abstract</link>
<description><![CDATA[
	
        Diaphragm-like stricture of the small intestine related to cytomegalovirus infection.
        Clin Gastroenterol Hepatol. 2010 Jan 28;
        Authors:  Shimizu T, Marusawa H, Yamashita Y
        
        PMID: 20117239 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/JFrw0Hz3bvE/nrgastro.2009.238">
<title>The expanding role of biologic therapy for IBD</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/JFrw0Hz3bvE/nrgastro.2009.238</link>
<description><![CDATA[The topic of biologic therapy for IBD has been selected for this Focus issue of Nature Reviews Gastroenterology & Hepatology because of the important implications it has for disease management. Four biologic agents are currently marketed for the treatment of IBD in the US ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/TvYxeicQ6q8/nrgastro.2009.224">
<title>IBD: High dietary intake of linoleic acid more than doubles the risk of ulcerative colitis</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/TvYxeicQ6q8/nrgastro.2009.224</link>
<description><![CDATA[A high dietary intake of linoleic acid—an essential n-6 polyunsaturated fatty acid found in red meats, polyunsaturated margarines and various cooking oils—more than doubles the risk of developing incident ulcerative colitis, according to the results of a new multicenter European study.Linoleic acid is converted ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/wQcBFsrtrH0/nrgastro.2009.229">
<title>H. Hepaticus and biliary disease</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/wQcBFsrtrH0/nrgastro.2009.229</link>
<description><![CDATA[Since the discovery of Helicobacter pylori, the association of other Helicobacter spp. with gastrointestinal disease has been of particular interest to clinicians. New evidence from Toshihide Hamada and colleagues suggests an association between colonization of the hepatobiliary system by H. hepaticus and ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/NkwWKyJJyQY/nrgastro.2009.230">
<title>Pancreas: New antibody may aid diagnosis of autoimmune pancreatitis</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/NkwWKyJJyQY/nrgastro.2009.230</link>
<description><![CDATA[An antibody present in almost all patients with autoimmune pancreatitis may be the most specific serologic marker yet identified for this disease, report Antonio Puccetti and colleagues in The New England Journal of Medicine.The pathogenesis of autoimmune pancreatitis is not well understood, and ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/amSggaFaNWg/nrgastro.2009.226">
<title>Obesity: Lifestyle counseling ineffective in tackling childhood obesity</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/amSggaFaNWg/nrgastro.2009.226</link>
<description><![CDATA[National policies in several countries, including the USA, UK and Australia, endorse the role of general practitioners in monitoring childhood obesity and undertaking any necessary counseling. However, Melissa Wake and colleagues suggest that these costly primary care guidelines are surplus to requirements, as surveillance followed ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/GzGNhifhpFU/nrgastro.2009.227">
<title>IBD: Thiopurines increase risk of lymphoproliferative disorders in patients with IBD</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/GzGNhifhpFU/nrgastro.2009.227</link>
<description><![CDATA[The evidence is conflicting as to whether long-term thiopurine therapy to suppress the immune system increases the risk of developing lymphomas in patients with IBD. Laurent Beaugerie and co-workers now present evidence from the large, prospective, observational CESAME study that patients with IBD receiving thiopurines ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/qEXhGB1gyos/nrgastro.2009.228">
<title>Obesity: Liraglutide induces weight loss</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/qEXhGB1gyos/nrgastro.2009.228</link>
<description><![CDATA[There are few safe and effective drugs available to treat obesity. Arne Astrup and colleagues conducted a clinical trial to assess the effect on bodyweight of liraglutide compared with the approved weight-loss agent orlistat or placebo in obese individuals. They found that liraglutide is well ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/0v7hugQRHhM/nrgastro.2009.231">
<title>Gallstones: Statin use is associated with a reduced risk of cholesterol gallstones</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/0v7hugQRHhM/nrgastro.2009.231</link>
<description><![CDATA[Findings from a new study “support the hypothesis that statin intake on a regular basis is associated with a risk reduction of developing a new gallstone diagnosis followed by cholecystectomy”, says Christoph Meier, one of the study authors.Approximately 10–20% of white adults in developed ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/KIUpfuYXvMA/nrgastro.2009.223">
<title>Hepatic artery thrombosis</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/KIUpfuYXvMA/nrgastro.2009.223</link>
<description><![CDATA[Hepatic artery thrombosis (HAT) is the most common vascular complication after liver transplantation, occurring in 2–5% of liver transplant recipients. As such, HAT is a major cause of morbidity and graft loss after liver transplantation. In many instances, HAT occurs soon after surgery for technical ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/E7DJwdv6Gno/nrgastro.2009.225">
<title>IBD: Is treatment with a third anti-TNF agent a safe and effective option in patients with Crohn&#x27;s disease?</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/E7DJwdv6Gno/nrgastro.2009.225</link>
<description><![CDATA[Treatment with a third anti-TNF (tumor necrosis factor) agent could be an effective therapeutic option for patients with Crohn's disease who have lost response, or developed intolerance, to two previous anti-TNF agents.Failure of, or intolerance to, an anti-TNF agent can be a significant problem ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/PWS_SP5rFRk/nrgastro.2009.239">
<title>IBD: Intensive GMA is more efficacious than weekly GMA for the treatment of ulcerative colitis</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/PWS_SP5rFRk/nrgastro.2009.239</link>
<description><![CDATA[Intensive treatment with granulocyte and monocyte adsorptive apheresis (GMA) is more efficacious for ulcerative colitis than routine weekly GMA treatment, according to the results of a new study from Japan.GMA selectively depletes granulocytes and monocytes from peripheral blood. This reduction in the number of ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/AdxKteCucx8/nrgastro.2009.233">
<title>GERD: Are functional heartburn and functional dyspepsia one disorder?</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/AdxKteCucx8/nrgastro.2009.233</link>
<description><![CDATA[The characteristics of functional heartburn remain poorly understood. Savarino  et al. have now demonstrated that functional heartburn has more in common with functional dyspepsia than with nonerosive reflux disease. This study suggests that there is substantial overlap between functional heartburn and functional dyspepsia, and possibly that these two disorders may actually be one functional esophagogastric disorder.]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/-hwsnj9qnj8/nrgastro.2009.234">
<title>Pancreas: Is there still a role for total pancreatectomy?</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/-hwsnj9qnj8/nrgastro.2009.234</link>
<description><![CDATA[The role of total pancreatectomy for pancreatic adenocarcinoma is controversial. Concerns have been raised about increased morbidity and mortality, and poorer long-term outcomes associated with total pancreatectomy compared with pancreaticoduodenectomy. Reddy and colleagues recently reported data that support the use of total pancreatectomy, when appropriate, in clinical practice.]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/6XbxW__Dlok/nrgastro.2009.235">
<title>Primary sclerosing cholangitis: What is the role of ursodeoxycholic acid in therapy for PSC?</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/6XbxW__Dlok/nrgastro.2009.235</link>
<description><![CDATA[Ursodeoxycholic acid (UDCA) is widely used for the treatment of chronic cholestatic liver diseases. However, a recent randomized, controlled trial has surprisingly shown that the use of high-dose UDCA in patients with primary sclerosing cholangitis (PSC) may be harmful; adverse events, such as death and liver transplantation, were significantly higher in patients who received UDCA compared with placebo.]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/caQFueSoVlk/nrgastro.2009.236">
<title>Liver: Management of non-acetaminophen-induced ALF</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/caQFueSoVlk/nrgastro.2009.236</link>
<description><![CDATA[The first prospective, double-blind, randomized controlled study of acetylcysteine for the treatment of patients with non-acetaminophen-induced acute liver failure supports its use in patients in the early stages of liver failure. Emergency liver transplantation still has a fundamental role in the management of patients with the most severe form of this syndrome.]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/HThTj-d5SYQ/nrgastro.2009.237">
<title>Diverticular disease: What is the best long-term treatment?</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/HThTj-d5SYQ/nrgastro.2009.237</link>
<description><![CDATA[Some patients who have diverticular disease develop complications or recurrent symptoms and medical therapy may be necessary. Findings from recent studies suggest that rifaximin, a poorly absorbed antibiotic, should be recommended for long-term treatment of diverticular disease; however, the anti-inflammatory drug mesalazine seems to be more promising in the long term.]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/B1w_heYkg1k/nrgastro.2009.220">
<title>The potential for disease modification in Crohn&#x27;s disease</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/B1w_heYkg1k/nrgastro.2009.220</link>
<description><![CDATA[The natural history of Crohn's disease is characterized by progression to complicated and disabling disease, often necessitating surgical interventions. There is either circumstantial or direct evidence to support the disease-modifying potential of several therapeutic agents. Healing of endoscopic lesions is an emerging surrogate marker of ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/Te9X2f3JLcw/nrgastro.2009.222">
<title>Top-down therapy for IBD: rationale and requisite evidence</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/Te9X2f3JLcw/nrgastro.2009.222</link>
<description><![CDATA[Several trials have shown that early treatment of Crohn's disease with immunomodulators and anti-TNF agents leads to a superior clinical outcome, including healing of the mucosa, compared with standard therapy alone. Mounting evidence indicates that mucosal healing is associated with a reduced risk of complications, ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/6HSvarjCaLc/nrgastro.2009.221">
<title>Optimizing the safety of biologic therapy for IBD</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/6HSvarjCaLc/nrgastro.2009.221</link>
<description><![CDATA[The introduction of biologic therapy for the treatment of IBD has substantially changed its management. The safety concerns associated with biologic therapies include the increased risk of infection, autoimmunity, development of lymphoma and demyelinating disease, and the risk of worsening heart failure. There are several ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/28nyTwXmuFU/nrgastro.2009.232">
<title>The pharmacoeconomics of biologic therapy for IBD</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/28nyTwXmuFU/nrgastro.2009.232</link>
<description><![CDATA[The past decade has been marked by the introduction and expanding use of biologic therapies for the induction and maintenance of response in patients with IBD. Although widely heralded for their efficacy, these agents have also stirred controversy over the potential economic impact that they ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/FvAvGOIQ-z4/nrgastro.2009.218">
<title>Future biologic targets for IBD: potentials and pitfalls</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/FvAvGOIQ-z4/nrgastro.2009.218</link>
<description><![CDATA[The treatment of patients with IBD has evolved towards biologic therapy, which seeks to target specific immune and biochemical abnormalities at the molecular and cellular level. Multiple genes have been associated with susceptibility to IBD, and many of these can be linked to alterations in ]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21224">
<title>Increased expression and cellular localization of spermine oxidase in ulcerative colitis and relationship to disease activity</title>
<link>http://dx.doi.org/10.1002%2Fibd.21224</link>
<description><![CDATA[Polyamines are important in cell growth and wound repair, but have also been implicated in inflammation-induced carcinogenesis. Polyamine metabolism includes back-conversion of spermine to spermidine by the enzyme spermine oxidase (SMO), which produces hydrogen peroxide that causes oxidative stress. In ulcerative colitis (UC), levels of spermine are decreased compared to spermidine. Therefore, we sought to determine if SMO is involved in UC.Colon biopsies and clinical information from subjects undergoing colonoscopy for evaluation of UC or colorectal cancer screening were utilized from 16 normal controls and 53 UC cases. Histopathologic disease severity was graded and the Mayo Disease Activity Index (DAI) and endoscopy subscore assessed. SMO mRNA expression was measured in frozen biopsies by TaqMan-based real-time polymerase chain reaction (PCR). Formalin-fixed tissues were used for SMO immunohistochemistry.There was a 3.1-fold upregulation of SMO mRNA levels in UC patients compared to controls (P = 0.044), and a 3.7-fold increase in involved left colon versus paired uninvolved right colon (P < 0.001). With worsening histologic injury in UC there was a progressive increase in SMO staining of mononuclear inflammatory cells. There was a similar increase in SMO staining with worsening endoscopic disease severity and strong correlation with the DAI (r = 0.653, P < 0.001). Inflammatory cell SMO staining was increased in involved left colon versus uninvolved right colon.SMO expression is upregulated in UC tissues, deriving from increased levels in mononuclear inflammatory cells. Dysregulated polyamine homeostasis may contribute to chronic UC by altering immune responses and increasing oxidative stress. (Inflamm Bowel Dis 2010;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21216">
<title>Inflammatory bowel diseases and health service: The necessity for a new strategy</title>
<link>http://dx.doi.org/10.1002%2Fibd.21216</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21214">
<title>Final adult height of children with inflammatory bowel disease is predicted by parental height and patient minimum height Z-score</title>
<link>http://dx.doi.org/10.1002%2Fibd.21214</link>
<description><![CDATA[This study was designed to elucidate the contribution of parental height to the stature of children with inflammatory bowel disease (IBD), who often exhibit growth impairment. Accordingly, we compared patients' final adult heights and target heights based on measured parental heights and examined predictors of final adult height in pediatric IBD patients.We prospectively analyzed the growth of 295 patients diagnosed between ages 1 and 18 (211 Crohn's disease [CD], 84 ulcerative colitis [UC]) and their family members (283 mothers, 231 fathers, 55 siblings).Twenty-two percent had growth impairment (height for age Z-score <-1.64, equivalent to <5th percentile on growth curve) in more than 1 measurement since diagnosis; most growth-impaired patients had CD (88% CD versus 12% UC). Parents of the growth-impaired group had lower mean height Z-scores compared to parents of nongrowth-impaired patients (-0.67 versus 0.02 for mothers [P < 0.001]; -0.31 versus 0.22 for fathers [P = 0.002]). For 108 patients who reached adult heights and had available parental heights, the growth-impaired group continued to demonstrate lower adult height Z-scores (-1.38 versus 0.07; P < 0.001). Adult heights were within 1 SD of target heights even for the growth-impaired group. Only 11.3% remained persistently growth-impaired in adulthood. Multivariate regression analysis demonstrated lower parental height and minimum patient height Z-score as significant predictors of lower final adult height in IBD.Parental height is a powerful determinant of linear growth even in the presence of chronic inflammation, and should be an integral part of the evaluation of growth in IBD children. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21213">
<title>Controversy over NOD2, inflammation, and defensins</title>
<link>http://dx.doi.org/10.1002%2Fibd.21213</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21212">
<title>New proteomic approaches for biomarker discovery in inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21212</link>
<description><![CDATA[There is an increasing interest in the discovery of new inflammatory bowel disease (IBD) biomarkers able to predict the future patterns of disease and to help in diagnosis, treatment, and prognosis. A biomarker is a substance that can be measured biologically and is associated with an increased risk of the disease. Biomarkers can be a genetic testing factor or proteins in biological samples such as serum, plasma, and cellular subpopulations. All of them should be studied to find out their utility in the management of IBD. Ulcerative colitis and Crohn's disease are relapsing and remitting chronic IBDs characterized by a global immune defect. The gold standard of their diagnosis is histological evaluation performed during endoscopic procedures. Several studies have focused on the identification and combination of less invasive diagnostic serum biomarkers. Nowadays, diagnostic serum tests are not able either to determine whether and when the relapse will occur once the disease is in remission state or to select a patient phenotype more responsive to a specific therapy and more susceptible to different types of complication. In this review we analyze and report the current understanding in IBD biomarkers and discuss potential future biomarkers and new developments of proteomics, such as subproteomics, as an innovative approach for the classification of patients according to their pattern of protein expression. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21205">
<title>Treatment-associated acute myeloid leukemia in a patient with Crohn&#x27;s disease on 6-mercaptopurine</title>
<link>http://dx.doi.org/10.1002%2Fibd.21205</link>
<description><![CDATA[No Abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21202">
<title>Lewis and Sumner syndrome following infliximab treatment in Crohn&#x27;s disease: A report of 2 cases</title>
<link>http://dx.doi.org/10.1002%2Fibd.21202</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21201">
<title>Response to Baumgart review</title>
<link>http://dx.doi.org/10.1002%2Fibd.21201</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21200">
<title>In vivo analysis of gut function and disease changes in a zebrafish larvae model of inflammatory bowel disease: A feasibility study</title>
<link>http://dx.doi.org/10.1002%2Fibd.21200</link>
<description><![CDATA[The aim of this study was to develop a model of inflammatory bowel disease (IBD) in zebrafish larvae, together with a method for the rapid assessment of gut morphology and function in vivo thereby enabling medium-throughput compound screening.Assays were performed using larval zebrafish from 3-8 days postfertilization (d.p.f.) in 96-well plates. Gut morphology and peristalsis were observed in vivo using fluorescent imaging following ingestion of fluorescent dyes. IBD was induced by addition of 2,4,6-trinitrobenzenesulfonic acid (TNBS) to the medium within the well. Pathology was assessed in vivo using fluorescent imaging and postmortem by histology, immunohistochemistry, and electron microscopy. Therapeutic compounds were evaluated by coadministration with TNBS.A novel method of investigating gut architecture and peristalsis was devised using fluorescent imaging of live zebrafish larvae. Archetypal changes in gut architecture consistent with colitis were observed throughout the gut. Significant changes in goblet cell number and tumor necrosis factor alpha (TNF-[alpha]) antibody staining were used to quantify disease severity and rescue. Prednisolone and 5-amino salicylic acid treatment ameliorated the disease changes. Candidate therapeutic compounds (NOS inhibitors, thalidomide, and parthenolide) were assessed and a dissociation was observed between efficacy assessed using a single biochemical measure (TNF-[alpha] staining) versus an assessment of the entire disease state.Gut physiology and pathology relevant to human disease state can be rapidly modeled in zebrafish larvae. The model is suitable for medium-throughput chemical screens and is amenable to genetic manipulation, hence offers a powerful novel premammalian adjunct to the study of gastrointestinal disease. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21225">
<title>Simple score to identify colectomy risk in ulcerative colitis hospitalizations</title>
<link>http://dx.doi.org/10.1002%2Fibd.21225</link>
<description><![CDATA[Patients hospitalized for ulcerative colitis (UC) are at high risk for colectomy. Despite growing interest in research using administrative data in inflammatory bowel disease, there is no available tool in such research to stratify disease severity or identify patients at high risk for colectomy.Using the Nationwide Inpatient Sample (NIS) 2004, we identified patients hospitalized for UC flare through appropriate ICD-9-CM discharge diagnosis codes (556.x). Our primary outcome of interest was undergoing total colectomy (45.8). Multivariate logistic regression models were constructed to identify independent predictors of colectomy. From this, a cumulative risk score was developed. Hospitalizations were divided into 3 strata (low, intermediate, high) based on the odds of colectomy.There were a total of 15,142 hospitalizations with a discharge diagnosis of UC included in our study among whom 366 patients underwent total colectomy (2.4%). Anemia (odds ratio [OR] 2.13), requirement for blood transfusion (OR 2.22), malnutrition (OR 4.53), and total parenteral nutrition (OR 4.30) were independent predictors of colectomy as were transfer in from another hospital (OR 2.06) and admission to a teaching hospital (OR 1.73). The cumulative colectomy risk score ranged from 0-8, with significantly higher risk of colectomy in the high-risk stratum (13.7%) compared to the intermediate-risk (4.2%, P < 0.001) and low-risk (1.3%, P < 0.001) strata. The risk score performed well in its discriminative ability with an area under the curve of 0.70.We propose a simple and novel risk score to stratify the severity of UC hospitalizations and predict colectomy in this population. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21203">
<title>To TNF or not to TNF: That is the question</title>
<link>http://dx.doi.org/10.1002%2Fibd.21203</link>
<description><![CDATA[No Abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21204">
<title>Phase I trial of sargramostim in pediatric Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21204</link>
<description><![CDATA[Improving granulocyte function may represent an effective therapy for Crohn's disease (CD). We performed a Phase I-2 trial of sargramostim (SRG) in children with CD.This was multicenter, open-label study in 6-16-year-old patients with moderate to severely active CD. Patients received either 4 or 6 [mu]g/kg SRG subcutaneously daily for 8 weeks, with and without concomitant corticosteroids (CS). The primary endpoint was identification of a safe and tolerable dose in children. The secondary endpoint was establishment of the pharmacokinetics (PK). Efficacy, a tertiary endpoint, was measured by the Pediatric CD Activity Index (PCDAI). Response was defined as a decrease from baseline of [ge]12.5 points and remission as absolute PCDAI of [le]10.In all, 22 patients were enrolled: 12 and 10 received 4 and 6 mg/kg, respectively; 19 completed the course. Both doses were found to be safe and well tolerated. Mild injection-site reactions occurred in 90% of patients. Three patients required dose reductions due to elevated absolute neutrophil counts. Following 4 [mu]g/kg the mean area under the curve (AUC) was 2.64 and 2.80 ngh/mL for the 6-11- and 12-16-year-old groups, respectively. The mean half-life (t1/2) was 1.22 and 1.59 hours, respectively. Following 6 [mu]g/kg, the mean AUC was 5.01 ngh/mL for the 12-16-year-old group, a 1.8-fold increase. A total of 16/18 patients (88%) achieved remission or response.Sargramostim at both 4 and 6 mg/kg was well tolerated. PK analysis suggested dose proportionality unaffected by CS exposure. Remission and response data are encouraging, but further trials are needed to assess efficacy. (Inflamm Bowel Dis 2010;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21195">
<title>CD95 is cytoprotective for intestinal epithelial cells in colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21195</link>
<description><![CDATA[CD95 is a member of the tumor necrosis factor receptor family. It is constitutively expressed on the basolateral membrane of intestinal epithelial cells (IECs) and under certain conditions induces apoptosis when crosslinked by its natural ligand, CD95L. A multitude of studies have been published addressing the question of where and under which conditions CD95L is produced in the gut in normal, inflammatory, and neoplastic situations and whether the apoptosis-inducing activity of CD95 contributes to pathology. Although some of these studies have considerably influenced our view on the role of the CD95/CD95L system compelling evidence for an involvement of the CD95/CD95L system in the physiological epithelial cell turnover is lacking.CD95 signaling deficiency in the colon was achieved in 2 ways. By transplanting bone marrow from wildtype mice into lethally irradiated mice expressing a signaling deficient mutant of CD95 (lprcg mice) and by tissue-specific deletion of CD95 in IECs. Mice were treated with either 3 cycles of dextran sulfate sodium (DSS) to induce colitis or by injection of azoxymethane (AOM) followed by 3 cycles of DSS to induce colon cancer. Disease index and the formation of neoplastic lesions in the colon were determined and histological analysis was performed.In each mouse model lacking CD95 activity in the colon mice were hypersensitive to DSS-induced colitis. In the CD95-deficient mice this did not have an effect on AOM/DSS-induced cancer formation.CD95 plays a role in protecting the colon from inflammation without contributing to colon cancer, under conclusions of increased inflammation. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21191">
<title>Cell death in the colonic epithelium during inflammatory bowel diseases: CD95/Fas and beyond</title>
<link>http://dx.doi.org/10.1002%2Fibd.21191</link>
<description><![CDATA[CD95 is a member of the death receptor family. It is a prototypical inducer of apoptosis that, upon binding of its cognate ligand (CD95L), forms a death-inducing signaling complex composed of adaptor molecules and initiator caspases that transmit the apoptosis signal. The CD95/CD95L system was implicated in the etiology of inflammatory bowel disease (IBD) based, primarily, on the finding that CD95 is highly expressed in the intestinal epithelial cells and that epithelial apoptosis is increased in IBD. In recent years it has been recognized that CD95, while playing an important role as an apoptosis-inducing receptor in the immune system, also has multiple nonapoptotic functions on nonimmune cells. This review critically discusses the data on the possible function of CD95 as an apoptosis-inducing receptor in IBD and discusses alternative mechanisms for epithelial cell loss in IBD. (Inflamm Bowel Dis 2010;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21207">
<title>Total nasolacrimal duct obstruction in 2 patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21207</link>
<description><![CDATA[No Abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21206">
<title>Activated factor XI and tissue factor in inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21206</link>
<description><![CDATA[No Abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21199">
<title>Evaluation of endoscopic and imaging modalities in the diagnosis of structural disorders of the ileal pouch</title>
<link>http://dx.doi.org/10.1002%2Fibd.21199</link>
<description><![CDATA[Computerized tomography enterography (CTE), gastrograffin enema (GGE), magnetic resonance imaging (MRI), and pouch endoscopy (PES) have commonly been used to assess ileal pouch disorders. However, their diagnostic utility has not been systematically evaluated. The aims of this study were to compare these imaging techniques to each other and to optimize diagnosis of pouch disorders by using a combination of these diagnostic modalities.Clinical data of patients from the Pouchitis Clinic from 2003 to 2008 who had a PES and at least 1 additional imaging modalities (CTE, GGE, or MRI) used for evaluation of ileal pouch disorders were retrospectively evaluated. We analyzed the accuracy, sensitivity, specificity, negative predictive value (NPV), and positive predictive value (PPV) with which these tests were able diagnose pouch inlet and distal small bowel and pouch outlet strictures, pouch fistulas, sinuses, and leaks. Subsequently, accuracy was recalculated by combining 2 imaging modalities to see if this could enhance accuracy.A total of 66 patients underwent evaluation with PES and 1 other imaging modality as follows: PES + CTE (n = 23), PES + GGE (n = 34), and PES + MRI (n = 26). The mean age was 41.5 ± 14.5 years, with 28 being female (42.4%). Sixty patients (90.9%) had J pouches and 59 (89.4%) had a preoperative diagnosis of ulcerative colitis. Overall, CTE, GGE, MRI, and PES all had reasonable accuracy for the diagnosis of small bowel and inlet strictures (73.9%-95.4%), outlet strictures (87.9%-92.3%), fistula (76.9%-84.8%), sinus (68.0%-93.9%), and pouch leak (83-93.9%). CTE had the lowest accuracy for small bowel and inlet strictures (73.9%) and MRI had the lowest accuracy for pouch sinus (68.0%). Combining 2 imaging tests can increase the accuracy of diagnosis to 100% for strictures, fistulas, sinus, and pouch leaks.CTE, GGE, MRI, and PES offer complementary information on disorders of the pouch and the combination of these tests increases diagnostic accuracy for complex cases. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21194">
<title>Direct comparison of two different mesalamine formulations for the maintenance of remission in patients with ulcerative colitis: A double-blind, randomized study</title>
<link>http://dx.doi.org/10.1002%2Fibd.21194</link>
<description><![CDATA[Mesalamine has been used as the first-line medication for the treatment of ulcerative colitis (UC). We directly compared the efficacy and safety of two different mesalamine formulations in the maintenance of remission in patients with UC.In a multicenter, double-blind, randomized study, 131 patients with quiescent UC were assigned to two groups: 65 to receive a pH-dependent release formulation of mesalamine at 2.4 g/day (pH-2.4 g) and 66 to receive a time-dependent release formulation of mesalamine at 2.25 g/day (Time-2.25 g). Both formulations were administered three times daily for 48 weeks. The primary endpoint was the proportion of patients without bloody stools.In the full analysis set (n = 130), the proportion of patients without bloody stools was 76.9% in the pH-2.4 g and 69.2% in the Time-2.25 g, demonstrating the noninferiority of pH-2.4 g to Time-2.25 g. No statistically significant difference in time to bloody stools was found between the two formulations (P = 0.27, log-rank test), but the time to bloody stools tended to be longer in pH-2.4 g compared to Time-2.25 g, and a similar trend was observed with regard to the time to relapse. No differences were observed between the safety profiles of the two formulations.The pH- and time-dependent release of mesalamine formulations were similarly safe and effective. Interestingly, the remission phase tended to be longer in the group that received the pH-dependent formulation compared to the group that received the time-dependent formulation (UMIN Clinical Trials Registry, no. C000000289). (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21193">
<title>Direct comparison of two different mesalamine formulations for the induction of remission in patients with ulcerative colitis: A double-blind, randomized study</title>
<link>http://dx.doi.org/10.1002%2Fibd.21193</link>
<description><![CDATA[Mesalamine is the first-line drug for the treatment of ulcerative colitis (UC). We directly compared the efficacy and safety of two mesalamine formulations for the induction of remission in patients with UC.In a multicenter, double-blind, randomized study, 229 patients with mild-to-moderate active UC were assigned to 4 groups: 66 and 65 received a pH-dependent release formulation of 2.4 g/day (pH-2.4 g) or 3.6 g/day (pH-3.6 g), respectively; 65 received a time-dependent release formulation of 2.25 g/day (Time-2.25 g), and 33 received placebo (Placebo). The drugs were administered three times daily for eight weeks. The primary endpoint was a decrease in the UC disease activity index (UC-DAI).In the full analysis set (n = 225) the decrease in UC-DAI in each group was 1.5 in pH-2.4 g, 2.9 in pH-3.6 g, 1.3 in Time-2.25 g and 0.3 in Placebo, respectively. These results demonstrate the superiority of pH-3.6 g over Time-2.25 g (P = 0.003) and the noninferiority of pH-2.4 g to Time-2.25 g. Among the patients with proctitis-type UC, a significant decrease in UC-DAI was observed in pH-2.4 g and pH-3.6 g as compared to Placebo, but not in Time-2.25 g. No differences were observed in the safety profiles.Higher dose of the pH-dependent release formulation was more effective for induction of remission in patients with mild-to-moderate active UC. Additionally, the pH-dependent release formulation was preferable to the time-dependent release formulation for patients with proctitis-type UC (UMIN Clinical Trials Registry, no. C000000288). (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21190">
<title>Thiopurine maintenance therapy for ulcerative colitis: The clinical significance of monitoring 6-thioguanine nucleotide</title>
<link>http://dx.doi.org/10.1002%2Fibd.21190</link>
<description><![CDATA[6-Mercaptopurine (6-MP) is an effective maintenance medication in patients with ulcerative colitis (UC), but toxic effects like myelosuppression limit its clinical benefit. In the blood, 6-thioguanine (6-TGN) is formed from 6-MP and mediates the therapeutic efficacy and most of the toxicities of 6-MP. The level of 6-TGN depends on the activity of thiopurine methyltransferase (TPMT), inherited as 1 of its 3 polymorphic forms with low, moderate, or normal/high activity. Accordingly, the 6-MP dose needs to be pharmacogenetically guided.Patients with quiescent UC received 6-MP as maintenance therapy and 6-TGN was assayed as its concentrations in red blood cells (RBCs) done by high-performance liquid chromatography. In a preliminary investigation, 30 mg/day 6-MP (n = 50) was given orally over 12 weeks to determine the time course of blood 6-TGN level. Then 257 patients were given 6-MP at 15-80 mg/day in a stepwise manner based on RBC 6-TGN, white blood cell count, and body weight to monitor 6-MP efficacy and safety profiles.At 30 mg/day 6-MP, RBC 6-TGN peaked over 4-8 weeks. In the main dosing study, the mean RBC 6-TGN level in patients who remained in remission during the 1-year observation time (n = 151) was 322.3 ± 119.5 pmole/8 × 108 RBC versus 204.8 ± 78.7 pmole/8 × 108 RBC in patients (n = 19) who relapsed (P < 0.001). Bone marrow suppression was seen almost exclusively at high 6-TGN concentration ranges. Further, a regression plot showed an inverse relationship between 6-TGN levels in RBC and TPMT enzyme activity.By regularly measuring RBC 6-TGN in patients with quiescent UC receiving 6-MP as maintenance therapy, we could monitor bone marrow suppression as well as other toxic side effects. Potentially, this strategy should enable physicians to avoid thiopurine-related adverse effects and identify individuals who may benefit most from 6-MP maintenance therapy. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20984">
<title>Surgical management of pyogenic complications of Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20984</link>
<description><![CDATA[Patients with Crohn's disease are prone to the development of pyogenic complications. These complications are most commonly in the form of perianal or intraabdominal abscesses and/or fistulas. Complications in these 2 distinct areas are managed differently; however, they are similar in the fact that initial treatment relies on medical or minimally invasive management to achieve a nonacute condition prior to definitive surgical procedure. This article reviews the current surgical management of obtaining pyogenic control in both anorectal and intraabdominal Crohn's disease. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21196">
<title>Combination of innate and adaptive immune alterations increased the likelihood of fibrostenosis in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21196</link>
<description><![CDATA[Mutations in the nucleotide oligomerization domain-2 (NOD2) gene and positive antibodies to microbial antigens have been found to be associated with the Crohn's disease (CD) phenotype, fibrostenosis. The aim of this study was to confirm these relationships in a large cohort of CD patients and to determine the correlation between the presence of NOD2 variants and antibodies to oligomannan, CBir, outer membrane porin-C (OmpC), and I2 in CD patients with fibrostenosis.Sera and DNA from 731 unrelated CD patients were tested for NOD2 variants (SNP 8, 12, and 13) and the antibodies. The results were correlated with CD phenotypes, fibrostenosis, internal penetrating, perianal penetrating, and ulcerative colitis (UC)-like as well as other clinical features.The presence of NOD2 allelic variants was primarily associated with fibrostenosis, secondarily with small bowel disease and small bowel surgery, and was inversely associated with UC-like disease. This association was present in patients with a fibrostenosis only (Vienna B2) and those with both stricturing and penetrating disease. The presence and level of antibodies to microbial antigens was also associated with the fibrostenosis phenotype. In the 316 patients with fibrostenosis the prevalence of NOD2 variants was significantly correlated with the antibody titer by quartile sum score. Further, when these patients with fibrostenosis were clustered by quartile sum score, the odds ratio for fibrostenosis was significantly higher in the patients with NOD2 variant alleles within each cluster, indicating synergy.Defects of innate (NOD2 variants) and adaptive (antibodies to microbial antigens) immunity act synergistically to increase the risk of the fibrostenosis phenotype. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21198">
<title>Safety of adalimumab in Crohn&#x27;s disease during pregnancy: Case report and review of the literature</title>
<link>http://dx.doi.org/10.1002%2Fibd.21198</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21197">
<title>When expression is not enough: The evolving thoughts on Fas/FasL and epithelial cell apoptosis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21197</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21189">
<title>Mortality in inflammatory bowel disease in the Netherlands 1991-2002: Results of a population-based study: The IBD South-Limburg cohort</title>
<link>http://dx.doi.org/10.1002%2Fibd.21189</link>
<description><![CDATA[The aim was to evaluate overall and disease-specific mortality in a population-based inflammatory bowel disease (IBD) cohort in the Netherlands, as well as risk factors for mortality.IBD patients diagnosed between 1 January 1991 and 1 January 2003 were included. Standardized mortality ratios (SMRs) were calculated overall and with regard to causes of death, gender, as well as age, phenotype, smoking status at diagnosis, and medication use.At the censoring date, 72 out of 1187 patients had died (21 Crohn's disease [CD], 47 ulcerative colitis [UC], and 4 indeterminate colitis [IC] patients). The SMR (95% confidence interval [CI]) was 1.1 (0.7-1.6) for CD, 0.9 (0.7-1.2) for UC and 0.7 (0.2-1.7) for IC. Disease-specific mortality risk was significantly increased for gastrointestinal (GI) causes of death both in CD (SMR 7.5, 95% CI: 2.8-16.4) and UC (SMR 3.4, 95% CI: 1.4-7.0); in CD patients, especially in patients 80 years at diagnosis. In contrast, UC patients had a decreased mortality risk from cancer (SMR 0.5, 95% CI; 0.2-0.9).In this population-based IBD study, mortality in CD, UC, and IC was comparable to the background population. The increased mortality risk for GI causes might reflect complicated disease course, with young and elderly patients at diagnosis needing intensive follow-up. Caution in interpreting the finding on mortality risk from cancer is needed as follow-up was probably to short to observe IBD-related cancers. (Inflamm Bowel Dis 2010;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21188">
<title>Budesonide treatment of patients with collagenous colitis restores normal eosinophil and T-cell activity in the colon</title>
<link>http://dx.doi.org/10.1002%2Fibd.21188</link>
<description><![CDATA[The aim of this study was to assess the activity of eosinophils, neutrophils, and CD4+ as well as CD8+ T-cells in 11 patients with active collagenous colitis (CC) before and after 8 weeks of budesonide treatment (9 mg once daily) compared to 10 healthy individuals.Clinical symptoms were recorded and intestinal biopsy samples were taken and analyzed by flow cytometry. Eosinophils with a high surface expression of CD44 and low CD9 expression were classified as activated. Neutrophil activity was assessed by their expression of CD66b, and CD69 was used as an activation marker for T-cells.All patients responded to the treatment. The eosinophils in active CC showed increased activity compared to controls. The activity was back to control levels after treatment. Neutrophils were not activated in CC patients before or after treatment. CD8+ T-cells from untreated CC patients had a lower activity than controls, and a tendency of lower activity was observed on CD4+ T-cells. After treatment, the activity was increased on both types of T-cells and was not different from controls.In the present study we demonstrated that the inflammation in CC is characterized by activated eosinophils but there is no neutrophil activity. CD4+ and CD8+ T-cells are increased in numbers in active CC but, surprisingly, they had a lower grade of activity than in control subjects. The major finding of this study is that budesonide treatment restores the normal activation of eosinophils and T-cells, accompanied by clinical remission. (Inflamm Bowel Dis 2010;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21186">
<title>Laparoscopic surgery for recurrent ileocolic Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21186</link>
<description><![CDATA[Laparoscopic (LAP) surgery is increasingly performed for primary ileocolic Crohn's disease (CD), but its application in patients with recurrent ileocolic CD is less well described. Our aim was to assess whether or not a laparoscopic approach was safe, feasible, and conferred meaningful short-term benefits in this patient population.Patients undergoing LAP surgery for recurrent ileocolic CD at our institution from 1998-2008 were identified using a prospectively maintained database. Potential risk factors for conversion to open surgery and overall patient outcomes were assessed with univariate analysis.Forty patients were identified, of which 30 (75%) were LAP-completed and 10 (25%) were LAP-converted. The groups did not differ with respect to clinicopathological features. LAP-converted patients were significantly more likely to require adhesiolysis than LAP-completed patients (100% versus 67%, P = 0.04). There was 1 intraoperative complication in a converted patient. LAP-converted patients had longer times to soft diet (4 versus 3 days, P = 0.03) and longer length of stay (7 versus 4 days, P = 0.003). The groups did not differ with respect to incidence of postoperative complications or frequency of readmission within 30 days. There was no mortality.In up to 20% of patients with recurrent ileocolic, successful laparoscopic re-resection may be prevented by adhesions. Conversion increased the length of stay without increasing morbidity. We conclude that LAP surgery can be safely performed in selected patients with recurrent ileocolic CD and leads to short-term benefits. (Inflamm Bowel Dis 2010;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21184">
<title>Outcome after surveillance of low-grade and indefinite dysplasia in patients with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21184</link>
<description><![CDATA[The management of low-grade (LGD) and indefinite dysplasia (IND) in patients with ulcerative colitis (UC) remains controversial, as outcomes after a diagnosis of LGD or IND in previous studies vary widely.All patients evaluated were from a single institution referral center who had a history of UC and a diagnosis of either LGD or IND between 1994 and 2008 as confirmed by 2 expert gastrointestinal (GI) pathologists. Data were collected by chart review of electronic and paper medical records. All patients who did not undergo a colectomy within 90 days of their dysplasia diagnosis were included in the final analysis. Hazard ratios for risk factors as well as incidence rates and Kaplan-Meier estimates were used to calculate the progression to high-grade dysplasia (HGD) or colorectal cancer (CRC).Thirty-five patients were included in the analysis, of whom 2 patients with IND and 2 patients with LGD developed HGD or CRC over a mean duration of 49.8 months. In total, the incident rate for advanced neoplasia for all patients was 2.7 cases of HGD or CRC per 100 person-years at risk. For flat and polypoid LGD the incident rate of advanced neoplasia was 4.3 and 1.5 cases per 100 person-years at risk, respectively. Patients with primary sclerosing cholangitis (PSC) had an incident rate of 10.5 cases per 100 years of patient follow-up.We report a low rate of progression to HGD or CRC in patients who underwent surveillance for LGD or IND; polypoid dysplasia showed less risk of progression than flat dysplasia. (Inflamm Bowel Dis 2010;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21183">
<title>Preserved Na+/H+ exchanger isoform 3 expression and localization, but decreased NHE3 function indicate regulatory sodium transport defect in ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21183</link>
<description><![CDATA[A major causative factor of diarrhea in ulcerative colitis (UC) patients is the loss of Na+ absorptive capacity of the inflamed colonic mucosa. Potential contributing mechanisms include reduced driving force for active transport, and impaired expression, mislocalization, or defective transport function of Na+ absorptive proteins. We therefore studied the expression, brush border membrane (BBM) localization, and transport capacity of the major intestinal Na+ absorptive protein, the Na+/H+ exchanger isoform 3 (NHE3) in biopsies from UC patients.In UC and control biopsies, inflammation was graded histologically, NHE3, tumor necrosis factor alpha (TNF-[alpha]), villin, as well as other housekeeping genes were analyzed by quantitative real-time polymerase chain reaction (PCR), BBM localization of NHE3 determined by immunohistochemistry, and confocal microscopy. Na+ absorptive capacity was assessed by 22Na+ isotope fluxes and NHE3 transport activity measured microfluorometrically in BCECF-loaded surface colonocytes within isolated crypts.In mildly, moderately, and severely inflamed sigmoid colon of UC patients, neither NHE3 mRNA expression nor the abundance of NHE3 in the BBM was significantly altered compared to other structural components of the BBM. However, Na+ absorption was strongly reduced by [ap]80% and acid-activated NHE3 transport activity was significantly decreased in the surface cells of sigmoid colonic crypts even in moderately inflamed mucosa.In the colonic mucosa of patients with active UC, NHE3 transport capacity was found significantly decreased despite correct NHE3 location and abundance in the brush border, independent of current treatment. These findings suggest functional NHE3 transport as a novel factor for inflammatory diarrhea in UC patients. (Inflamm Bowel Dis 2010;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21178">
<title>Enhanced expression of proproliferative and antiapoptotic genes in ulcerative colitis-associated neoplasia</title>
<link>http://dx.doi.org/10.1002%2Fibd.21178</link>
<description><![CDATA[Inflammatory bowel diseases including long-standing ulcerative colitis (UC) have an increased risk of evolving into colorectal cancer (CRC). The overexpression of some proproliferative and antiapoptotic genes, such as survivin, telomerase catalytic subunit (hTERT), integrin-linked kinase (ILK), and regulatory factors c-MYB and Tcf-4, has been implicated in the development and progression of several human malignancies including CRC.In this study we analyzed the expression alterations of these markers and proinflammatory enzymes cyclooxygenase 2 (COX-2) and inducible nitric oxide synthase (iNOS) during the transition of colonic mucosa from chronic inflammation to epithelial neoplasia in biopsies of UC patients using quantitative real-time polymerase chain reaction and immunohistochemistry; additionally, we compared the expression profiles of this gene panel in samples of patients with CRC after tumor resection and in human tumor xenografts of SW620 malignant colonic cells.The transcript levels of survivin, c-MYB, COX-2, iNOS, and Tcf-4 showed a statistically significant increase during neoplastic transformation of UC patient colonic mucosa, whereas hTERT and ILK were not elevated. In contrast, the specimens of CRC showed upregulated expression of not only survivin, c-MYB, Tcf-4, COX-2, and iNOS but also hTERT. A similar expression profile was observed in human tumor xenografts in which all transcripts with the exception of c-MYB were upregulated.These results suggest that telomerase and ILK activation occurs during the later stages of carcinoma progression, whereas upregulation of survivin, c-MYB, and Tcf-4 is a feature of the early stage of development of neoplasia, and thus, they might serve as early indicators for UC-associated colorectal carcinogenesis. (Inflamm Bowel Dis 2010;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21165">
<title>Periportal cuffing in inflammatory bowel diseases: Mystery of stars and stripes</title>
<link>http://dx.doi.org/10.1002%2Fibd.21165</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21179">
<title>Serum anti-glycan antibodies predict complicated Crohn&#x27;s disease behavior: A cohort study</title>
<link>http://dx.doi.org/10.1002%2Fibd.21179</link>
<description><![CDATA[A high proportion of patients with Crohn's disease (CD) over time develop complications like fistulae and strictures, requiring surgery. We tested a panel of antiglycan antibodies for predicting the occurrence of complications and CD-related surgery in an adult patient cohort.Serum samples of 149 CD patients of the German inflammatory bowel disease (IBD) network were tested for the presence of anti-laminarin IgA (Anti-L), anti-chitin IgA (Anti-C), anti-chitobioside IgA (ACCA), anti-laminaribioside IgG (ALCA), anti-mannobioside IgG (AMCA), and anti-Saccaromyces cerevisiae IgG (gASCA) carbohydrate antibodies by enzyme-linked immunosorbent assay (ELISA) (IBDX® panel, Glycominds, Lod, Israel) in a blinded fashion. Clinical data were available on occurrence of complicated disease or CD-related surgery as well as disease activity, onset, and location.The median follow-up of the patients without any previous complication or surgery at time of sample procurement was 53.7 months. Overall, 26.3% developed a complication and 17.1% underwent CD-related surgery, respectively. Positivity for gASCA, AMCA, ACCA, and Anti-L alone or an increasing frequency of positive serum antibodies independently predicted a faster progression toward a more severe disease course. Once a complication or surgery had occurred only positivity for Anti-L or more than 3 markers out of the whole panel indicated progression to an additional surgery or complication. The antibody status of most patients remained stable over time.This is the first study showing the clinical value of serum antiglycan antibodies for prediction of a more complicated disease course in adult patients with CD. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21177">
<title>Enhanced translocation of bacteria across metabolically stressed epithelia is reduced by butyrate</title>
<link>http://dx.doi.org/10.1002%2Fibd.21177</link>
<description><![CDATA[The gut microflora in some patients with Crohn's disease can be reduced in numbers of butyrate-producing bacteria and this could result in metabolic stress in the colonocytes. Thus, we hypothesized that the short-chain fatty acid, butyrate, is important in the maintenance and regulation of the barrier function of the colonic epithelium.Confluent monolayers of the human colon-derived T84 or HT-29 epithelial cell lines were exposed to dinitrophenol (DNP (0.1 mM), uncouples oxidative phosphorylation) + Escherichia coli (strain HB101, 106 cfu) ± butyrate (3-50 mM). Transepithelial resistance (TER), and bacterial internalization and translocation were assessed over a 24-hour period. Epithelial ultrastructure was assessed by transmission electron microscopy.Epithelia under metabolic stress display decreased TER and increased numbers of pseudopodia that is consistent with increased internalization and translocation of the E. coli. Butyrate (but not acetate) significantly reduced the bacterial translocation across DNP-treated epithelia but did not ameliorate the drop in TER in the DNP+E. coli exposed monolayers. Inhibition of bacterial transcytosis across metabolically stressed epithelia was associated with reduced I-[kappa]B phosphorylation and hence NF-[kappa]B activation.Reduced butyrate-producing bacteria could result in increased epithelial permeability particularly in the context of concomitant exposure to another stimulus that reduces mitochondria function. We speculate that prebiotics, the substrate for butyrate synthesis, is a valuable prophylaxis in the regulation of epithelial permeability and could be of benefit in preventing relapses in IBD. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21176">
<title>Variants at the 3p21 locus influence susceptibility and phenotype both in adults and early-onset patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21176</link>
<description><![CDATA[To date, a number of high-profile studies have yielded over 50 inflammatory bowel disease (IBD) disease genes/loci. The polymorphisms rs9858542 (BSN) and rs3197999 (MST1), on 3p21 locus, have been found associated with susceptibility to IBD. We aimed to replicate these associations in adult and early-onset cohorts of IBD Italian patients, by analyzing also potential gene-gene interactions with variants in NOD2/CARD15, IL23R, ATG16L1, and IRGM genes, and investigating genotype-phenotype correlation.In all, 1808 patients with IBD, 855 with Crohn's disease (CD) and 953 with ulcerative colitis (UC), including 539 patients with their initial diagnosis <19 years of age, and 651 controls were analyzed for SNPs rs9858542 and rs3197999.BSN and MST1 were significantly associated with either CD (Prs9858542 2.5 × 10-7; Prs3197999 3.9 × 10-7), and UC (Prs9858542 = 3.1 × 10-4; Prs3197999 = 8 × 10-4). Prevalence of these variants was significantly increased in both adult and early-onset IBD patients. After stepwise logistic regression, the 2 variants were associated in adult UC with distal colitis (Prs9858542 = 0.013, odds ratio [OR] = 2.04, 95% confidence interval [CI] = 1.16-3.59; Prs3197999 = 0.018, OR 1.9, 95% CI 1.2-3.3), while the rs3197999 variant was inversely associated with occurrence of extraintestinal manifestations in adult CD(P = 0.017, OR 0.6, 95% CI 0.4-0.9).We confirmed the association of BSN and MST1 with IBD susceptibility, either in the adult or the early-onset cohorts. These variants appeared to influence either the distal location of the disease in the UC cohort and extraintestinal manifestations in CD patients. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21162">
<title>Should patients under long-term anti-TNF therapies be followed for tuberculosis contamination?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21162</link>
<description><![CDATA[No Abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21181">
<title>Management of inflammatory bowel diseases: A changing paradigm. Can we finally change the disease course?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21181</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21187">
<title>Risk of ischemic stroke in patients with Crohn&#x27;s disease: A population-based nested case-control study</title>
<link>http://dx.doi.org/10.1002%2Fibd.21187</link>
<description><![CDATA[Observational studies have linked Crohn's disease (CD) to an increased risk of venous thromboembolic complications. Case reports of ischemic stroke in CD patients have raised the question of a similar association, but data from observational studies are lacking.Using data from the UK General Practice Research Database we conducted a nested case-control analysis within a population-based cohort of 8054 patients with and 161,078 patients without CD. A total of 1748 cases of ischemic stroke were identified to whom 17,348 controls were matched on age, sex, and year of cohort entry. Adjusted odds ratios (ORs) of ischemic stroke associated with CD were calculated by conditional logistic regression. Stratified analyses were performed for age and sex.While CD was not associated with an overall increased risk of ischemic stroke (OR 1.10, 95% confidence interval [CI] 0.85-1.43), stratified analyses revealed an increase in risk in younger patients (<50 years: OR 2.93; 95% CI 1.44-5.98) but not in elderly patients ([ge]50 years: OR 0.99; 95% CI 0.75-1.30; P for interaction <0.01). The interaction with age remained statistically significant even after changing the cutoff value for the younger and older age group to 45, 55, or 60 years in a sensitivity analysis. There was no interaction with sex (P = 0.79).The study indicates that younger patients with CD may be under an increased risk of ischemic stroke. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21185">
<title>Low-dose naltrexone for treatment of duodenal Crohn&#x27;s disease in a pediatric patient</title>
<link>http://dx.doi.org/10.1002%2Fibd.21185</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21175">
<title>Characterization of the novel ST2/IL-33 system in patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21175</link>
<description><![CDATA[ST2 has been proposed to be a regulator of inflammation and Th1/Th2 balance. ST2L is the IL-33 membrane receptor and belongs to the IL-1R family. The soluble variant, ST2s, is identical to the extracellular region of ST2L and competes for IL-33 binding, inhibiting receptor signaling. Although ST2s has been associated with inflammatory processes in patients with sepsis, trauma, asthma, and autoimmunity, until now there are no reported studies showing the role of ST2/IL-33 in inflammatory bowel disease (IBD).Expression of ST2 and IL-33 was determined in serum and colonic biopsies from IBD patients. ST2 transcript and protein was determined by reverse-transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA)/immunoblot, respectively, and IL-33 protein by ELISA. Intestinal mucosa localization of ST2 and IL-33 was conducted by immunofluorescence.ST2s transcript in the colonic mucosa was mainly expressed in UC patients rather than Crohn's disease or control; however, ST2L mRNA remained constant in all samples. Total ST2 protein was significantly higher in mucosa samples from patients with active UC, with a predominant induction of ST2s that strongly correlates with serum ST2 levels. Mucosa IL-33 levels were higher in UC patients and serum levels were barely detected in all patient groups. ST2 and IL-33 are both abundantly expressed in the cytoplasm of epithelial cells of control subjects; however, in ulcerative colitis patients ST2 decreases and IL-33 showed cytoplasm-nuclear redistribution.The novel association between the ST2/IL-33 system and IBD seems to identify that variations in this axis might regulate the inflammatory process in these diseases. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21174">
<title>Genome wide association (GWA) predictors of anti-TNF[alpha] therapeutic responsiveness in pediatric inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21174</link>
<description><![CDATA[Interindividual variation in response to anti-TNF[alpha] therapy may be explained by genetic variability in disease pathogenesis or mechanism of action. Recent genome-wide association studies (GWAS) in inflammatory bowel disease (IBD) have increased our understanding of the genetic susceptibility to IBD. The aim was to test associations of known IBD susceptibility loci and novel "pharmacogenetic" GWAS identified loci with primary nonresponse to anti-TNF[alpha] in pediatric IBD patients and develop a predictive model of primary nonresponse.Primary nonresponse was defined using the Harvey Bradshaw Index (HBI) for Crohn's disease (CD) and partial Mayo score for ulcerative colitis (UC). Genotyping was performed using the Illumina Infinium platform. Chi-square analysis tested associations of phenotype and genotype with primary nonresponse. Genetic associations were identified by testing known IBD susceptibility loci and by performing a GWAS for primary nonresponse. Stepwise multiple logistic regression was performed to build predictive models.Nonresponse occurred in 22 of 94 subjects. Six known susceptibility loci were associated with primary nonresponse (P < 0.05). Only the 21q22.2/BRWDI loci remained significant in the predictive model. The most predictive model included 3 novel "pharmacogenetic" GWAS loci, the previously identified BRWD1, pANCA, and a UC diagnosis (R2 = 0.82 and area under the curve [AUC] = 0.98%). The relative risk of nonresponse increased 15-fold when number of risk factors increased from 0-2 to [ge]3.The combination of phenotype and genotype is most predictive of primary nonresponse to anti-TNF[alpha] in pediatric IBD. Defining predictors of response to anti-TNF[alpha] may allow the identification of patients who will not benefit from this class of therapy. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21133">
<title>Elevated IL-13R[alpha]2 in intestinal epithelial cells from ulcerative colitis or colorectal cancer initiates MAPK pathway</title>
<link>http://dx.doi.org/10.1002%2Fibd.21133</link>
<description><![CDATA[Chronic inflammation in ulcerative colitis (UC) is a sizeable risk factor for colorectal cancer (CRC). Interleukin-13 (IL-13) is elevated in the UC mucosa and may induce dysregulated signaling in neighboring intestinal epithelial cells (IECs) and thus function as a tumorogenic cytokine.Expression of IL-13 receptor chains on IECs obtained from control or chronically inflamed mucosa and colonic tumors was quantified by flow cytometry and immunoblot. IL-13R[alpha]1 and IL-13R[alpha]2 expression was significantly increased on IEC from UC and CRC patients compared to control and Crohn's disease (CD) subjects. Purified IEC from these subjects and cell lines expressing varying ratios of IL-13R[alpha]1 and IL-13R[alpha]2 chains were stimulated with IL-13 in vitro to investigate by immunoblot the activation of the signal transducer and activator of transcription 6 (STAT6) and mitogen activated protein kinase (MAPK) signaling pathways.Despite similarly elevated receptor expression in UC and CRC, IL-13 does not activate the STAT6 or MAPK pathways in UC, while in colonic tumors only the STAT6 pathway is activated. Using neutralizing antibodies and cell lines expressing a range of surface densities for IL-13R[alpha]1 and IL-3R[alpha]2, we demonstrate that IL-13R[alpha]2 serves a dual role, initiating MAPK signaling at low concentrations and as an inhibitory, decoy receptor at high IL-13R[alpha]2 to IL-13R[alpha]1 ratios.IL-13R[alpha]2 is both a decoy receptor and induces MAPK signal transduction, depending on its relative expression and the local concentration of IL-13, which together modulate the balance and intensity of the signaling pathways initiated in UC and CRC. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21127">
<title>Efficacy and safety of certolizumab pegol induction therapy in an unselected Crohn&#x27;s disease population: Results of the FACTS survey</title>
<link>http://dx.doi.org/10.1002%2Fibd.21127</link>
<description><![CDATA[Switzerland was the first country to approve certolizumab pegol (Cimzia, CZP) for the treatment of patients with moderate to severe Crohn's disease (CD) in September 2007. This phase IV study aimed to evaluate the efficacy and safety of CZP in a Swiss multicenter cohort of practice-based patients.Baseline and Week 6 evaluation questionnaires were sent to all Swiss gastroenterologists in hospitals and private practices. Disease activity was assessed with the Harvey-Bradshaw Index (HBI) and adverse events were evaluated according to WHO guidelines.Fifty patients (31 women, 19 men) were included; 56% had complicated disease (stricture or fistula) and 52% had undergone prior CD-related surgery. All patients had prior exposure to systemic steroids, 96% to immunomodulators, 78% to infliximab, and 50% to adalimumab. A significant decrease in HBI was observed at Week 6 (versus Week 0) following induction therapy with CZP 400 mg subcutaneously at Weeks 0, 2, and 4 (12.6 ± 4.7 Week 0 versus 6.2 ± 4.4 Week 6, P < 0.001). Response and remission rates at Week 6 were 54% and 40%, respectively. We identified 8/11 CD patients undergoing a 50% fistula response (P = 0.021). The frequency of adverse drug reactions attributed to CZP was 6%. CZP was continued in 80% of patients beyond Week 6.In a population of CD patients with complicated disease behavior, CZP induced a response and remission in 54% and 40% of patients, respectively. This series provides the first evidence of the effectiveness of CZP in perianal fistulizing CD. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21180">
<title>Ocular manifestations in a community-based cohort of patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21180</link>
<description><![CDATA[Ophthalmologic diseases in patients with inflammatory bowel disease (IBD) have been reported with varying frequency, mostly from tertiary referral centers. The aim was to describe the spectrum of ophthalmologic conditions in patients with IBD in a community setting and to compare it with a control non-IBD cohort.A prospective cohort of patients with Crohn's disease (CD), ulcerative colitis (UC), and non-IBD controls underwent evaluation by an ophthalmologist, including visual acuity, slit-lamp exam, and assessment of lacrimal output.The ophthalmologic exam was completed in 112 subjects; 48 with CD, 40 with UC, and 24 controls. Active intestinal disease was present in 52/88 (59%) of the IBD patients, and 79/88 (89%) were taking 5-aminosalicylates (5-ASAs). The IBD and control populations had similar age and gender profiles. Patients with IBD were more likely to report ocular symptoms (odds ratio [OR] 5.6, 95% confidence interval [CI] 1.5-20), particularly dry eyes (OR 5.3, 95% CI 1.4-19), than the control population. On objective exam, 42% of IBD patients had evidence of dry eyes. In a univariate analysis, 5-ASA use was associated with an increased risk of ocular symptoms (OR 7.4, 95% CI 0.9-64), and 5-ASA use >3 g per day was associated with an increased odds ratio of dry eyes (OR 15, 95% CI 1.9-122). Active disease was not associated with eye symptoms or dry eyes. Other eye conditions such as episcleritis, uveitis, or cataracts were infrequent in this cohort.Patients with IBD in the community frequently have dry eyes. This is associated with 5-ASA use, particularly doses >3 g per day. Whether this is a surrogate marker of disease severity is unclear. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21173">
<title>Can fecal calprotectin or lactoferrin identify postoperative recurrence in Crohn&#x27;s disease?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21173</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21135">
<title>Interleukin 21 expression is increased in rectal biopsies from patients with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21135</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21134">
<title>CD24 is upregulated in inflammatory bowel disease and stimulates cell motility and colony formation</title>
<link>http://dx.doi.org/10.1002%2Fibd.21134</link>
<description><![CDATA[We investigated whether CD24 (reportedly a stem cell marker and adhesion molecule) was expressed in regenerative mucosa in inflammatory bowel disease (IBD) and whether it could be functionally relevant.CD24 expression was examined in 10 cases of IBD and the relationship of CD24 with Wnt signaling was tested using dominant negative (DN)-TCF4 expression. For functional evaluation, CD24 was 1) cloned and forcibly expressed in HCT116 (which expresses very low levels of CD24) and 2) knocked-down by RNA interference in HT29 (which expresses high levels of CD24). The effect of altered CD24 expression on proliferation/apoptosis, staurosporine-induced apoptosis, colony formation in soft agar, migration, and invasion was examined.CD24 was not expressed in normal tissue, while 10/10 cases of IBD showed CD24 upregulation. Inhibition of Wnt signaling with DN-TCF4 caused CD24 downregulation. Forced expression of CD24 did not influence cell proliferation, apoptosis, or staurosporine-induced apoptosis but it did significantly enhance colony forming efficiency (P < 0.01). Furthermore, there was increased transwell migration (P < 0.001) and invasion (P < 0.03) and there was increased cell migration in wounding assays. Conversely, knockdown of CD24 reduced transwell migration (P < 0.01) and invasion (P < 0.01) and reduced cell motility in wounding assays. CD24 knockdown did not influence proliferation, apoptosis resistance, or staurosporine-induced apoptosis.This is the first study to report upregulation of CD24 in regenerating tissue in IBD. This may be regulated by Wnt signaling and can confer enhanced colony forming ability and enhanced cell motility - features that may be important in tissue healing in the colon. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21131">
<title>Quality and publication success of abstracts of randomized clinical trials in inflammatory bowel disease presented at Digestive Disease Week</title>
<link>http://dx.doi.org/10.1002%2Fibd.21131</link>
<description><![CDATA[The incorporation of abstracts from scientific meetings into systematic reviews and practice guidelines may reduce publication bias and delays in implementing therapeutic interventions.All abstracts of Phase III randomized controlled trials in inflammatory bowel disease accepted at Digestive Disease Week (1998-2003) were identified. MedLine, PubMed (1997-current), EMBASE, and Google Scholar were searched for subsequent full publications. Characteristics of methodology and outcomes of the abstracts and articles were analyzed.The 5-year cumulative publication rate of the 82 eligible abstracts was 78%. Abstracts that presented negative results were less likely to be published than those with positive findings, particularly after the first 2 years (hazard ratio 6.45; 95% confidence interval [CI]: 2.22-18.7) with 5-year cumulative publication rates of (50% versus 91%, respectively, P < 0.001). The median time to publication was longer for negative than positive abstracts (58 versus 26 months, P < 0.001). Abstracts selected for oral presentation were more likely to be published than poster presentations (89% versus 69%; P = 0.03). A change in primary outcome results was observed in 28% (n = 18) of abstracts compared to that in the final publication, and 6% (n = 4) had a statistically significant change resulting in a change of study conclusions.Our findings suggest that the use of abstract data would enable detection and mitigation of publication bias. Improving the uniformity and quality of abstract reporting of randomized clinical trials at scientific meetings may facilitate their incorporation in practice guidelines and systematic reviews. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21130">
<title>Nutriose, a prebiotic low-digestible carbohydrate, stimulates gut mucosal immunity and prevents TNBS-induced colitis in piglets</title>
<link>http://dx.doi.org/10.1002%2Fibd.21130</link>
<description><![CDATA[We investigated a prebiotic low-digestible carbohydrate (LDC) as a possible food ingredient to stimulate bowel functions in the treatment of inflammatory bowel disease. The study aimed to assess a fermentable dextrin fiber (Nutriose) and its relationship to the immune management of the disease and the microbiota profile in colitis-bearing piglets.In a randomized placebo-controlled parallel blind preclinical study, 32 male piglets were fed LDC (4% Nutriose) or dextrose placebo for 44 days before being challenged with trinitrobenzene sulfonic acid (TNBS) to induce colitis. We followed the microbiota profile using real-time polymerase chain reaction (PCR) targeted to 9 bacterial genera. Secretory IgA was evaluated by enzyme-linked immunosorbent assay (ELISA). Inflammatory protein profiles were monitored in blood and colonic tissues. Both histological scoring of biopsy samples and live endoscopic scoring were used to measure colitis development.Prior and continuing LDC supplementation alleviated the symptoms of colitis (body weight loss, bloody stools) induced by a TNBS challenge. This effect was associated with an improvement in endoscopic and histological scores. LDC was shown to selectively downregulate some of the proinflammatory factors and their concomitant pyretic events and to stimulate the Th2-related immune pathway (IL-10 and s-IgA).At the dose tested, LDC is a well-tolerated prebiotic agent able to not only stimulate butyrogenic bacteria strains and reduce intestinal transit disorders and energy intake, but also to prevent chronic inflammatory intestinal injuries. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21129">
<title>Asymmetric endoscopic inflammation of the ileal pouch: A sign of ischemic pouchitis?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21129</link>
<description><![CDATA[Pouchitis is associated with dysbiosis and dysregulated mucosal immunity, although secondary pouchitis with special etiologic factors, such as ischemia, can occur. The aim was to describe a disease phenotype of the ileal pouch with an endoscopic appearance suggestive of ischemia.We identified consecutive patients with endoscopic asymmetric inflammation of the pouch (inflammation of side of the pouch with a completely normal other limb of the pouch one limb and a sharp demarcation along the staple suture line). Patients with Crohn's disease (CD) of the pouch or antibiotic-responsive pouchitis, matched for duration of the pouch, served as controls. Histology slides of mucosal biopsies were re-reviewed independently by 2 blinded gastrointestinal pathologists. Demographic, clinical, endoscopic, histologic, and imaging characteristics were compared between the groups.Ten patients with "ischemic" pouchitis, 15 with CD of the pouch, and 15 with antibiotic-responsive pouchitis were studied. Pyloric gland metaplasia was observed only in the groups with CD of the pouch (23.1%) or antibiotic-responsive pouchitis (13.3%). Of patients with "ischemic" pouchitis, 80% had extracellular hemosiderin or hematoidin deposits (versus 30.8% those with CD of the pouch and 13.3% of those with pouchitis, P = 0.003). The majority of patients (80%) with "ischemic" pouchitis did not respond to conventional antibiotic therapy. It appeared that subsequent abdominal surgeries after pouch construction and a history of postoperative portal vein thrombi were associated with "ischemic" pouchitis.Endoscopic asymmetric inflammation of the pouch may represent an ischemia-associated pouchitis with characteristic clinical, radiographic, and histologic features. Its hemodynamic, cellular, and molecular basis of mechanism warrants further study. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21128">
<title>Health-related quality of life of youth with inflammatory bowel disease: A comparison with published data using the PedsQL 4.0 generic core scales</title>
<link>http://dx.doi.org/10.1002%2Fibd.21128</link>
<description><![CDATA[This study compared youth and parent-proxy reports of health-related quality of life (HRQoL) among youth with inflammatory bowel disease (IBD) to published comparison group data and examined concordance between youth and parent-proxy reports of HRQoL.One hundred thirty-six youth and parent-proxy reports on the PedsQL 4.0 Generic Core Scales were compared to published data from chronically ill, acutely ill, and healthy comparison groups using independent samples t-tests. Reporter agreement was examined using paired samples t-tests and intraclass correlations (ICCs).Youth with IBD reported lower psychosocial functioning than the healthy comparison group, higher physical and social functioning than the chronically ill group, and lower school functioning than all published comparison groups. Parent-proxy reports of youth HRQoL were higher than the chronically ill group, but lower than the healthy group on all scales except psychosocial functioning. Youth with active IBD reported lower physical health domain scores than youth with inactive disease. Concordance between youth and parent-proxy reports was moderate, with the lowest agreement in school and social functioning.Youth with IBD and their parents rate HRQoL as lower than healthy youth but do not perceive the impact of IBD to be as limiting as in other chronic conditions. Youth report suggests that IBD may be particularly detrimental to HRQoL in the school functioning domain. Moderate agreement between parent and youth reports substantiates continued use of multiple informants in studies of pediatric HRQoL. Inflamm Bowel Dis 2010]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21171">
<title>The path to Crohn&#x27;s disease: Is mucosal pathology a secondary event?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21171</link>
<description><![CDATA[Current models of Crohn's disease (CD) invoke an initial disturbance of the epithelial interface between the gut mucosa and intestinal microbiota. This "outside-in" paradigm, mirroring the pathophysiology of acute gastroenteritis, suggests that mucosal damage by luminal bacteria is an early, initiating factor in the etiopathogenesis of disease. However, a number of features of CD argue against a primary mucosal process, including phenotypic studies of CD patients that point to a macrophage defect and genetic studies that predict impaired innate immunity to intracellular bacteria. Intracellular pathogens, such as Listeria, Salmonella, and Mycobacteria, invade via the gastrointestinal tract with minimal or no acute mucosal pathology. These organisms then infect and persist in lymphatic tissues before inducing pathology, in the gut or elsewhere, as a secondary process. In a disease resulting from impaired macrophage responses to intracellular pathogens, mucosal damage could instead represent a terminal event in the pathogenesis of disease. Such an "inside-out" model is also compatible with observations on postoperative disease relapses where subepithelial pathology precedes ulceration. This alternative disease paradigm suggests that clinical and experimental research efforts should be directed at deeper processes in the gut wall and attached mesentery to understand how intracellular bacteria could initiate or exacerbate this chronic inflammatory disease. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21170">
<title>Ulcerative colitis in northern Portugal and Galicia in Spain</title>
<link>http://dx.doi.org/10.1002%2Fibd.21170</link>
<description><![CDATA[Clinical and therapeutic patterns of ulcerative colitis (UC) are variable in different world regions. The purpose of this study was to examine two close independent southern European UC populations from 2 bordering countries and observe how demographic and clinical characteristics of patients can influence the severity of UC.A cross-sectional study was conducted during a 15-month period (September 2005 to December 2006) based on data of 2 Web registries of UC patients. Patients were stratified according to the Montreal Classification and disease severity was defined by the type of treatment taken.A total of 1549 UC patients were included, 1008 (65%) from northern Portugal and 541 (35%) from Galicia (northwest Spain). A female predominance (57%) was observed in Portuguese patients (P < 0.001). The median age at diagnosis was 35 years and median years of disease was 7. The majority of patients (53%) were treated only with mesalamine, while 15% had taken immunosuppressant drugs, and 3% biologic treatment. Most patients in both groups were not at risk for aggressive therapy. Extensive colitis was a predictive risk factor for immunosuppression in northern Portugal and Galicia (odds ratio [OR] 2.737, 95% confidence interval [CI]: 1.846-4.058; OR 5.799, 95% CI: 3.433-9.795, respectively) and biologic treatment in Galicia (OR 6.329, 95% CI: 2.641-15.166). Younger patients presented a severe course at onset with more frequent use of immunosuppressors in both countries.In a large population of UC patients from two independent southern European countries, most patients did not require aggressive therapy, but extensive colitis was a clear risk factor for more severe disease. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21169">
<title>Subepithelial dendritic B cells in orofacial granulomatosis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21169</link>
<description><![CDATA[Orofacial granulomatosis (OFG) is a chronic, disfiguring, granulomatous inflammation of the lips and oral mucosa. The pathogenesis is unknown, but it has been linked previously to Crohn's disease (CD) and more recently to dietary sensitivity. The oral mucosa is an immunologically responsive site associated with the generation of protective mucosal and systemic immune responses to vaccination and also hyperresponsiveness to allergens in some individuals. Classically, immune responses in oral mucosa are considered to be mediated by mucosa-associated lymphoid tissues (MALT), secondary lymphoid follicles that are intimately associated with epithelia.Immunohistochemistry was used to investigate the inflammatory infiltrate in OFG and control tissue samples. Polymerase chain reaction (PCR), cloning of PCR products, and sequencing were used to characterize the local immunoglobulin gene profile in OFG.We describe large, active, dendritic B cells in oral mucosa that were not associated with any organized lymphoid tissues in the local subepithelial microenvironment. They express activation induced cytidine deaminase, which is essential for immunoglobulin gene diversification by somatic hypermutation and class switch recombination. IgE is also expressed by these B cells. They do not align with any other previously described B-cell subset in secondary lymphoid tissues in terms of morphology, proliferative activity, or phenotype.These subepithelial dendritic B cells may contribute to the immune responsiveness of the oral mucosa, including IgE-mediated allergic responses. In patients with OFG, further understanding of the role these cells play in oral immunity may lead to novel therapeutic possibilities. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21168">
<title>Magnetic resonance follow-through imaging for evaluation of disease activity in ileal Crohn&#x27;s disease: An observational, retrospective cohort study</title>
<link>http://dx.doi.org/10.1002%2Fibd.21168</link>
<description><![CDATA[Magnetic resonance follow-through (MRFT) is a new cross-sectional imaging modality with the potential to accurately stage ileal Crohn's disease (CD), while avoiding ionizing radiation and the discomfort associated with enteroclysis. We aimed to assess the reliability of this technique in assessing the extent and activity of ileal CD, and to assess its influence on subsequent management.Out of a total of 342 patients undergoing MRFT between 2004 and 2008, 221 were performed in 191 patients with confirmed CD. Case notes were reviewed in detail with documentation of all investigations pre- and post-MRFT. Agreement between inflammatory markers, histopathology, and MRFT findings was determined.Overall, 116/221 (52.5%) of MRFTs showed active ileal CD, and 76/221 (34.4%) quiescent CD, while 29/221 (13.1%) were suboptimal. Overall, 66 strictures and 18 fistulae were identified. There was substantial agreement between active ileal CD on MRFT and histopathology (n = 59; [kappa] = 0.66; P = 0.0006; sensitivity 85.1%, specificity 85.7%) and fecal calprotectin (n = 14; [kappa] = 0.72; P = 0.047), while C-reactive protein (CRP) showed moderate agreement (n = 107; [kappa] = 0.402; P = 0.00028). Management was influenced by MRFT reports following active (52/84, 62% treated medically) or quiescent (48/62, 77.4% managed conservatively) disease. Fibrotic strictures were predominantly treated surgically (7/14, 50%). In all, 13/32 (40.6%) patients with inflammatory ileal strictures required surgery, mostly due to steroid-resistant disease. Overall, 75 MR findings were documented in 221 MRFTs, including 1 renal cancer.MRFT provides accurate information on ileal CD activity, with close agreement to inflammatory markers and histopathology. It represents a substantial advance in the staging of CD, while avoiding painful enteroclysis and radiation exposure in young patients. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21167">
<title>Targeting TGF-[beta]1 by employing a vaccine ameliorates fibrosis in a mouse model of chronic colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21167</link>
<description><![CDATA[Intestinal fibrosis and stricture formation are major complications of inflammatory bowel disease (IBD), for which there are currently few effective treatments. We sought to investigate whether targeting transforming growth factor-beta1 (TGF-[beta]1), a key profibrotic mediator, with a peptide-based virus-like particle vaccine would be effective in suppressing intestinal fibrosis by using a mouse model of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced chronic colitis.The vaccine was prepared by inserting a peptide derived from mouse TGF-[beta]1 into a carrier hepatitis B core antigen using gene recombination methods. Chronic colitis was induced in BALB/c mice by 8 weekly TNBS administrations. Mice were subcutaneously injected with vaccine, carrier, or phosphate-buffered saline (PBS) in 2 separate studies: either before or after acute inflammatory responses commenced.Sera from vaccinated mice exhibited significantly elevated levels of TGF-[beta]1-specific immunoglobulin G (IgG), which inhibited TGF-[beta]1-induced luciferase production in mink lung epithelial cells. In the chronic colitis model, mice receiving vaccine showed improved body weight gain and significantly reduced colonic collagen deposition. Hematoxylin and eosin staining and semiquantitative scoring indicated that vaccination even ameliorated colonic inflammation. Cytokine profile analysis revealed that levels of TGF-[beta]1, interleukin (IL)-17, and IL-23 in vaccinated mouse colon tissues were decreased, and that percentages of IL-17-expressing CD4+ lymphocytes in mesenteric lymph node cells were reduced. Furthermore, Smad3 phosphorylation, a key event in TGF-[beta] signaling, was decreased in colonic tissue in vaccinated mice.This TGF-[beta]1 peptide-based vaccine, which suppressed excessive TGF-[beta]1 bioactivity, may prevent the development of intestinal fibrosis and associated complications, presenting a novel approach in the treatment of IBD. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21166">
<title>Methotrexate for maintenance of remission in chronic active Crohn&#x27;s disease: Long-term single-center experience and meta-analysis of observational studies</title>
<link>http://dx.doi.org/10.1002%2Fibd.21166</link>
<description><![CDATA[According to current guidelines methotrexate (MTX) should be considered as a second-line immunomodulator in patients with chronic active Crohn's disease (CD) if purine analogs are not tolerated or there is a lack of efficacy. However, its therapeutic role remains controversial to the present day.Medical records of all eligible patients treated in the outpatient clinic of the Johann Wolfgang Goethe-University Hospital between December 2000 and January 2009 were reviewed.Sixty-three patients were identified. The mean duration of treatment was 100 weeks (range, 2-364 weeks) with a mean cumulative dose of MTX of 2130 mg (range, 40-9005 mg). In 50 (79%) patients started on MTX clinical remission could be achieved within 3 months of treatment. The cumulative probability of these patients to maintain remission was 95.3%, 89.5%, 70.6%, and 62.8% at 6 months, 1, 2, and 3 years of treatment, respectively. The respective figures of the meta-analysis were 94%, 86%, 75%, 53%, and 43. Drug-related side effects were reported in 50 patients (79%), leading to withdrawal of MTX in 21 cases (33%).Along with previous observations our data demonstrate the efficacy of MTX as a second-line immunomodulator in chronic active CD. However, its use is limited due to intolerable side effects in a large proportion of patients. The results should encourage further research in order to establish the definite significance of MTX in chronic active CD. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21164">
<title>Impact of prior irregular infliximab dosing on performance of long-term infliximab maintenance therapy in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21164</link>
<description><![CDATA[Infliximab is efficacious in the management of moderate to severe Crohn's disease (CD). There are limited data regarding performance of infliximab in patients who require reinitiation of maintenance dosing following previous irregular exposure.This was a retrospective, observational study of CD patients treated with maintenance infliximab beyond 3 years. Maintenance infliximab infusion regimens were categorized as scheduled maintenance (SM) (maintenance infusions q [le]8 weeks after loading) or prior irregular (PI) (no loading, gap in therapy >8 weeks prior to or during maintenance therapy). We examined differences in need for medical and surgical hospitalizations as well as associated healthcare costs between the 2 groups.In all, 104 CD patients met criteria for 3-year maintenance infliximab treatment (SM n = 64; PI n = 40). The rates of CD-related surgeries (60.9% and 55.0%, P = not significant [N.S.]) and medical hospitalizations (35.9% and 37.5%, P = N.S.) prior to infliximab initiation was similar between the 2 groups. However, the rate of medical (26.5% versus 47.5%, P = 0.035) and surgical hospitalizations (21.8% versus 48.7%, P = 0.009) were significantly lower in the SM compared to the PI group. During the third year of treatment the excess costs per patient for the PI group compared to the SM group amounted to $11,464 in spite of both cohorts being on SM therapy.Patients who begin and continue an uninterrupted maintenance dosing regimen had a lower incidence of hospitalization and surgery than those who received an irregular or interrupted regimen prior to beginning an SM regimen. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21132">
<title>Lipopolysaccharide exposure is linked to activation of the acute phase response and growth failure in pediatric Crohn&#x27;s disease and murine colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21132</link>
<description><![CDATA[Systemic exposure to lipopolysaccharide (LPS) has been linked to clinical disease activity in adults with inflammatory bowel disease (IBD). We hypothesized that markers of LPS exposure and the acute phase response (APR) would be increased in pediatric IBD patients with growth failure, and that LPS signaling would be required for induction of the APR in murine colitis.Serum markers of LPS exposure, endotoxin core IgA antibody (EndoCAb), and the APR, LPS binding protein (LBP) were quantified in pediatric IBD patients and controls. LBP and cytokine production were determined after administration of trinitrobenzene sulfonic acid (TNBS) enemas to mice with genetic deletion of Toll-Like receptor 4 (TLR4), and wildtype (WT) controls.Serum EndoCAb and LBP were significantly elevated in patients with Crohn's disease (CD), compared to disease controls with ulcerative colitis (UC) and healthy controls (P < 0.001). This was independent of disease activity or location. CD patients with elevated serum EndoCAb and LBP exhibited linear growth failure which persisted during therapy. Serum LBP increased in WT mice following TNBS administration, in conjunction with increased serum TNF-[alpha], IL-6, and IL-10, and expansion of regulatory T-cell numbers. Both the APR and expansion of foxp3+ T cells were abrogated in TLR4-deficient mice, in conjunction with a reduction in acute weight loss.LPS exposure and a persistent APR are associated with growth failure in pediatric CD. LPS signaling is required for the APR in murine colitis. Therapies targeting this pathway may benefit the subset of patients with refractory growth failure. (Inflamm Bowel Dis 2010)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21159">
<title>Randomized, double-blind, placebo-controlled trial of the oral interleukin-12/23 inhibitor apilimod mesylate for treatment of active Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21159</link>
<description><![CDATA[Interleukin-12 (IL-12) and interleukin-23 (IL-23) are inflammatory cytokines linked to the Th-1 and Th-17 phenotypes associated with Crohn's disease (CD). We investigated the activity and safety of apilimod mesylate (formerly STA-5326), an oral IL-12 and IL-23 inhibitor, in patients with active CD.We performed a multicenter, Phase 2, randomized, double-blinded, placebo-controlled study to evaluate the efficacy of apilimod mesylate in treating 220 adult patients with moderate-to-severe CD (Crohn's Disease Activity Index [CDAI] score 220-450). Patients were stratified according to C-reactive protein (CRP) levels and corticosteroid use and were randomly assigned to receive placebo or apilimod mesylate 50 mg daily or 100 mg daily. The study was divided into an induction phase (43 days) and a maintenance phase (125 days). The primary analysis involved a comparison of the proportion of patients experiencing clinical response, defined as at least a 100-point decrease in CDAI score from baseline at day 29. Data on adverse events were also collected.In all, 220 of the planned 282 patients were enrolled when the Data Monitoring Committee determined that the drug was not efficacious as a treatment and closed enrollment. A clinical response was experienced by 18 patients (24.7%) in the 50-mg daily (QD) group (n = 73) and 19 patients (25.7%) in the 100 mg QD group (n = 74), as compared with 21 patients (28.8%) in the placebo group (n = 73) on day 29 (P = 0.71 for each comparison). No significant adverse safety signal was observed.Apilimod was well-tolerated but did not demonstrate efficacy over placebo in patients with active CD. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21156">
<title>Validation of the Spanish version of a questionnaire to measure quality of care through the eyes of patients with inflammatory bowel disease (QUOTE-IBD)</title>
<link>http://dx.doi.org/10.1002%2Fibd.21156</link>
<description><![CDATA[Crohn's disease (CD) and ulcerative colitis (UC) are chronic immunoinflammatory diseases that place a considerable burden on patients, their families, and society. Quality of care plays an important role for patients. A questionnaire to measure quality of care through the eyes of patients with inflammatory bowel disease (QUOTE-IBD) has been designed and validated specifically for the English language and culture. The objective was to translate the QUOTE-IBD into Spanish and to determine its validity in patients with IBD.This is a prospective study in 2 phases: first, translation and validation of the Spanish QUOTE-IBD. Translation was based on the validated QUOTE-IBD. Second, once the complete translation was finished, comprehension of the items was assessed with a specific questionnaire in a reduced number of patients. Criterion validity was assessed with the Pearson's correlation coefficient between scores of the QUOTE-IBD and visual analog scales (VAS). In order to analyze the reproducibility of the Spanish QUOTE-IBD, the questionnaire was completed by stable patients twice, with a span of time of at least 4 weeks.A total of 103 patients (CD: 61, UC: 42) were included in the study. Pearson's correlation coefficient between total care Spanish QUOTE-IBD and VAS of health care items was 0.34 (P < 0.001). Correlations among all 6 care dimensions score of Spanish QUOTE-IBD and VAS were statistically significant (P < 0.01). Results of first and second administration of total care and dimensional care scores of Spanish QUOTE-IBD in 46 stable patients were not different.The Spanish QUOTE-IBD has proved to be a valid instrument to measure the quality of health care for patients with CD and UC. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21163">
<title>Single-port access laparoscopic surgery for complex Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21163</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21160">
<title>Outcome of medical treatment of stricturing and penetrating Crohn&#x27;s disease: A retrospective study</title>
<link>http://dx.doi.org/10.1002%2Fibd.21160</link>
<description><![CDATA[Outcomes of medical treatment in patients with stricturing and penetrating Crohn's disease (CD) are not well characterized.Adults with stricturing and penetrating CD who underwent medical treatment from 2004 to 2008 were evaluated. We assessed response rates to medical treatment, time to relapse or surgery, and postoperative complications.In all, 53 patients underwent medical therapy. 60% had stricturing disease, 11% had penetrating, and 28% had both. Disease location was ileal in 38%, colonic in 2%, and ileocolonic in 60%. At 30, 60, and 90 days, 54%, 60%, and 64% experienced a response to medical therapy, respectively. At 30 days, 75% of patients with ileal CD responded to therapy compared to 38% of patients with ileocolonic CD (P = 0.026). Overall, 64% of patients required surgery. Patients with ileocolonic disease required surgery at 0.55 years versus 1.07 years in patients with ileal disease (P = 0.023). 24% of patients experienced an anastomotic leak, fistula, or abscess (IASC). 29% of patients with penetrating disease developed IASC compared to 6% of patients with stricturing disease (P = 0.047). 32% of patients on biologic therapy had IASC compared to 0% of those not on biologics (P = 0.059).The outcomes of medical treatment of stricturing or penetrating CD are poor, as 64% ultimately require surgery. Important factors that seem to be associated with either failed therapy include ileocolonic or colonic disease location. We report a high rate of IASC, especially in patients with penetrating disease and those treated with biologic therapy. This should be considered prior to attempted medical therapy. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21155">
<title>TLR9 mRNA expression is upregulated in patients with active ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21155</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21150">
<title>Angiopoietin-2 in experimental colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21150</link>
<description><![CDATA[The pathophysiology of inflammatory bowel disease (IBD) includes leukocyte infiltration, blood and lymphatic remodeling, weight loss and protein enteropathy. The roles of angiopoietin-2 (Ang-2) in initiating gut inflammation, leukocyte infiltration and angiogenesis are not well understood.Disease activity index, histopathological scoring, myeloperoxidase assay, immunohistochemistry and sodium dodecyl sulphate- polyacrylamide gel electrophoretic methods were employed in the present study to addess the roles of Ang-2 in experimental colitis.Several important differences were seen in the development of experimental IBD in Ang-2-/- mice. Although weight change and disease activity differ only slightly in WT and Ang-2-/- + DSS treated mice, leukocyte infiltration, inflammation and blood and lymphatic vessel density is significantly attenuated compared to WT + DSS mice. Gut capillary fragility and water export (stool blood and form) appear significantly earlier in Ang-2-/- + DSS mice vs. WT. Colon lengths were also significantly reduced in Ang-2-/- and gut histopathology was less severe in Ang-2-/- compared to WT + DSS. Lastly, the decrease in serum protein content in WT + DSS was less severe in Ang-2-/- + DSS, thus protein losing enteropathy (PLE) a feature of IBD is relieved by Ang-2-/-.These data demonstrate that in DSS colitis, Ang-2 mediates inflammatory hemangiogenesis, lymphangiogenesis and neutrophil infiltration to reduce some, but not all clinical features of IBD. The implications for Ang-2 manipulation in the development of IBD and other inflammatory diseases and treatments involving Ang-2 are discussed. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21122">
<title>Fine-scale geographic variations of inflammatory bowel disease in France: Correlation with socioeconomic and house equipment variables</title>
<link>http://dx.doi.org/10.1002%2Fibd.21122</link>
<description><![CDATA[In a previous study we found a north-south gradient for Crohn's disease (CD) incidence in France. The aim of the present study was to determine if socioeconomic factors may influence the geographic distribution of CD and ulcerative colitis (UC) in France.Using the national health insurance databases, incidence rates of CD and UC were estimated for each of 341 metropolitan "job areas" in 2000-2002. Relationships between incidence rates and relevant contextual variables from the 1999 French census were tested for significance using a Poisson regression. Mapping of smoothed relative risks (sRR) for CD and UC at the scale of job areas, using a Bayesian approach and adjusting for significant contextual variables, was carried out in order to search for geographic variations.CD incidence rates were negatively related to the percentage of farmers and to the percentage of housing with bathroom and toilets and positively related to the unemployment rate and to the percentage of households below the poverty threshold. Mapping of sRR for CD showed a clear north-south gradient, which was slightly improved after including the percentage of farmers and the percentage of housing with toilets. In UC we found no significant correlation between either incidence and socioeconomic variables or incidence and house equipment variables, and there was no north-south gradient. However, there was a positive and significant correlation between CD and UC incidence.The present study shows that geographic risk factors of CD in France are northern latitude, nonrural areas, and areas with poor sanitary house equipment. Among these factors the most important is northern latitude. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21161">
<title>Exogenous alkaline phosphatase for the treatment of patients with moderate to severe ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21161</link>
<description><![CDATA[Increased activity of intestinal alkaline phosphatase (AP) occurs locally in patients with ulcerative colitis (UC), aimed at repairing inflammatory tissue damage. We evaluated the safety and preliminary efficacy of exogenous AP administered to patients with UC in an open-label, first-in-patient exploratory trial, conducted in the Internal Medicine and Gastroenterology hospital departments in the Czech Republic and Italy.Twenty-one patients were enrolled (13 females), age 23-54 years, with steroid- and/or immunosuppressant-refractory, moderate/severe UC (Mayo score 6-11). Oral AP enzyme 30,000 U was administered daily for 7 days, intraduodenally. Efficacy outcomes were changes in Mayo score at Day 21 posttreatment; changes in Modified Truelove-Witts Severity index (MTWSI) at Days 21, 63; C-reactive protein and stool calprotectin levels at Days 7, 21, 63. Safety evaluations were adverse events and laboratory abnormalities reported up to Day 63 posttreatment.No clinically relevant adverse events causing withdrawal or considered serious, or laboratory abnormalities or antibody formation against AP were observed. Mayo scores were significantly decreased at Day 21, and MTWSI at Days 21 and 63. C-reactive protein and stool calprotectin levels were decreased at Days 21 and 63. Clinical response on the Mayo score after a single 7-day AP course was 48% at Day 21.In this uncontrolled trial, administration of exogenous AP enzyme daily over a 7-day course to patients with UC was associated with short-term improvement in disease activity scores, with clinical effects being observed within 21 days and associated with reductions in C-reactive protein and stool calprotectin. AP enzyme treatment was well tolerated and nonimmunogenic. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21158">
<title>Babesiosis in a patient on infliximab for Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21158</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21157">
<title>Campylobacter concisus and other Campylobacter species in children with newly diagnosed Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21157</link>
<description><![CDATA[Campylobacter concisus and other members of the Campylobacter genus have recently been suggested as possible etiological agents of Crohn's disease (CD). To further investigate this issue we determined the prevalence of these organisms in pediatric patients newly diagnosed with CD.DNA was extracted from fecal specimens collected from 54 children with CD, 27 noninflammatory bowel disease (non-IBD), and 33 healthy controls and subjected to polymerase chain reaction (PCR) sequencing.Detection of C. concisus DNA using a newly developed PCR assay targeting the 16S rRNA gene of C. concisus showed that 65% (35/54) of fecal samples from CD children were positive, a prevalence significantly higher than that in the healthy (33%, 11/33, P = 0.008) and non-IBD controls (37%, 10/27, P = 0.03). The prevalence of all Campylobacter DNA using genus-specific primers in children with CD was 72% (39/54), which was significantly higher than the 30% (10/33, P = 0.0002) and 30% (8/27, P = 0.0003) observed in healthy and non-IBD controls, respectively.Given the strengthening evidence for a significantly higher prevalence of C. concisus and other non-jejuni Campylobacter species in pediatric CD, investigation into the role of these non-jejuni Campylobacter species in the initiation of human IBD is clearly a priority. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21154">
<title>Safety of immunomodulators and biologics for the treatment of inflammatory bowel disease during pregnancy and breast-feeding</title>
<link>http://dx.doi.org/10.1002%2Fibd.21154</link>
<description><![CDATA[The aim of this article is to critically review available data regarding the safety of immunomodulators and biological therapies during pregnancy and breast-feeding in women with inflammatory bowel disease. Methotrexate and thalidomide can cause congenital anomalies and are contraindicated during pregnancy (and breast-feeding). Although thiopurines have a Food and Drug Administration (FDA) rating D, available data suggest that these drugs are safe and well tolerated during pregnancy. Although traditionally women receiving azathioprine or mercaptopurine have been discouraged from breast-feeding because of theoretical potential risks, it seems that these drugs may be safe in this scenario. Treatment with cyclosporine for steroid-refractory ulcerative colitis (UC) during pregnancy can be considered safe and effective, and the use of this drug should be considered in cases of severe UC as a means of avoiding urgent surgery. Breast-feeding is contraindicated for patients receiving cyclosporine. Biological therapies appear to be safe in pregnancy, as no increased risk of malformations has been demonstrated. Therefore, the limited clinical results available suggest that the benefits of infliximab and adalimumab in attaining response and maintaining remission in pregnant patients might outweigh the theoretical risks of drug exposure to the fetus. Stopping therapy in the third trimester may be considered, as it seems that transplacental transfer of infliximab is low prior to this. Certolizumab differs from infliximab and adalimumab in that it is a Fab fragment of an antitumor necrosis factor alpha monoclonal antibody, and therefore it may not be necessary to stop certolizumab in the third trimester. The use of infliximab is probably compatible with breast-feeding. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21153">
<title>Diagnostic value of noninvasive combined fluorine-18 labeled fluoro-2-deoxy-D-glucose positron emission tomography and computed tomography enterography in active Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21153</link>
<description><![CDATA[The role of combined localized positron emission tomography (lPET) and computed tomography enterography (CTe) in Crohn's disease is unclear. We examined if this imaging modality using fluorine-18 labeled-fluoro-2-deoxy-D-glucose (FDG) could more effectively identify disease activity.52 lPET-CTe scans were analyzed in this retrospective study. CTe scores and FDG uptake were quantified. Correlations of CTe scores and standard uptake value (SUV) with C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), short Inflammatory Bowel Disease Questionnaire (sIBDq), and Harvey-Bradshaw index (HBI) were estimated using Pearson analysis. Imaging scores were compared to medical outcome by logistics regression model.CTe scores correlated with SUV, but additional abnormal segments of small bowel were not identified. In all, 38 (79%) abnormal CTe segments demonstrated increased FDG uptake with mean SUVmax 4.77; 10 (21%) abnormal CTe segments lacked FDG accumulation, with mean SUVmax 1.27. There was no correlation between SUVmax and CRP, ESR, sIBDq, or HBI. There were no significant differences in clinical indices, biochemical parameters, and presence of multiple abnormal segments between medical responders and uptake were associated with failed medical therapy (P = 0.001).PET scanning added to CTe did not identify additional abnormal segments when compared to CTe alone. Abnormal segments with mucosal enhancement on CTe that did not accumulate FDG were significantly associated with failure of medical therapy. A larger trial is warranted to confirm if combined lPET-CTe has an important role in the clinical management of stricturing Crohn's disease. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21147">
<title>Prevalence of hepatitis B and C and risk factors for nonvaccination in inflammatory bowel disease patients in Northeast France</title>
<link>http://dx.doi.org/10.1002%2Fibd.21147</link>
<description><![CDATA[Data regarding the prevalence of hepatitis C (HCV) and hepatitis B (HBV) in inflammatory bowel disease (IBD) patients are conflicting.In all, 315 IBD (252 Crohn's disease [CD] and 63 ulcerative colitis [UC]) patients were consecutively recruited between June 2005 and May 2009.The median age was 33 years (interquartile range [IQR]: 24-43) and median disease duration was 5 years (IQR: 2-11). Present and/or past HBV and HCV infection was found in 2.86% of 315 patients (CD: HBsAg 0.79%, anti-HBc 2.78%, anti-HCV 0.79%; UC: HBsAg 1.59%, anti-HBc 1.59%, anti-HCV 1.59%). Effective vaccination (anti-HBs without anti-HBc) was present in 48.9% of 315 patients. In multivariate analysis, age at diagnosis over 31 years (odds ratio [OR] 0.29; 95% confidence interval [CI] 0.15-0.58; P = 0.005), disease duration over 7 years (OR 0.43; 95% CI 0.23-0.83; P = 0.005), age at inclusion over 33 years (OR 0.44; 95% CI 0.20-0.94; P = 0.005), and CD (OR 0.29; 95% CI 0.15-0.58; P = 0.005) were associated with the lack of effective vaccination. Two HBsAg-positive patients, including 1 under curative nucleoside/nucleotide analog treatment, had received 6 and 7 infliximab infusions, and 1 HCV RNA-positive subject had been receiving corticosteroid and azathioprine therapies for 12 and 33 months, respectively. No viral reactivation occurred in these patients.The prevalence of HBV and HCV infection in French IBD patients is similar to that of the general population. While the ECCO recommends an effective HBV vaccination in IBD, half of the patients were not vaccinated. The nonvaccination risk factors identified in our study may allow targeted vaccination coverage. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21149">
<title>Tissue factor -1208D&#x3E;I polymorphism is associated with D-dimer levels in patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21149</link>
<description><![CDATA[No abstract]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21148">
<title>Novel model of TH2-polarized chronic ileitis: The SAMP1 mouse</title>
<link>http://dx.doi.org/10.1002%2Fibd.21148</link>
<description><![CDATA[SAMP1/Yit mice develop spontaneous, segmental, transmural ileitis recapitulating many features of Crohn's disease (CD). The ileitic phenotype may have arisen during crosses of SAMP1 mice selected for the presence of skin lesions. We hereby describe that the original SAMP1 strain similarly develops ileitis. Our aim was to characterize the histopathological and immunological features of this model and assess its responsiveness to standard inflammatory bowel disease (IBD) therapy.The time course of histopathological features of ileitis was assessed. Immune compartments were characterized by flow cytometry. Ileal cytokine profiles and transcription factors were determined by real-time reverse-transcription polymerase chain reaction (RT-PCR). Finally, response to corticosteroid therapy and its effect on immune compartments and cellularity was evaluated.Histological features and time course of disease were conserved, compared to those reported in SAMP1/Yit strains, with similar expansion of CD19+, CD4+, and CD8+ effector (CD44high CD62Llow), and central memory lymphocytes (CD44highCD62Lhigh). However, different from SAMP1/YitFc mice, analysis of ileal cytokine profiles revealed initial TH1 polarization followed by TH2-polarized profile accompanied by prominent eosinophilia during late disease. Lastly, corticosteroids attenuated ileitis, resulting in decreased lymphocyte subsets and cellularity of compartments.Here we report that the ileitic phenotype of SAMP1-related strains was already present in the original SAMP1 strain. By contrast, the cytokine profile within the terminal ilea of SAMP1 is distinct from the mixed TH1/TH2 profile of SAMP1/YitFc mice during late disease, as it shows predominant TH2 polarization. Dissemination of these strains may advance our understanding of CD pathogenesis, which in 60% of patients involves the terminal ileum. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21146">
<title>Cdcs1 a major colitis susceptibility locus in mice; Subcongenic analysis reveals genetic complexity</title>
<link>http://dx.doi.org/10.1002%2Fibd.21146</link>
<description><![CDATA[The cytokine-deficiency-induced colitis susceptibility (Cdcs)1 locus is a major modifier of murine inflammatory bowel disease (IBD) and was originally identified in experimental crosses of interleukin-10-deficient (Il10-/-) mice. Congenic mice, in which this locus was reciprocally transferred between IBD-susceptible C3H/HeJBir-Il10-/- and resistant C57BL/6J-Il10-/- mice, revealed that this locus likely acts by inducing innate hypo- and adaptive hyperresponsiveness, associated with impaired NF-[kappa]B responses of macrophages. The aim of the present study was to dissect the complexity of Cdcs1 by further development and characterization of reciprocal Cdcs1 congenic strains and to identify potential candidate genes in the congenic interval.In total, 15 reciprocal congenic strains were generated from Il10-/- mice of either C3H/HeJBir or C57BL/6J genetic backgrounds by 10 cycles of backcrossing. Colitis activity was monitored by histological grading. Candidate genes were identified by fine mapping of congenic intervals, sequencing, microarray analysis, and a high-throughput real-time reverse-transcription polymerase chain reaction (RT-PCR) approach using bone marrow-derived macrophages.Within the originally identified Cdcs1-interval, 3 independent regions were detected that likely contain susceptibility-determining genetic factors (Cdcs1.1, Cdcs1.2, and Cdcs1.3). Combining results of candidate gene approaches revealed Fcgr1, Cnn3, Larp7, and Alpk1 as highly attractive candidate genes with polymorphisms in coding or regulatory regions and expression differences between susceptible and resistant mouse strains.Subcongenic analysis of the major susceptibility locus Cdcs1 on mouse chromosome 3 revealed a complex genetic structure. Candidate gene approaches revealed attractive genes within the identified regions. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21144">
<title>MDP-NOD2 stimulation induces HNP-1 secretion, which contributes to NOD2 antibacterial function</title>
<link>http://dx.doi.org/10.1002%2Fibd.21144</link>
<description><![CDATA[Human neutrophil peptide 1 (HNP-1) is a defensin with antibacterial activity secreted by various cells as a component of the innate immune host defense. NOD2 is a cytoplasmic protein that recognizes bacterial derived muramyl dipeptide, and is involved in bacterial clearance. The aim of the present study was to investigate the relationship between antibacterial activity of NOD2 and HNP-1 expression in epithelial cell lines.Gentamicin protection assay using Salmonella typhimurium was performed in Caco-2 cells. The mRNA level was determined by quantitative reverse-transcription polymerase chain reaction (RT-PCR) and defensin expression was assessed by Western blot and enzyme-linked immunosorbent assay (ELISA). Nuclear factor-[kappa]B activation was assessed using pIV luciferase and Renilla plasmids. A NOD2 mutant was generated by site-directed mutagenesis.Among the defensins tested, only HNP-1 expression is induced in colonic epithelial model HCT116 cells after MDP-LD stimulation. HNP-1 secretion is significantly increased after MDP-LD stimulation in the cell supernatant of intestinal epithelial cells expressing endogenous NOD2, but not in cells that lack endogenous NOD2 expression. HNP-1 is required for NOD2-dependent NF-[kappa]B activation after MDP-LD stimulation since hnp-1 siRNA transfection abrogated the response to MDP-LD stimulation. The antibacterial function of NOD2 against S. typhimurium was impaired when expression of HNP-1 was blocked by siRNA.HNP-1 secretion depends on NOD2 stimulation by MDP-LD and contributes to antibacterial activity in intestinal epithelial cells expressing endogenous NOD2, but not NOD2 3020insC mutant associated with increased susceptibility to Crohn's disease. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21138">
<title>Surgery for low-grade colorectal dysplasia in ulcerative colitis: Decisions, decisions</title>
<link>http://dx.doi.org/10.1002%2Fibd.21138</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21114">
<title>A33 antigen-deficient mice have defective colonic mucosal repair</title>
<link>http://dx.doi.org/10.1002%2Fibd.21114</link>
<description><![CDATA[A33 antigen is a transmembrane protein expressed predominantly in normal intestinal epithelium and most colon cancers and cell lines. The function of A33 antigen is unclear, but indirect evidence indicates a role in cell adhesion, trafficking, and the gut immune response. The aim of this study was to determine the contribution made by A33 antigen in mediating colonic repair following colitis induction in the A33 antigen-deficient mutant mouse.Colitis was induced by treatment with TNBS/ethanol. A33 antigen-deficient or wildtype mice were sacrificed at 0, 3, 7, and 14 days after colitis induction and morphological damage, mucosal proliferation, and inflammatory cell infiltration were quantified. In a subsequent study, following the induction of colitis mice were monitored for 22 days and morbidity and mortality determined.Mice lacking A33 antigen expression were compromised in their ability to resolve TNBS-induced damage and exhibited distinct crypt pathology. In A33 antigen-deficient mice morphological damage remained unresolved at 14 days postcolitis induction. Increases in colonic cell proliferation were delayed in A33 antigen-deficient mice, and the rate of crypt fission was increased after TNBS treatment. Commensurate with these observations, polymorphonuclear cell infiltration was suppressed in the absence of A33 antigen. Mortality following colitis induction was 20% higher in A33 antigen-deficient mice than in wildtype controls.Mice deficient in A33 antigen expression show impaired resolution of hapten-induced mucosal damage, leading to increased mortality, associated with impaired epithelial cell proliferation and a suppressed adaptive immune response. This study suggests a contribution for A33 antigen in the colonic healing response following mucosal damage. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21124">
<title>TL1A produced by lamina propria macrophages induces Th1 and Th17 immune responses in cooperation with IL-23 in patients with Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21124</link>
<description><![CDATA[Tumor necrosis factor (TNF)-like protein 1A (TL1A) is a member of the TNF superfamily and contributes to the pathogenesis of Crohn's disease (CD) by stimulating T-helper (Th) 1 cells. In addition to Th1, recent studies have focused on the role of Th17 cells in the pathogenesis of CD. Here we tried to clarify the role of TL1A in Th1 and Th17 immunity in CD.TL1A expression was assessed by quantitative reverse-transcription polymerase chain reaction (RT-PCR) in lamina propria (LP) macrophages (LP-M[phis]s) from normal controls (NC) and patients with CD or ulcerative colitis (UC). Purified LP CD4+ T cells were stimulated with TL1A and/or IL-23 and interferon gamma (IFN-[gamma]) and interleukin (IL)-17 levels were analyzed. We also examined the effect of TL1A on naïve CD4+ T-cell differentiation.We found that LP-M[phis]s are a major producer of TL1A. TL1A expression was markedly enhanced in LP-M[phis]s from CD patients compared with NC or UC patients. IL-23, in addition to TL1A, was induced in LP-M[phis]s by commensal bacteria stimulation. TL1A and IL-23 synergistically promoted the production of IFN-[gamma] and IL-17 by LP T cells, while TL1A alone did not induce cytokine production. Furthermore, TL1A promoted Th17 differentiation from naïve T cells by LP-M[phis]s; however, IL-23 did not show any synergistic effects on Th17 differentiation.TL1A expressed in LP-M[phis]s might play an important role in the pathogenesis of CD by inducing Th1 and Th17 immunity. IL-23 differentially regulated these functions of TL1A on memory and naïve T cells. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21152">
<title>Natural history of Crohn&#x27;s disease: Comparison between childhood- and adult-onset disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21152</link>
<description><![CDATA[Childhood-onset Crohn's disease (CD) might reflect a more severe form of disease. To test this hypothesis we analyzed the long-term natural history of CD in an adult cohort of patients with childhood-onset compared to adult-onset CD.We selected 206 childhood-onset CD patients among 2992 adult patients with a diagnosis of CD established before December 31, 2000. Disease characteristics were prospectively assessed during follow-up until December 2007 and compared to adult-onset CD patients matched 2 to 1 on gender, year of CD diagnosis, and disease location.Compared to adult-onset CD, patients with childhood-onset CD were more likely to have a severe disease, with an increased year-by-year disease activity index (37% of patient-years in childhood-onset group versus 31% in the adult-onset group, P < 0.001). Immunosuppressant requirement was also increased with a 10-year cumulative risk of 54 ± 3% in childhood-onset CD group versus 45 ± 2%, in the adult-onset CD group (P < 0.001). Cumulative risks of stricturing and penetrating complications and surgical resections were not statistically different between groups. Accordingly, these events occurred at a younger age in the childhood-onset CD group. At the age of 30 years the actuarial risk of having undergone an extensive intestinal resection was 48 ± 5% in the childhood-onset group versus 14 ± 2% in the adult-onset group (P < 0.001).Patients with childhood-onset CD exhibit a more active disease and require more immunosuppressive therapy. This feature is observed irrespective of the disease location, suggesting an intrinsic more severe phenotype. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21151">
<title>Interleukin-19 protects mice from innate-mediated colonic inflammation</title>
<link>http://dx.doi.org/10.1002%2Fibd.21151</link>
<description><![CDATA[Inflammatory bowel disease (IBD) results from the chronic dysregulation of the mucosal immune system and the aberrant activation of both the innate and the adaptive immune responses. We used two complementary models of colonic inflammation to examine the roles of interleukin (IL)-19 in colonic inflammation and thus its possible role in IBD.Using gene-targeting, we generated IL-19-deficient mice. To study the activation of the innate immune response during colonic inflammation we characterized an innate immune-mediated model of colitis induced by dextran sulfate sodium (DSS). DSS can induce not only acute colitis but also chronic colitis. In addition to the acute DSS-induced colitis model, we used a chronic DSS-induced colitis model that is associated with the activation of both Th1 and Th2 cytokines as well as innate immune response in the colon.We show that IL-19-deficient mice are more susceptible to experimental acute colitis induced by DSS, and this increased susceptibility is correlated with the accumulation of macrophages and the increased production of IFN-[gamma], IL-1[beta], IL-6, IL-12, TNF-[alpha], and KC. Additionally, cytokine production in IL-19-deficient macrophages was enhanced on stimulation of lipopolysaccharide (LPS) through reduced phosphorylation of STAT1 and STAT3. Moreover, our results clearly demonstrate that IL-19 is required for B-cell infiltration during chronic DSS-induced colitis, which may be mediated by IL-13 and IL-6.The finding that IL-19 drives pathogenic innate immune responses in the colon suggests that the selective targeting of IL-19 may be an effective therapeutic approach in the treatment of human IBD. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21145">
<title>Inflammatory bowel disease in young people: The case for transitional clinics</title>
<link>http://dx.doi.org/10.1002%2Fibd.21145</link>
<description><![CDATA[The incidence of inflammatory bowel disease (IBD) is increasing among adolescents. In all, 25% of patients are diagnosed before the age of 16, when they are traditionally transferred from the pediatric to the adult service.We conducted a retrospective case-controlled study to characterize patients treated in a novel transitional adolescent-young adult IBD clinic. This compared disease extent, radiation exposure, therapeutic strategy, and requirement for surgery in 100 adolescents with controls from our adult IBD clinic matched for disease duration.The median (range) ages for the adolescent and adult population was 19 (16-28) and 43 (24-84), with a median age at diagnosis of 15 (3-26) and 39 (13-82) respectively (P < 0.001). Crohn's disease was significantly more common in the adolescents. Disease distribution was ileocolonic in 69% of adolescents and 28% of adults, restricted to the ileum in 20% of adolescents and 47% of adults, and colonic only in 11% and 22%, respectively. Upper gastrointestinal involvement occurred in 23% of adolescents, but was not seen in adults (P < 0.01). Total ulcerative colitis was seen in 67% of adolescents and 44% of adults (P < 0.01). Contrary to previous data adolescents did not receive more ionizing radiation than adults. Requirement for immunosuppressive therapy was higher in the adolescent group (53% versus 31%, respectively, P < 0.01). Likewise, 20% of adolescents had required biological therapy compared to only 8% in the adult cohort (P < 0.05).Gastroenterologists should recognize that IBD is more complex when presenting in adolescence and our data support the creation of specific adolescent transitional clinics. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21142">
<title>Genome-wide gene expression analysis of mucosal colonic biopsies and isolated colonocytes suggests a continuous inflammatory state in the lamina propria of patients with quiescent ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21142</link>
<description><![CDATA[Genome-wide gene expression (GWGE) profiles of mucosal colonic biopsies have suggested the existence of a continuous inflammatory state in quiescent ulcerative colitis (UC). The aim of this study was to use DNA microarray-based GWGE profiling of mucosal colonic biopsies and isolated colonocytes from UC patients and controls in order to identify the cell types responsible for the continuous inflammatory state.Adjacent mucosal colonic biopsies were obtained endoscopically from the descending colon in patients with active UC (n = 8), quiescent UC (n = 9), and with irritable bowel syndrome (controls, n = 10). After isolation of colonocytes and subsequent extraction of total RNA, GWGE data were acquired using Human Genome U133 Plus 2.0 GeneChip Array (Affymetrix, Santa Clara, CA). Data analysis was carried out by principal component analysis and projection to latent structure-discriminant analysis using the SIMCA-P 11 software (Umetrics, Umeå, Sweden).A clear separation between active UC, quiescent UC, and control biopsies were found, whereas the model for the colonocytes was unable to distinguish between quiescent UC and controls. The differentiation between quiescent UC and control biopsies was governed by unique profiles containing gene expressions with significant fold changes. These primarily belonged to the family of homeostatic chemokines, revealing a plausible explanation for the abnormal regulated innate immune response seen in patients with UC.This study has demonstrated the presence of a continuous inflammatory state in quiescent UC, which seems to reflect an altered gene expression profile of lamina propria cells. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21141">
<title>Magnetic resonance imaging for Crohn&#x27;s disease: Is this really the end of colonoscopy?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21141</link>
<description><![CDATA[No abstract]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21139">
<title>The good, the bad, and the ugly: Adverse events and Crohn&#x27;s therapies</title>
<link>http://dx.doi.org/10.1002%2Fibd.21139</link>
<description><![CDATA[No abstract]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21137">
<title>Perianal fistulae in Crohn&#x27;s Disease: Current and future approaches to treatment</title>
<link>http://dx.doi.org/10.1002%2Fibd.21137</link>
<description><![CDATA[Perianal fistulae are common in Crohn's disease but rarely heal without treatment. The main aim of treatment is to effectively close the fistula without affecting sphincter integrity and continence. Traditional surgical and medical approaches are not without their limitations and may result in either comorbidity, such as fecal incontinence, or incomplete healing of the fistulae. Over the last 2 decades these limitations have led to a paradigm shift toward the use of biomaterials, and more recently cell-based therapies, which have met with variable degrees of success. This review discusses the traditional and current methods of treatment, as well as emerging and possible alternative approaches that may improve fistula healing. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21136">
<title>Fecal calprotectin variability in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21136</link>
<description><![CDATA[No abstract]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21123">
<title>Colocolic intussusception in a patient with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21123</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21140">
<title>Clostridium difficile and inflammatory bowel disease: More questions than answers?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21140</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21143">
<title>Crohn&#x27;s disease patient with right lower quadrant abdominal pain for 20 years due to an appendiceal neuroma (Fibrous obliteration of the appendix)</title>
<link>http://dx.doi.org/10.1002%2Fibd.21143</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21119">
<title>Ulcerative colitis in a Southern European country: A national perspective</title>
<link>http://dx.doi.org/10.1002%2Fibd.21119</link>
<description><![CDATA[The incidence, prevalence, and even the clinical behavior of ulcerative colitis (UC) are highly variable in different world regions. In previous studies, Portugal was reported as having a milder clinical behavior. The aim of this study was to apply the Montreal Classification in a large group of UC Portuguese patients in order to describe their clinical characteristics and evaluate variables potentially useful for outcome prediction.A cross-sectional study based on data collected from a nationwide online registry was undertaken.In all, 2863 patients with UC were included. Twenty-one percent had ulcerative proctitis, 52% left-sided colitis, and 28% extensive colitis. Sixty percent of patients had taken steroids, 14% immunosuppressors, 1% biologicals, and 4.5% were submitted to surgery. Patients with extensive colitis had more severe activity, needing more steroids, immunosuppressors, and surgery. At the time of diagnosis 61% were less than 40 years old and 5% less than 16. Younger patients also had a more aggressive initial course. Thirty-eight percent of patients had only taken salicylates during the disease course and were characterized by a lower incidence of systemic symptoms at presentation (3.8% versus 8.8%, P < 0.001), fewer extraintestinal manifestations (7.7% versus 24.0%, P < 0.001), and a higher prevalence of proctitis (32.1% versus 10.0%).A more aggressive phenotype was found in extensive colitis and in the initial course of younger patients, with an increased need for steroids and immunosuppressors. In addition, a significant percentage of patients, particularly with proctitis, showed a milder clinical evolution and were maintained in remission only with salicylates. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21113">
<title>Cerebral thromboembolic events in pediatric patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21113</link>
<description><![CDATA[There is a recognized association between pediatric inflammatory bowel disease (IBD) and cerebral thromboembolic events (CTEs). Historical reporting had described the association as strongest between ulcerative colitis (UC), rather than Crohn's disease (CD). We describe the incidence and outcome of CTE in pediatric IBD patients from a single center over 5 years and the relative proportion of stroke reported in the literature in patients with UC and CD before and after January 2000.Demographic data were extracted on all newly diagnosed cases of IBD in our center from January 2003 to January 2008 to ascertain patient characteristics, disease type, risk factors for CTE, modality of neuroimaging, and outcome. A literature search was performed to identify all articles describing stroke in pediatric IBD. All identified studies were stratified into those published before and after January 1 2000.In all, 154 new patients diagnosed with IBD (male 56%) (UC 30%, CD 64%, IBD unclassified [IBDU] 6%) were reviewed. Four cases of CTE occurred in our population over 5 years (2.6%). All patients had a risk factor for CTE. Fifteen case series were identified with 32 patients. There was a significant increase in the proportion strokes affecting patients with CD reported after January 2000 (P = 0.02).CTE affects a proportion of pediatric IBD patients. Although resolution of physical impairment is the norm, significant morbidity exists. Our study suggests a secular trend toward CTE in CD. Primary prevention with the identification and amelioration of identifiable risk factors should be the clinical objective in future studies. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21126">
<title>Association between blood flow and inflammatory state in a T-cell transfer model of inflammatory bowel disease in mice</title>
<link>http://dx.doi.org/10.1002%2Fibd.21126</link>
<description><![CDATA[Adoptive transfer of naive T-lymphocyte subsets into lymphopenic mice initiates chronic gut inflammation that mimics several aspects of inflammatory bowel disease (IBD). Patients with IBD can have profound alterations in intestinal blood flow, but whether the same is true in the T-cell transfer model has yet to be determined.In the current study, chronic intestinal inflammation was induced in recombinase-activating gene-1-deficient (RAG-/-) mice by adoptive transfer of CD4+ T-lymphocytes obtained from interleukin-10 deficient (IL-10-/-) mice.Four weeks later, widespread colonic inflammation was observed in the reconstituted recipients, in contrast to 2 control sets of mice injected with a different subset of lymphocytes or with vehicle alone. We observed that the resulting pathology induced in the reconstituted RAG-/- mice was divided distinctly into 2 subsets: 1 with blood flow near normal with very high inflammation scores, and the other with severely attenuated blood flow but with much lower signs of inflammation. Colonic and ileal blood flow rates in the latter subset of CD4+ mice averaged only [ap]30% compared to the mice with higher inflammation scores. The lower blood flow rates were associated with greatly reduced red blood cell concentrations in the tissue, suggesting a possible loss of vascular density.In this model of chronic intestinal inflammation, mild inflammation was associated with significant decreases in blood flow. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21125">
<title>Turner&#x27;s syndrome, autoimmune thyroiditis, and Crohn&#x27;s disease in the same patient: A combination emphasizing the role of X-chromosome in inflammatory bowel disease patients</title>
<link>http://dx.doi.org/10.1002%2Fibd.21125</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21121">
<title>Recurrent cytomegalovirus infection in ileal pouch-anal anastomosis for ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21121</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21117">
<title>Teduglutide, a novel mucosally active analog of glucagon-like peptide-2 (GLP-2) for the treatment of moderate to severe Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21117</link>
<description><![CDATA[Teduglutide, an analog of glucagon-like peptide-2 (GLP-2), is associated with trophic effects on gut mucosa. Its role in the treatment of active Crohn's disease (CD) was assessed in a pilot, randomized, placebo-controlled, double-blinded, dose-ranging study.Subjects with moderate-to-severe CD were randomized 1:1:1:1 to placebo or 1 of 3 doses of teduglutide (0.05, 0.10, or 0.20 mg/kg daily) delivered as a daily subcutaneous injection for 8 weeks. The primary outcome measure was the percentage of subjects in each group that responded to treatment, defined as a decrease in Crohn's Disease Activity Index (CDAI) score to  100 points. At week 8 there was an optional 12-week open-label period of treatment with teduglutide 0.10 mg/kg/d.One hundred subjects were enrolled and 71 completed the study. The mean baseline CDAI score was 290.8 ± 57.6 and was similar across groups. There were numerically higher response and remission rates in all teduglutide-treated groups as compared with placebo, although the percentage of subjects who achieved a clinical response or remission was more substantial, and seen as early as week 2 of treatment in the highest dose (0.2 mg/kg/d) group (44% response and 32% remission versus 32% response and 20% remission in the placebo group). Of subjects who had not achieved remission during the 8-week placebo-controlled phase in the higher-dose group, 50% achieved remission during the more prolonged, open-label treatment phase. Plasma citrulline was similar across groups at baseline, but increased substantially over time in all teduglutide groups when compared with placebo at week 8. Adverse events were not different between placebo and active treatment groups.Teduglutide is a novel and potentially effective therapy for inducing remission and mucosal healing in patients with active moderate-to-severe CD. Further clinical investigation of this growth factor is warranted. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21112">
<title>The position of the amino group on the benzene ring is critical for mesalamine&#x27;s improvement of replication fidelity</title>
<link>http://dx.doi.org/10.1002%2Fibd.21112</link>
<description><![CDATA[Individuals with ulcerative colitis are at high risk of developing colitis-associated cancer. 5-Aminosalicylate (5-ASA) protects from cancer by its antiinflammatory activity as well as by altering cell growth, inducing apoptosis, and reducing replication errors. So far neither 5-ASA's structural specificity nor its pharmacophore group have been identified. Here we compared 5-ASA with its analogs (4-ASA and 3-ASA) and its metabolite N-acetyl-5-ASA (NAc-5-ASA).Superoxide scavenging was analyzed by lucigenin-amplified chemiluminescence. Cell growth, cell cycle distribution, and replication fidelity at a (CA)13 microsatellite were measured in HCT116 and HT29 colon epithelial cells by MTT and flow cytometry. Nuclear protein extracts were blotted for replication protein A (RPA), claspin, p53, and p53Ser15.All compounds inhibited the growth of colon epithelial cells at a similar level and displayed potent scavenging properties, with 3-ASA being the most active, followed by 5-ASA, 4-ASA, and NAc-5-ASA. Besides 5-ASA, only 4-ASA caused an increase in the S-phase population (56%-69% and 49%-62% in HCT116 and HT29 cells, respectively). This was accompanied by nuclear recruitment of replication proteins RPA and claspin as well as phosphorylation of p53Ser15, both of which were weaker or absent with 3-ASA or NAc-5-ASA. 5-ASA was the only compound that lowered mutations at a (CA)13 microsatellite.5-ASA shares its growth inhibitory and superoxide scavenging properties with its structural analogs and metabolite, but the position of the amino group is critical for reducing replication errors. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21110">
<title>Pityriasis lichenoides chronica induced by adalimumab therapy for Crohn&#x27;s disease: Report of 2 cases successfully treated with methotrexate</title>
<link>http://dx.doi.org/10.1002%2Fibd.21110</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21120">
<title>Relationships between inflammatory bowel disease and perinatal factors: Both maternal and paternal disease are related to preterm birth of offspring</title>
<link>http://dx.doi.org/10.1002%2Fibd.21120</link>
<description><![CDATA[The aims of this study were to explore the influences of familial, maternal, and paternal inflammatory disease (IBD) on perinatal outcomes in the offspring and the risk for development of IBD related to perinatal factors.Eighty-five patients with Crohn's disease (CD) and 86 with ulcerative colitis (UC) were included from a population-based incidence study enrolled 1990-1994. Family and birth records of these patients, as well as of their 207 infants, were drawn from the Norwegian Medical Birth Registry, established in 1967, and compared with the national birth cohort from the same period.Maternal (odds ratio [OR] = 2.15, 95% confidence interval [CI]: 1.36, 3.39) and paternal IBD (OR = 3.02, 95% CI: 1.82, 5.01) influenced the risk of preterm birth (<37 weeks), which further increased if the affected parents had a first-degree relative with IBD (OR = 4.29, 95% CI: 1.59, 11.63). Maternal CD was associated with lower birth weight in the offspring (crude difference: 271.79 g, 95% CI: 87.83, 455.77, versus controls). Maternal UC increased the risk of perinatal bacterial infection in the offspring (OR = 6.03, 95% CI: 2.03, 17.91). IBD patients (2.3%) were less likely to be delivered by cesarean section than controls (8.1%) (OR = 0.27, CI: 95%: 0.10, 0.73).Familial, maternal, and paternal IBD were linked to preterm birth, which might be explained by genetic mechanisms. The present protective effect of cesarean sections needs further clarification in future studies. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21118">
<title>Small bowel resection rates in Crohn&#x27;s disease and the indication for surgery over time: Experience from a large tertiary care center</title>
<link>http://dx.doi.org/10.1002%2Fibd.21118</link>
<description><![CDATA[Our primary aim was to determine if the rate of small bowel resection (SBR) has declined over time among Crohn's disease (CD) patients seen at a single academic institution. A secondary aim was to establish whether the indication for surgery has changed.Patients with a primary or secondary ICD-9 code for CD (555.0-555.9) who underwent SBR at the University of Pittsburgh were included. Patients were divided into 4 separate time periods based on when they had surgery: 1995-1998 (Period 1), 1999-2001 (Period 2), 2002-2004 (Period 3), and 2005-2007 (Period 4). Medical records were reviewed for the 6 months preceding surgery. Use of 5-ASAs, immunomodulators (IMs), tumor necrosis factor (TNF) antagonists, and corticosteroids were noted. Disease behavior was defined as nonstricturing, nonpenetrating (B1), stricturing (B2), and penetrating (B3). Proportions of patients undergoing SBR were calculated according to calendar cohort and these rates were examined for time trends.In all, 227 unique patients were analyzed for a total of 236 surgeries. The rates of 5-ASA, IM, and corticosteroid use were similar across the 4 time periods. By contrast, TNF antagonist usage progressively increased over time (0%, 18%, 34%, 35%; P = 0.0002). The annual rate of SBR per period did not change (1.6%, 1.9%, 1.6%, 1.9%; P = 0.93). Similarly, the disease behavior did not change over time.While the frequency of TNF antagonist use in CD at the University of Pittsburgh has increased over time, the rate of SBR and indication for surgery has remained unchanged. These findings may be explained by long-standing, complicated disease refractory to medical therapy. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21107">
<title>Perforin deficiency attenuates inflammation and tumor growth in colitis-associated cancer</title>
<link>http://dx.doi.org/10.1002%2Fibd.21107</link>
<description><![CDATA[Patients with inflammatory bowel disease (IBD) have a markedly increased risk to develop colon cancer, but there are only limited data about the host antitumor response in such colitis-associated cancer. In the present study we aimed at assessing the role of perforin-dependent effector mechanisms in the immune response in a murine model of colitis-associated colon cancer.Wildtype and perforin-deficient mice were analyzed in a mouse model of colitis-associated colon cancer using azoxymethane (AOM) and dextran sodium sulfate (DSS).Tumors of wildtype mice showed infiltration of CD4+, CD8+ T cells, natural killer (NK) cells, high numbers of apoptotic cells, and expression of the transcription factor eomesodermin and cytotoxic effector proteins, suggesting a potential role of the antitumor immune response in AOM/DSS tumorigenesis. Furthermore, perforin deficiency resulted in reduced apoptosis of epithelial cells as compared to wildtype mice, whereas tumor infiltration by NK cells, CD8+, and CD4+ T cells was unchanged. However, perforin-deficient mice surprisingly developed significantly fewer tumors than wildtype mice. Subsequent studies identified an important role of perforin in regulating colitis activity, as perforin deficiency caused a significant reduction of DSS colitis activity and proinflammatory cytokine production as compared to wildtype controls.Perforin is involved in both the antitumor immune response and the regulation of activity of mucosal inflammation in colitis-associated cancer. Our data emphasize the possible consequences for therapeutic strategies targeting colitis-associated colon cancer. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21111">
<title>Mapping of inflammatory bowel disease in northern France: Spatial variations and relation to affluence</title>
<link>http://dx.doi.org/10.1002%2Fibd.21111</link>
<description><![CDATA[Geographic variations in the incidence of inflammatory bowel disease (IBD) may reflect variations in the distribution of environmental etiologic factors. We assessed spatial variation in the incidence of IBD in northern France and analyzed its association with a deprivation index.All cases of IBD included in the EPIMAD registry between 1990 and 2003 were extracted. The standardized incidence ratio (SIR) was calculated for each canton in the region. The association between incidence and deprivation was assessed using the Townsend deprivation index.The mean annual incidence rates of Crohn's disease (CD) and ulcerative colitis (UC) were 6.2 × 10-5 and 3.8 × 10-5, respectively. The mean cumulative numbers of cases by canton were 18.4 (1-183) for CD and 11.3 (0-148) for UC. For both CD and UC, mapping depicted spatial heterogeneity in the SIR with spatial autocorrelation. A high relative risk (RR) of CD was observed in mainly rural and periurban cantons of the region. For UC, a high RR was found in cantons of the south and the center of Pas-de-Calais. No significant correlation was observed between spatial variations in IBD and deprivation.The incidence of IBD is associated with spatial heterogeneity in northern France. The noteworthy predominance of CD in agricultural areas warrants further investigations. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21109">
<title>Transmission ratio distortion of DLG5 R30Q: Evidence for prenatal selection?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21109</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21108">
<title>Butyrate utilization by the colonic mucosa in inflammatory bowel diseases: A transport deficiency</title>
<link>http://dx.doi.org/10.1002%2Fibd.21108</link>
<description><![CDATA[The short-chain fatty acid butyrate, which is mainly produced in the lumen of the large intestine by the fermentation of dietary fibers, plays a major role in the physiology of the colonic mucosa. It is also the major energy source for the colonocyte. Numerous studies have reported that butyrate metabolism is impaired in intestinal inflamed mucosa of patients with inflammatory bowel disease (IBD). The data of butyrate oxidation in normal and inflamed colonic tissues depend on several factors, such as the methodology or the models used or the intensity of inflammation. The putative mechanisms involved in butyrate oxidation impairment may include a defect in beta oxidation, luminal compounds interfering with butyrate metabolism, changes in luminal butyrate concentrations or pH, and a defect in butyrate transport. Recent data show that butyrate deficiency results from the reduction of butyrate uptake by the inflamed mucosa through downregulation of the monocarboxylate transporter MCT1. The concomitant induction of the glucose transporter GLUT1 suggests that inflammation could induce a metabolic switch from butyrate to glucose oxidation. Butyrate transport deficiency is expected to have clinical consequences. Particularly, the reduction of the intracellular availability of butyrate in colonocytes may decrease its protective effects toward cancer in IBD patients. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21106">
<title>CXCL12 Is a constitutive and inflammatory chemokine in the intestinal immune system</title>
<link>http://dx.doi.org/10.1002%2Fibd.21106</link>
<description><![CDATA[Inflammatory bowel disease (IBD) is characterized by increased lymphocytic infiltrate to the lamina propria (LP) and upregulation of inflammatory chemokines and receptors. CXCL12 is a constitutive chemokine involved in lung, brain, and joint inflammation. We hypothesized that CXCL12 and its receptor, CXCR4, would have a constitutive and inflammatory role in the gut.Intestinal epithelial cells (IECs) and T lymphocytes were isolated from intestinal mucosa of IBD and control patients undergoing bowel resection. Autologous T cells were isolated from peripheral blood (PB). CXCL12 and CXCR4 expression by IECs was assessed by polymerase chain reaction and immunohistochemistry, lymphocyte phenotype by flow cytometry, and migration by Transwells.IECs expressed CXCL12 and expression was increased and more diffuse in IBD compared to normal crypts (ulcerative colitis [UC] > Crohn's disease [CD], inflamed > noninflamed). CXCR4 was expressed by IECs, LP T cells (LPTs), and PB T cells (PBTs), and CXCR4+ cells were increased in IBD LP in situ. PBTs and LPTs from all patients had a high and comparable migration toward CXCL12 (P < 0.0001 and P < 0.05 vs. medium, respectively). Migration toward IBD-IEC-derived supernatant was significantly higher compared to normal. Antibodies against CXCR4 and CXCL12 blocked migration.CXCL12 is expressed by normal IECs and upregulated and differentially distributed in IBD IECs. CXCR4 is expressed by IECs and LPTs, and CXCR4+ cells are significantly increased in IBD LP. CXCL12 is chemotactic for both PBTs and LPTs. Thus, CXCL12 and CXCR4 have a constitutive and inflammatory role in the intestinal mucosa and their selective therapeutic manipulation may be considered in IBD management. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21098">
<title>Does psychological counseling alter the natural history of inflammatory bowel disease?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21098</link>
<description><![CDATA[There is increasing evidence that psychological stress can increase mucosal inflammation and worsen the course of inflammatory bowel disease (IBD). We have now assessed whether psychotherapy by a counselor specially trained in the management of IBD can influence the course of disease.Using retrospective case note review, we compared the course of IBD in 24 patients (13 ulcerative colitis; 11 Crohn's disease), during the year before (year 1) and the year after referral (year 2) for supportive outpatient psychotherapy to an IBD counselor, to that of 24 IBD controls who were matched to individual cases for age, sex, disease, duration of disease, medication at baseline, and for relapse rate in year 1. Counselor assessments were made using a visual analog scale 0-6 (0 denotes poor, 6 excellent response to counseling). The results are shown as median (range).Patients were referred for counseling because of disease-related stress (14 patients), work problems (3), concerns about surgery (5), and bereavement (2); they received 6 (1-13) 1-hour sessions in year 2. In the year after starting counseling (year 2), patients had fewer relapses (0 [0-2]) and outpatient attendances (3.5 [1-10]) than in the year before referral (year 1) (2 [0-5], P = 0.0008; and 6.5 [1-17], P = 0.0006, respectively; furthermore, steroid usage (1 course [0-4] before, 0 [0-2] after, P = 0.005) and relapse-related use of other IBD medications declined during psychotherapy (1 drug [0-5] before, 0 [0-2] after, P = 0.002). There were no differences in any of these measures between years 1 and 2 in the control group. Numbers of hospital admissions did not change between year 1 and 2 in either group. In the 20 patients who attended >1 session counseling helped solve stress-related difficulties (counselor's score 4 [3-5]), the counselor scored them 4 (3-6) overall in psychological well-being after the counseling sessions.IBD-focused counseling may improve not only psychological well-being, but also the course of IBD in individuals with psychosocial stress. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21097">
<title>TLR5 is not required for flagellin-mediated exacerbation of DSS colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21097</link>
<description><![CDATA[The two forms of human inflammatory bowel disease, Crohn's disease (CD) and ulcerative colitis (UC), are both associated with loss of tolerance to gut microbial antigens. The dominant antigen recognized by antibody and T-cell responses in patients with CD is bacterial flagellin. Flagellin is also the only known ligand for Toll-like receptor 5 (TLR5), a key protein in innate immunity. Although flagellin activates TLR5 to produce inflammatory responses in many cell types in the gut, there is conflicting evidence as to whether TLR5 is harmful or protective in CD and murine colitis models. A recent study found that administration of flagellin enemas to mice along with dextran sodium sulfate (DSS) made their colitis worse.We sought to determine whether this exacerbation was due to TLR5 ligation, or to TLR5-independent adaptive immune responses to flagellin as an antigen, by using a transposon insertional mutant of the Escherichia coli H18 flagellin, 2H3, which lacks TLR5 stimulatory activity.We found that flagellin enemas produced only a mild exacerbation of DSS colitis, and that 2H3 was equivalent to or worse than wildtype flagellin. Moreover, we found that DSS colitis was more severe in TLR5-/- mice than wildtype C57BL/6 mice.Together, these results suggest that flagellin-mediated exacerbation of colitis is independent of TLR5. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21086">
<title>5-aminosalicylic acid interferes in the cell cycle of colorectal cancer cells and induces cell death modes</title>
<link>http://dx.doi.org/10.1002%2Fibd.21086</link>
<description><![CDATA[Epidemiological data suggests that 5-aminosalicylic acid (5-ASA), a nonsteroidal antiinflammatory drug used in the treatment of inflammatory bowel diseases, prevents colorectal cancer development in these patients, although the mechanisms remain incompletely understood.Here we report that 5-ASA prevents growth of several colorectal cancer cell lines by interfering in the cell cycle, i.e., an S-phase and G2/M phase arrest, dependent on 5-ASA dosage and concentration, together with an increased mitotic index. In addition, prolonged cell cycle arrest by repeated 5-ASA treatment induced apoptosis and caused abnormal spindle organization leading to mitotic catastrophe, another form of cell death.These observations illustrate that 5-ASA has chemopreventive and chemotherapeutic properties. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21116">
<title>Association between Helicobacter pylori infection and inflammatory bowel disease: A meta-analysis and systematic review of the literature</title>
<link>http://dx.doi.org/10.1002%2Fibd.21116</link>
<description><![CDATA[Epidemiologic data suggest a protective effect of Helicobacter pylori infection against the development of autoimmune disease. Laboratory data illustrate H. pylori's ability to induce immune tolerance and limit inflammatory responses. Numerous observational studies have investigated the association between H. pylori infection and inflammatory bowel disease (IBD). Our aim was to perform a systematic review and meta-analysis of this association.Medline, EMBASE, bibliographies, and meeting abstracts were searched by 2 independent reviewers. Of 369 abstracts reviewed, 30 promising articles were reviewed in detail. Twenty-three studies met our inclusion criteria (subject N = 5903). Meta-analysis was performed with the metan command in Stata 10.1.Overall, 27.1% of IBD patients had evidence of infection with H. pylori compared to 40.9% of patients in the control group. The estimated relative risk of H. pylori infection in IBD patients was 0.64 (95% confidence interval [CI]: 0.54-0.75). There was significant heterogeneity in the included studies that could not be accounted for by the method of IBD and H. pylori diagnosis, study location, or study population age.These results suggest a protective benefit of H. pylori infection against the development of IBD. Heterogeneity among studies and the possibility of publication bias limit the certainty of this finding. Further studies investigating the effect of eradication of H. pylori on the development of IBD are warranted. Because environmental hygiene and intestinal microbiota may be strong confounders, further mechanistic studies in H. pylori mouse models are also necessary to further define the mechanism of this negative association. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21105">
<title>Analysis of 39 Crohn&#x27;s disease risk loci in Swedish inflammatory bowel disease patients</title>
<link>http://dx.doi.org/10.1002%2Fibd.21105</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21104">
<title>Epstein-Barr virus and parvovirus B19 coinfection in a Crohn&#x27;s disease patient under azathioprine</title>
<link>http://dx.doi.org/10.1002%2Fibd.21104</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21103">
<title>Ileal pouch for everyone, even when we are not sure of the diagnosis before or at colectomy?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21103</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21102">
<title>Body mass index and disease activity at treatment initiation: Potential new predictors of response to azathioprine therapy in IBD</title>
<link>http://dx.doi.org/10.1002%2Fibd.21102</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21100">
<title>Current thinking on recurrence: Does anastomotic surgical technique affect recurrence rates in Crohn&#x27;s patients?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21100</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21099">
<title>Incidence of stricturing and penetrating complications of Crohn&#x27;s disease diagnosed in pediatric patients</title>
<link>http://dx.doi.org/10.1002%2Fibd.21099</link>
<description><![CDATA[The development of disease complications is poorly characterized in pediatric patients with Crohn's disease (CD).We retrospectively determined the cumulative incidence of stricturing and penetrating complications of CD prior to first surgery utilizing data from 989 consecutively enrolled CD patients (age 0-17 years at diagnosis) collected between January 2000 and November 2003 and stored in the Pediatric IBD Consortium Registry.Mean age at diagnosis was 11.5 ± 3.8 (standard deviation) years. Median follow-up time was 2.8 years. Prior to first surgery, the cumulative incidence of stricturing or penetrating complications was 27% at 5 years and 38% at 10 years from the diagnosis of inflammatory bowel disease. The cumulative incidence of complicated disease was lowest in isolated colonic disease (P = 0.009). Penetrating complications that followed stricturing complications prior to first surgery occurred within 2 years of stricturing complications (cumulative incidence was 13% at 2 years from diagnosis of stricturing disease). Stricturing complications that followed penetrating complications prior to first surgery occurred within 8 years of penetrating complications (cumulative incidence was 26% at 8 years from diagnosis of penetrating complications).Strictures, abscesses, and fistulas are common in pediatric CD. Earlier aggressive management may be indicated. Prospective study is required to identify genetic and serologic markers that predict a patient's risk for the development of complicated disease and to determine optimal treatment regimens. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21096">
<title>Plasma chromogranin A in patients with inflammatory bowel disease: A possible explanation</title>
<link>http://dx.doi.org/10.1002%2Fibd.21096</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21080">
<title>Effect of EP4 agonist (ONO-4819CD) for patients with mild to moderate ulcerative colitis refractory to 5-aminosalicylates: A randomized phase II, placebo-controlled trial</title>
<link>http://dx.doi.org/10.1002%2Fibd.21080</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21115">
<title>Lessons from geographic mapping of IBD in France</title>
<link>http://dx.doi.org/10.1002%2Fibd.21115</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21082">
<title>Adalimumab for cutaneous metastatic Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21082</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21101">
<title>Getting the steak without the sizzle: Is MR enterography as good as CT enterography?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21101</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21068">
<title>Antigen-presenting cells exposed to Lactobacillus acidophilus NCFM, Bifidobacterium bifidum BI-98, and BI-504 reduce regulatory T cell activity</title>
<link>http://dx.doi.org/10.1002%2Fibd.21068</link>
<description><![CDATA[The effect in vitro of six different probiotic strains including Lactobacillus acidophilus NCFMTM, Lactobacillus salivarius Ls-33, Lactobacillus paracasei subsp. paracasei YS8866441, Lactobacillus plantarum Lp-115, Bifidobacterium bifidum BI-504 and BI-98 was studied on splenic enteroantigen-presenting cells (APC) and CD4+CD25+ T-regulatory cells (Tregs) in splenocyte-T cell proliferation assays.Splenocytes exposed to enteroantigen +/- probiotics were used to stimulate cultured CD4+CD25- T cells to which titrated numbers of Tregs were added. Cytokine assays were performed by use of neutralizing antibodies and ELISA.Exposure of APCs to enteroantigens and the series of probiotic strains mentioned above did not influence the stimulatory capacity of APCs on proliferative enteroantigen-specific T cells. However, exposure to B. bifidum BI-98, BI-504 and L. acidophilus NCFMTM consistently reduced the suppressive activity of Tregs. The suppressive activity was analyzed using fractionated components of the probiotics, and showed that a component of the cell wall is responsible for the decreased Treg activity in the system. The probiotic-induced suppression of Treg function is not mediated by changes in APC-secretion of the inflammatory cytokines IL-6 or IL-1b.We conclude that certain probiotic strains can modify APCs to cause reduced Treg activity. This effect apparently depends on a direct APC-to-Treg cell contact. The APC-mediated suppressive effect on Treg function of certain probiotic strains may constrain the anti-inflammatory activity, which is often desired from probiotic therapy. This unexpected function of certain probiotic strains should be taken into consideration when designing adjuvant therapies with these bacteria, or when probiotic strains are selected for improvement of gut-associated inflammation like IBD. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21055">
<title>Age distribution of IBD hospitalization</title>
<link>http://dx.doi.org/10.1002%2Fibd.21055</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21053">
<title>Widespread but not localized neoplasia in inflammatory bowel disease worsens the prognosis of colorectal cancer</title>
<link>http://dx.doi.org/10.1002%2Fibd.21053</link>
<description><![CDATA[Patients with inflammatory bowel disease (IBD) are at increased risk of colorectal cancer (CRC). Recently, new phenotypes of CRC in IBD have been suggested. Studies of the prognosis of CRC in IBD have shown conflicting results. The aim of the study was to analyze factors for prognosis in CRC-IBD, including the impact of the new phenotypes.By using the nationwide, population-based Cancer Registry of Norway, we compared survival of a CRC-IBD cohort with CRC in the background population (all-CRC), adjusting for the topographical distribution of dysplasia at cancer diagnosis (widespread versus localized neoplasia in IBD) and other factors. We also analyzed prognostic factors within CRC-IBD.The mean age at CRC diagnosis was 43 years in widespread, 52 years in localized neoplasia IBD, and 70 years in all-CRC (P < 0.05). Adjusted for cofactors, prognosis of CRC-IBD was poorer compared to all-CRC (mortality rate ratio [MRR] 3.71, 95% confidence interval [CI]: 2.54-5.42, P < 0.001). Prognosis of widespread neoplasia IBD was poorer compared to all-CRC (MRR 4.27, 95% CI: 2.83-6.44, P < 0.001) and compared to localized neoplasia IBD (MRR 3.58, 95% CI: 0.87-14.72, P = 0.076). Survival was not significantly different between localized neoplasia IBD and all-CRC (P = 0.132).The results demonstrate lower age and poorer survival of CRC in IBD compared to CRC in the background population. The unfavorable effect of IBD on prognosis of CRC was pronounced in widespread neoplasia IBD. The diagnosis of this phenotype seems to be an important prognostic sign in patients with CRC in IBD. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21016">
<title>High gene expression of MDR1 (ABCB1) is associated with medical treatment response and long-term remission in patients with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21016</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21094">
<title>A new tool to measure the burden of Crohn&#x27;s disease and its treatment: Do patient and physician perceptions match?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21094</link>
<description><![CDATA[Health-related quality of life (HRQOL) is difficult to efficiently measure in the clinic setting. Our aim was to develop and test a simple tool to measure the burden of Crohn's disease (CD) and its treatment and to compare how patients and their physicians perceive the impact of CD on HRQOL.A cross-sectional, self-administered questionnaire was distributed to patients with CD. The questionnaire included a feeling thermometer to measure disease and treatment burden, which was compared to the Short Inflammatory Bowel Disease Questionnaire (SIBDQ). At that visit, the patient's physician completed a questionnaire containing the feeling thermometer and the Harvey Bradshaw index (HBI). Nonparametric tests were use to report results.In all, 113 surveys were completed. The median age of respondents was 40 years and 68% were female. Using the feeling thermometer (scale 0-100), patients reported their current health as a median of 70 (interquartile range [IQR] 50-80) and their disease specific burden as 20 (IQR 10-40). Treatment-specific burden was 6.9 (IQR 1.3-20). Physicians perceived their patients' current health as a median of 71.3 (IQR 57.5-90) with a disease burden of 12.5 (IQR 5-30). Spearman's rho between the burden of symptoms measured by the feeling thermometer and the SIBDQ was -0.71. The correlation between patient and physician perception of current health was 0.73.Two questions using the feeling thermometer provide a quick and accurate assessment of the burden of CD on patients. Physicians' perception of the burden of disease was similar to their patients. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21092">
<title>Platelet-activating factor-induced NF-[kappa]B activation and IL-8 production in intestinal epithelial cells are Bcl10-dependent</title>
<link>http://dx.doi.org/10.1002%2Fibd.21092</link>
<description><![CDATA[Platelet-activating factor (PAF), a potent proinflammatory phospholipid mediator, has been implicated in inducing intestinal inflammation in diseases such as inflammatory bowel disease (IBD) and necrotizing enterocolitis (NEC). However, its mechanisms of inducing inflammatory responses are not fully understood. Therefore, studies were designed to explore the mechanisms of PAF-induced inflammatory cascade in intestinal epithelial cells.Nuclear factor kappa B (NF-[kappa]B) activation was measured by luciferase assay and enzyme-linked immunosorbent assay (ELISA), and interleukin 8 (IL-8) production was determined by ELISA. B-cell lymphoma 10 (Bcl10), caspase recruitment domain-containing membrane-associated guanylate kinase protein 3 (CARMA3), and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) mRNA and protein levels were assessed by real-time reverse-transcription polymerase chain reaction (RT-PCR) and Western blot, respectively. siRNA silencing of Bcl10 was used to examine its role in PAF-induced NF-[kappa]B activation and IL-8 production. The promoter region of the Bcl10 gene was cloned with the PCR method and promoter activity measured by luciferase assay.The adaptor protein Bcl10 appeared to play an important role in the PAF-induced inflammatory pathway in human intestinal epithelial cells. Bcl10 was required for PAF-induced I[kappa]B[alpha] phosphorylation, NF-[kappa]B activation, and IL-8 production in NCM460, a cell line derived from normal human colon, and Caco-2, a transformed human intestinal cell line. PAF also stimulated Bcl10 interactions with CARMA3 and MALT1, and upregulated Bcl10 expression in these cells via transcriptional regulation.These findings highlight a novel PAF-induced inflammatory pathway in intestinal epithelial cells, requiring Bcl10 as a critical mediator and involving CARMA3/Bcl10/MALT1 interactions. The proinflammatory effects of PAF play prominent roles in the pathogenesis of IBD and this pathway may present important targets for intervention in chronic inflammatory diseases of the intestine. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21091">
<title>Circulating levels of chemerin and adiponectin are higher in ulcerative colitis and chemerin is elevated in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21091</link>
<description><![CDATA[Chemerin is an adipokine that stimulates chemotaxis of cells of the innate immune system. Inflammatory bowel disease (IBD) is linked to an impaired immune response and, therefore, we hypothesized that systemic chemerin may be altered in IBD patients.Serum was collected from patients with Crohn's disease (CD, 230 patients), ulcerative colitis (UC, 80 patients), and healthy controls (HC, 80 probands). Chemerin and adiponectin, which has already been measured in the serum of similar cohorts by others, were determined by enzyme-linked immunosorbent assay (ELISA).Chemerin was elevated in IBD compared to HC and was higher in male CD than UC patients. Female and male CD patients had lower adiponectin levels compared to UC, and adiponectin was lower in female CD patients compared to female HC. Adiponectin tended to be higher in female and male UC patients compared to HC and this difference became significant in the whole study group. Correlations with disease activity were only found in males. Here, chemerin was higher in CD patients on remission but was reduced in UC with nonactive disease. Adiponectin was higher in UC with inactive disease. Treatment with corticosteroids was linked to elevated adiponectin in male CD patients and higher chemerin in female UC patients. Unlike adiponectin, which was elevated in female serum in all cohorts, chemerin was only higher in female UC patients.These findings further indicate potential regulatory functions of adipokines in intestinal inflammation that are partly gender-dependent and that may even be associated with the distinct immunopathogenesis of UC and CD. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21090">
<title>Female gender and surgery impair relationships, body image, and sexuality in inflammatory bowel disease: Patient perceptions</title>
<link>http://dx.doi.org/10.1002%2Fibd.21090</link>
<description><![CDATA[There is a paucity of literature on the impact of inflammatory bowel disease (IBD) on relationships, body image, and sexual function from a patient perspective. This study sought to describe patients' perceptions of these issues.In all, 347 patients, age 18-50 years, from a hospital-based IBD database were surveyed by post. Quantitative and qualitative data were obtained on demographics, relationships, quality of life (QoL), body image, and sexual function. Comparisons were made by diagnosis, gender, and operative status. Univariate and multivariable analyses and logistic regressions were performed; P < 0.05 was regarded as significant.The response rate was 62.5%. Overall, 88.5% reported impaired QoL; 50.2% a negative effect on relationship status; and 66.8% impaired body image (females 74.8% versus males 51.4%, P = 0.0007; operated 81.4% versus nonoperated 51.3%, P = 0.0003). A greater proportion of women reported decreased frequency of sexual activity, as did operated subjects (female 66.3% versus male 40.5%, P < 0.0001; operated 68.5% versus nonoperated 50.4%, P = 0.0113). Women and operated subjects also more often reported decreased libido (female 67.1% versus male 41.9% P = 0.0005; operated 67.4% versus nonoperated 52.6%, P = 0.035). 9.7% omitted medication because of perceived negative effect(s) on sexual function. Logistic regression revealed that female gender negatively affected body image, libido, and sexual activity, while limited resection surgery negatively affected body image (all P < 0.005).A large proportion of patients perceive IBD to negatively affect many aspects of sexuality. Females and operated subjects more frequently perceived these negative effects. These findings are important in overall clinical care of patients with IBD and should be addressed. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21089">
<title>Crohn&#x27;s proctitis: A distinct entity</title>
<link>http://dx.doi.org/10.1002%2Fibd.21089</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21087">
<title>Mesalamine (pentasa)-induced painful skin lesions</title>
<link>http://dx.doi.org/10.1002%2Fibd.21087</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21084">
<title>Prospective randomized open-label multicenter phase I/II dose escalation trial of visilizumab (HuM291) in severe steroid-refractory ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21084</link>
<description><![CDATA[Visilizumab is a humanized IgG2 monoclonal anti-CD3 antibody. We evaluated its safety and dose response in severe intravenous steroid-refractory ulcerative colitis (UC).In all, 104 patients were treated. In Stage I, 73 patients were randomly assigned to receive intravenous visilizumab 5, 7.5, 10, or 12.5 [mu]g/kg/day for 2 consecutive days. In Stage II, 33 patients received visilizumab at the optimal clinical dose (OCD) of 5 [mu]g/kg/day for 2 days. Symptomatic response and remission were defined by the modified Truelove-Witts severity index. Clinical response and remission were defined by the Mayo score.The rates of symptomatic response at day 15 in the 5, 7.5, 10, or 12.5 [mu]g/kg dose groups were 71%, 70%, 50%, and 61%, respectively, in Stage I and in 54% in Stage II. The symptomatic remission rates were 35%, 5%, 22%, and 11% in Stage I and 18% in Stage II. The rates of clinical response at day 30 in the 5, 7.5, 10, or 12.5 [mu]g/kg dose groups were 71%, 65%, 50%, and 67%, respectively, in Stage I and 55% in Stage II. The clinical remission rates were 6%, 5%, 0%, and 11% in Stage I and 6% in Stage II. All patients experienced adverse events. Serious adverse events included abdominal abscess, cytomegalovirus infection, atrial fibrillation, herpes zoster, and esophageal candidiasis.Treatment with visilizumab induced symptomatic response and clinical response. Results with 5 [mu]g/kg/day were similar to those observed with higher doses (NCT00267306 at ). (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21077">
<title>Course of inflammatory bowel disease in patients infected with human immunodeficiency virus</title>
<link>http://dx.doi.org/10.1002%2Fibd.21077</link>
<description><![CDATA[Human immunodeficiency virus (HIV) infection depletes CD4+ lymphocytes, which may benefit patients with inflammatory bowel disease (IBD). The aim was to compare the course of IBD in HIV patients with a matched group of IBD seronegative patients.A total of 20 IBD (14 Crohn's disease, 6 ulcerative colitis) HIV infected patients and 40 matched control seronegative IBD patients (2 controls per case) were compared regarding relapse of their disease. The CD4+ count was followed every 6 months and a value of [le]500 cells/[mu]L was used to define patients with immunosuppression. Relapse rates per year of follow-up were compared among the 2 groups and survival curves for cumulative remission rates were compared with a log-rank test. Multivariate analysis was used to discriminate among the impact of different variables on the risk of IBD relapse.The median duration of follow-up was 8.4 years (range 0.6-18 years). The mean relapse rate for the HIV+IBD group was 0.016/year of follow-up as compared to 0.053/year of follow-up for the IBD-matched control group (P = 0.032). Regarding the HIV-positive/IBD group, 14 patients were immunosuppressed at any given time during the follow-up period. None of these patients experienced an IBD relapse, whereas 3 out of the 6 without immunosuppression relapsed (P = 0.017). According to the multivariate analysis, HIV status was the only risk factor independently associated with a lower probability of IBD relapse.HIV infection reduces the relapse rates in IBD patients and this may be attributed to the lower CD4+ counts seen in these patients. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21070">
<title>Glucocorticoid bioactivity does not predict response to steroid therapy in severe pediatric ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21070</link>
<description><![CDATA[The pathophysiological basis for corticosteroid (CS) failure in ulcerative colitis (UC) is unknown. A transactivation glucocorticoid bioassay (GBA) was developed to measure the biological activity of CS by quantifying glucocorticoid response elements. This approach eliminates differences in bioavailability, chemistry, affinity, and other potential differences between the various steroids regarding their ability to activate the glucocorticoid receptor. In this multicenter prospective study, we aimed to evaluate whether CS bioavailability plays a role in CS refractoriness in severe pediatric UC.GBA (using COS-1 transfected cells) was measured in the serum of 50 children (52% males, age 13.4 ± 3.5 years) admitted for acute severe UC on the third day of CS treatment. Demographic, clinical, and laboratory data were prospectively recorded.Of the children enrolled, 16 (32%) failed CS therapy and required infliximab (n = 14) or colectomy (n = 2) within a median of 10 days (interquartile range [IQR] 6.5-14.5). Reflecting internal validity of the assay, GBA was highly correlated with the last CS dose and the time interval to bloodletting (r = -0.41 and r = -0.54, respectively; P < 0.001). There was no statistically significant difference in the GBA levels between responders and nonresponders (249 nM versus 200 nM cortisol equivalent, P = 0.18). In a multivariate regression model adjusted for time elapsed from CS and the administered dose, GBA did not predict response to CS (P = 0.34).The lack of correlation of GBA level and treatment outcome lends support to the hypothesis that the bioavailability, type, and dosing of intravenous CS are not associated with response or failure to the drug. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21081">
<title>Oral valganciclovir for colonic dilatation in ulcerative colitis associated with human cytomegalovirus infection</title>
<link>http://dx.doi.org/10.1002%2Fibd.21081</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21074">
<title>Detailed haplotype-tagging study of germline variation of MUC19 in inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21074</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21073">
<title>T-cell regulation of neutrophil infiltrate at the early stages of a murine colitis model</title>
<link>http://dx.doi.org/10.1002%2Fibd.21073</link>
<description><![CDATA[T-cells are a main target for antiinflammatory drugs in inflammatory bowel disease. As the innate immune system is also implicated in the pathogenesis of these diseases, T-cell suppressors may not only inhibit T-cell-dependent production of proinflammatory mediators but also affect innate immune cell function. Specifically, these drugs may impair innate immune cell recruitment and activation through inhibition of T-cells or act independent of T-cell modulation. We explored the extent of immune modulation by the T-cell inhibitor tacrolimus in a murine colitis model.We assessed the effects of tacrolimus on trinitro-benzene sulphonic acid (TNBS) colitis in wildtype and Rag2-deficient mice. The severity of colitis was assessed by means of histological scores and weight loss. We further characterized the inflammation using immunohistochemistry and by analysis of isolated intestinal leukocytes at various stages of disease.Tacrolimus-treated wildtype mice were less sensitive to colitis and had fewer activated T-cells. Inhibition of T-cell function was associated with strongly diminished recruitment of infiltrating neutrophils in the colon at the early stages of this model. In agreement, immunohistochemistry demonstrated that tacrolimus inhibited production of the neutrophil chemoattractants CXCL1 and CXCL2. Rag2-deficient mice displayed an enhanced baseline level of lamina propria neutrophils that was moderately increased in TNBS colitis and remained unaffected by tacrolimus.Both the innate and the adaptive mucosal immune system contribute to TNBS colitis. Tacrolimus suppresses colitis directly through inhibition of T-cell activation and by suppression of T-cell-mediated recruitment of neutrophils. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21071">
<title>Guillain-Barr&#xE9; syndrome during a relapse of ulcerative colitis: A case report</title>
<link>http://dx.doi.org/10.1002%2Fibd.21071</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21058">
<title>Age distribution of IBD hospitalization</title>
<link>http://dx.doi.org/10.1002%2Fibd.21058</link>
<description><![CDATA[The ages of patients with Crohn's disease (CD) and ulcerative colitis (UC) are characterized by a bimodal distribution. The present study used hospital statistics to compare the age distribution of inflammatory bowel disease (IBD) among different countries.Hospital statistics from the period 1994 to 2007 were obtained through special requests to the national statistical offices of 9 European countries. Hospitalization was expressed as age- and sex-specific rates per 10,000 living people.Hospitalization rates of different countries varied between 1.2 and 4.3 discharges per 10,000 for CD and between 0.7 and 4.7 discharges per 10,000 for UC. Countries with high CD rates were associated with similarly high UC rates (r = 0.955, P < 0.0001). In all countries alike, the age-distribution of CD hospitalization was characterized by a large peak in younger patients followed by a small peak in older patients. UC hospitalization was characterized by a small peak in younger patients followed by a large peak in older patients.The bimodal age distribution of IBD hospitalization can be explained in terms of varying exposure to 2 separate environmental risk factors that affected consecutive age groups differently over the course of the 20th century. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21057">
<title>Effect of natural commensal-origin DNA on toll-like receptor 9 (TLR9) signaling cascade, chemokine IL-8 expression, and barrier integritiy of polarized intestinal epithelial cells</title>
<link>http://dx.doi.org/10.1002%2Fibd.21057</link>
<description><![CDATA[The intestinal epithelium is constantly exposed to high levels of genetic material like bacterial DNA. Under normal physiological conditions, the intestinal epithelial monolayer as a formidable dynamic barrier with a high-polarity structure facilitates only a controlled and selective flux on components between the lumen and the underlining mucosa and even is able to facilitate structure-based macromolecules movement. The aim of this study was to test the effect of natural commensal-origin DNA on the TLR9 signaling cascade and the barrier integrity of polarized intestinal epithelial cells (IECs).Polarized HT-29 and T84 cells were treated with TNF-[alpha] in the presence or absence of DNA from Lactobacillus rhamnosus GG (LGG) and Bifidobacterium longum. TLR9 and interleukin-8 (IL-8) mRNA expression was assessed by semiquantitative and TaqMan real-time reverse-transcription polymerase chain reaction. Expression of TLR9 protein, degradation of inhibitor of kappa B alpha (I[kappa]B[alpha]), and p38 mitogen-activated protein kinase (p38 MAP) phosphorylation were assessed by Western blotting. To further reveal the role of TLR9 signaling, the TLR9 gene was silenced by siRNA. IL-8 secretion was measured by an enzyme-linked immunosorbent assay. Nuclear factor-kappa B (NF-[kappa]B) activity was assessed by the electrophoretic mobility shift assay (EMSA) and NF-[kappa]B-dependent luciferase reporter gene assays. As an indicator of tight junction formation and monolayer integrity of epithelial cell monolayers, transepithelial electrical resistance (TER) was repetitively monitored. Transmonolayer movement of natural commensal-origin DNA across monolayers was monitored using qRT-PCR and nested PCR based on bacterial 16S rRNA genes.In response to apically applied natural commensal-origin DNA, polarized HT-29 and T84 cells enhanced expression of TLR9 in a specific manner, which was subsequently associated with attenuation of TNF-[alpha]-induced NF-[kappa]B activation and NF-[kappa]B-mediated IL-8 expression. TLR9 silencing abolished this inhibitory effect. Apically applied LGG DNA attenuated TNF-[alpha]-enhanced NF-[kappa]B activity by reducing I[kappa]B[alpha] degradation and p38 phosphorylation. LGG DNA did not decrease the TER but rather diminished the TNF-[alpha]-induced TER reduction. Translocation of natural commensal-origin DNA into basolateral compartments did not occur under tested conditions.Our study indicates that TLR9 signaling mediates, at least in part, the anti-inflammatory effects of natural commensal-origin DNA on the gut because TLR9 silencing abolished the inhibitory effect of natural commensal-origin DNA on TNF-[alpha]-induced IL-8 secretion in polarized IECs. The nature of the TLR9 agonist, the polarity of cells, and the tight junction integrity of IECs has to be taken into account in order to predict the outcome of TLR9 signaling. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21088">
<title>Assessing disease activity in ulcerative colitis: Patients or their physicians?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21088</link>
<description><![CDATA[We aimed to determine the optimal approach to assess disease activity (i.e., biological inflammation) in ulcerative colitis (UC) by comparing patients' and physicians' rating of the disease.This was a prospective, multicenter, double-cohort study. The first cohort was composed of 94 children with UC (parent proxy when required) and their physicians who provided independent clinical report and global assessment of disease, rated on a 100 mm visual analog scale. Constructs of disease activity (including mucosal inflammation, laboratory tests, Mayo score, and the Pediatric UC Activity Index), were scored by an independent blinded physician and used to compare validity of the assessment. Of the 94 children, 43 were seen at a follow-up visit and provided a global rating of change in disease activity. To ascertain whether age influences assessment accuracy, a second cohort of 86 adult UC patients were analyzed in a similar way.In both cohorts the physician global assessment had higher correlations with all constructs of disease activity than did the patient' global assessment (for colonoscopic score r = 0.76 vs. r = 0.29, P = 0.002). Even with abdominal pain, a subjective item, the physician's rating had higher correlation than the patient's rating. Similarly, the physician rating of change better reflected change in disease activity than that of the patient rating.For indirect measurement of biological activity on the basis of symptoms and signs, clinician assessments are superior to those of patients. Patient assessments, physician assessments, and direct measurement of disease activity provide complementary information in clinical research. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21085">
<title>Value of fractional exhaled nitric oxide (FENO) for the diagnosis of pulmonary involvement due to inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21085</link>
<description><![CDATA[Pulmonary involvement due to inflammatory bowel disease (IBD) is frequent when evaluating a patient with IBD and pulmonary involvement remains complicated. Most of the patients are asymptomatic and the methods used are mostly invasive or expensive procedures. The aim of this prospective study is to evaluate the value of the fractional exhaled nitric oxide (FENO) level for the diagnosis of pulmonary involvement due to IBD and to investigate any correlation between FENO level and disease activity.Thirty-three nonsmoker patients with IBD (25 ulcerative colitis [UC] and 8 Crohn's Disease [CD]) who were free of corticosteroid treatment and 25 healthy subjects as a control group were enrolled in this study. All patients with IBD were investigated for pulmonary involvement with medical history, physical examination, chest roentgenogram, oxygen saturation, blood eosinophil levels, pulmonary function tests (PFTs), high-resolution computed tomography (HRCT), and FENO level.Pulmonary involvement was established in 15 patients (45.5%) with IBD. The FENO level was higher in patients with pulmonary involvement than without pulmonary involvement and healthy controls independent from the pulmonary symptoms, eosinophil count, duration of disease, activity of disease, and surgery history (FENO: 32 ± 20; 24 ± 8; 14 ± 8 ppb, respectively) (P < 0.05). In addition, diffusion capacity (DLCO) was found to be significantly lower in patients with CD compared with UC (P < 0.05).This study showed that an increased FENO level may be used for identifying patients with IBD who need further pulmonary evaluation. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21083">
<title>Azathioprine maintains long-term steroid-free remission through 3 years in patients with steroid-dependent ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21083</link>
<description><![CDATA[Studies assessing the efficacy of azathioprine (AZA) in steroid-dependent ulcerative colitis (SD-UC) are scarce. The purpose of this trial was to explore the efficacy of AZA in maintaining steroid-free remission in SD-UC patients and the factors associated with sustained response.In this observational cohort study, 42 subjects with SD-UC were recruited for AZA therapy during a 3-year period. AZA was adjusted for a target dose of 2-3 mg/kg/day. Steroid therapy was tapered off following a standardized regimen. The primary endpoint was the annual rate of steroid-free response to AZA. Secondary endpoints included clinical recurrence, yearly steroid dose, and safety of treatment.On an intention-to-treat basis, the proportion of patients remaining in steroid-free remission at 12, 24, and 36 months was 0.55, 0.52, and 0.45, respectively. A significant decrease in the flare-ups rate and in requirement for steroids were observed during 3 years on AZA compared with the previous year (P = 0.000 for both). Patients with and without sustained response were comparable according to demographics, extent of disease, dose of AZA, steroids, and 5-aminosalicylate (5-ASA) use. Only disease duration <36 months was associated with off-steroids remission (P = 0.02, odds ratio [OR] 3.12, 95% confidence interval [CI] 1.89-7.64). The AZA benefit-risk profile was favorable.In this open-label observational trial AZA showed sustained efficacy for maintenance of clinical remission off steroids and steroid sparing through 3 years of therapy in SD-UC. Patients with earlier UC are those who most probably will have sustained steroid-free remission at the end of 12 months while on AZA. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21056">
<title>Prevalence of Clostridium difficile infection in Polish pediatric patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21056</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21045">
<title>Mind-body complementary alternative medicine use and quality of life in adolescents with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21045</link>
<description><![CDATA[Mind-body complementary and alternative medicine (CAM) modalities (e.g., relaxation or meditation) for symptom management have not been well studied in adolescents with inflammatory bowel disease (IBD). The purposes of this study were to: 1) determine the prevalence of 5 types of mind-body CAM use, and consideration of use for symptom management; 2) assess characteristics associated with regular mind-body CAM use; and 3) examine whether regular and/or considered mind-body CAM use are associated with health-related quality of life (HRQOL).Sixty-seven adolescents with IBD ages 12-19 recruited from a children's hospital completed a questionnaire on CAM use and the Pediatric Quality of Life Inventory. Logistic regression models were estimated for regular and considered CAM use.Participants mean (SD) age was 15.5 (2.1) years; 37 (55%) were female; 53 (79%) were white; and 20 (30%) had moderate disease severity. Adolescents used prayer (62%), relaxation (40%), and imagery (21%) once/day to once/week for symptom management. In multivariate analyses, females were more likely to use relaxation (odds ratio [OR] = 4.38, 95% confidence interval [CI] = 1.25-15.29, c statistic = 0.73). Younger adolescents were more likely to regularly use (OR = 0.63, 95% CI = 0.42-0.95, c statistic = 0.72) or consider using (OR = 0.77, 95% CI = 0.59-1.00, c statistic = 0.64) meditation. Adolescents with more severe disease (OR = 4.17, 95% CI = 1.07-16.29, c statistic = 0.83) were more willing to consider using relaxation in the future. Adolescents with worse HRQOL were more willing to consider using prayer and meditation for future symptom management (P < 0.05).Many adolescents with IBD either currently use or would consider using mind-body CAM for symptom management. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21095">
<title>Significant association of appendiceal neoplasms and ulcerative colitis rather than Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21095</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21079">
<title>Exposure of mouse colon to dietary bile acid supplement induces sessile adenomas</title>
<link>http://dx.doi.org/10.1002%2Fibd.21079</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21061">
<title>On the role of ischemia in the pathogenesis of IBD: A review</title>
<link>http://dx.doi.org/10.1002%2Fibd.21061</link>
<description><![CDATA[Inflammatory bowel disease (IBD) is a chronic intestinal disorder comprising 2 distinct but often overlapping diseases: Crohn's disease and ulcerative colitis. Although much research to identify the etiology of IBD has focused on genetic constitution, infectious causes, and immune dysregulation, its exact cause and pathogenesis remain incompletely understood. Mesenteric blood flow, the intestinal microcirculation, and intestinal ischemia also have been proposed as etiologic, although they remain less-explored themes despite evidence suggesting a contributory role in IBD pathogenesis. The anatomy, architecture, and function of the splanchnic microcirculation will be reviewed here with regard to the development of intestinal microvascular ischemia, a pathologic process that appears to precede the classic changes that characterize IBD. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21078">
<title>Veto on vedolizumab (MLN0002) for Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21078</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21069">
<title>Fecal calprotectin mirrors inflammation of the distal ileum and bowel function after restorative proctocolectomy for pediatric-onset ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21069</link>
<description><![CDATA[The goal was to cross-sectionally assess fecal calprotectin after restorative proctocolectomy for pediatric-onset ulcerative colitis (UC).Fecal calprotectin, histology of the distal ileum, inflammation biochemistry, episodes of pouchitis, and bowel function were cross-sectionally determined at early adulthood in 32 patients who had undergone proctocolectomy with ileoanal anastomosis for UC at a mean (SD) age of 12.0 ± 4.1 years.A total of 15 (47%) patients showed increased (>100 [mu]g/g) fecal calprotectin (669 ± 866 [mu]g/g), although their serum C-reactive protein (5.2 ± 3.8 mg/L), erythrocyte sedimentation rate (13 ± 13 mm/h), and white blood cell count (6.7 ± 1.7 E9/L) were normal or slightly elevated. Calprotectin correlated positively with the histological neutrophil count of the distal ileum (r = 0.715; P < 0.001), the frequency of pouchitis (r = 0.468; P < 0.01), and with the maximum daily frequency of bowel actions (r = 0.610; P < 0.001). Mean fecal calprotectin was 71 ± 50 [mu]g/g among patients with no history of pouchitis (n = 10), 290 ± 131 [mu]g/g among patients with a single episode of pouchitis (n = 15), and 832 ± 422 [mu]g/g among those with recurrent pouchitis (P = 0.019 between recurrent pouchitis and no pouchitis). Sensitivity, specificity, positive predictive value, and negative predictive value for fecal calprotectin concentration over 300 [mu]g/g to detect recurrent pouchitis were 57%, 92%, 67%, and 89%, respectively.Neutrophilic inflammation of the distal ileum, as reflected by fecal calprotectin, is common after restorative proctocolectomy for pediatric-onset UC. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21075">
<title>Cytokine mRNA expression in steroid-na&#xEF;ve patients with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21075</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21067">
<title>Endoscopic ultrasound to guide the combined medical and surgical management of pediatric perianal Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21067</link>
<description><![CDATA[Perianal fistulas are a debilitating manifestation of Crohn's disease (CD) in the pediatric population and present a management challenge. The aims of this study were to describe our experience using endoscopic ultrasound (EUS) to guide management of perianal CD (PCD) in a pediatric population, and determine whether using EUS to monitor healing after seton placement improves outcomes.We conducted a retrospective study of 2 cohorts: pediatric subjects with PCD who underwent EUS and pediatric subjects who underwent seton placement between 2002 and 2007.In all, 25 children underwent a total of 42 EUS procedures. Of 28 EUSs performed to evaluate suspected perianal disease, complex fistulizing disease was identified in 15 (54%). Setons were placed after most EUSs demonstrating complex fistulizing disease and after none demonstrating superficial or no fistulizing disease. Of 14 EUSs performed to monitor healing around a seton, 7 (50%) demonstrated persistent peri-seton inflammation. Setons were more often left in place after an EUS revealing persistent inflammation (86% versus 0%), and the patients were more likely to have a biologic initiated or changed (57% versus 0%). Among all subjects who underwent seton placement, time from seton removal to recurrence was longer for those followed by EUS compared to those followed by physical exam only; however, we were not powered to test for statistical significance.EUS to guide the combined medical and surgical management of PCD is feasible in the pediatric population. Larger prospective studies are needed to determine if EUS-directed management improves outcomes in pediatric patients with PCD. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21054">
<title>Similar geographic variations of mortality and hospitalization associated with IBD and Clostridium difficile colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21054</link>
<description><![CDATA[Superinfection with Clostridium difficile can aggravate the symptoms of preexisting inflammatory bowel disease (IBD). The study served to assess whether the geographic variation of IBD within the United States might be influenced by C. difficile infection.Hospitalization data of the Healthcare Cost and Utilization Project (HCUP) from 2001-2006 and mortality data from 1979-2005 of the US were analyzed by individual states. Hospitalization and mortality associated with Crohn's disease (CD), ulcerative colitis (UC), and C. difficile colitis were correlated with each other, using weighted least square linear regression with the population size of individual states as weight.Among the hospitalization rates, there were strong correlations between both types of IBD, as well as each type of IBD with C. difficile colitis. Similarly, among the mortality rates there were strong correlations between both types of IBD, as well as each type of IBD with C. difficile colitis. Lastly, each type of hospitalization rate was also strongly correlated with each type of mortality rate. In general, hospitalization and mortality associated with IBD tended to be frequent in many of the northern states and infrequent in the Southwest and several southern states.The similarity in the geographic distribution of the 3 diseases could indicate the influence of C. difficile colitis in shaping the geographic patterns of IBD. It could also indicate that shared environmental risk factors influence the occurrence of IBD, as well as C. difficile colitis. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21051">
<title>Does primary sclerosing cholangitis impact quality of life in patients with inflammatory bowel disease?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21051</link>
<description><![CDATA[Impairment of health-related quality of life (HRQoL) is an important concern in inflammatory bowel disease (IBD; ulcerative colitis [UC], Crohn's disease [CD]). Between 2%-10% of patients with IBD have primary sclerosing cholangitis (PSC). There has been limited examination of the disease-specific HRQoL in this population compared to non-PSC IBD controls.This was a retrospective, case-control study performed at a tertiary referral center. Cases comprised 26 patients with a known diagnosis of PSC and IBD (17 UC, 9 CD). Three random controls were selected for each case after matching for IBD type, gender, age, and duration of disease. Disease-specific HRQoL was measured using the Short Inflammatory Bowel Disease Questionnaire (SIBDQ). Disease activity for CD was measured using the Harvey-Bradshaw index (HB) and using the UC activity index for UC. Independent predictors of HRQoL were identified.There was no significant difference in the age, gender distribution, or disease duration between PSC-IBD and controls. There was no difference in use of immunomodulators or biologics between the 2 groups. Mean SIBDQ score was comparable between PSC-IBD patients (54.5) and controls (54.1), both for UC and CD. Likewise, the disease activity scores were also similar (2.8 versus 3.1, P = 0.35). On multivariate analysis, higher disease activity score (-1.33, 95% confidence interval [CI] 95% CI -1.85 to -0.82) and shorter disease duration were predictive of lower HRQoL. Coexisting PSC did not influence IBD-related HRQoL. There was a higher proportion of permanent work disability in PSC-IBD (7.7%) compared to controls (0%).PSC does not seem to influence disease-specific HRQoL in our patients with IBD but is associated with a higher rate of work disability. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21032">
<title>Need for standardization in population-based quality of life studies: A review of the current literature</title>
<link>http://dx.doi.org/10.1002%2Fibd.21032</link>
<description><![CDATA[In this systematic review we focus on the current use of and knowledge on health related quality of life in unselected, population-based IBD cohorts. We made a systematic literature search and included for comprehensive review papers that described a population-based cohort and that used validated HRQoL instruments. We show that even studies defined by the authors as population-based do not always meet the criteria set for being population-based. The heterogeneity of the study populations we have reviewed emphasizes that "population-based" must be defined very meticulously and that study populations need to be scrutinized with regard to all characteristics of the cohort before one can compare their results. Different definitions of study populations as population-based affect outcomes. We also show that use of the same HRQoL questionnaires does not guarantee comparable results as there are several different versions of the questionnaires, the different translations are not always comparable and at last there are several methods of computing and presenting the data. Detailed accumulation of knowledge and thorough meta analyses is therefore difficult hence we find it necessary to raise a discussion on the need of standardization in this field of research and we make some simple recommendations on factors we find important. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21049">
<title>Sulfasalazine-induced nephrotic syndrome in a patient with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21049</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21047">
<title>TNF-[alpha] is an important pathogenic factor contributing to reactivation of cytomegalovirus in inflamed mucosa of colon in patients with ulcerative colitis: Lesson from clinical experience</title>
<link>http://dx.doi.org/10.1002%2Fibd.21047</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21044">
<title>Development of glomerulonephritis early in the course of Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21044</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21040">
<title>Gastrointestinal manifestations in primary immune disorders</title>
<link>http://dx.doi.org/10.1002%2Fibd.21040</link>
<description><![CDATA[The gastrointestinal tract is the largest lymphoid organ in the body containing T and B lymphocytes, macrophages, and dendritic cells. Despite the fact that these cells are constantly confronted with antigen primarily in the form of food and bacteria, immune responses in the gut are tightly regulated to maintain homeostasis. Without this balance of active immunity and tolerance, mucosal inflammation may ensue, and manifest as Crohn's disease, ulcerative colitis, pernicious anemia, or celiac sprue. Therefore, it is not unreasonable that inflammatory diseases of the gut are commonly encountered in patients with primary immune deficiencies. The exact pathogenesis of gastrointestinal diseases in the setting of primary immunodeficiency remains unknown, however, both humoral and cell-mediated immunity appear to play a role in preventing intestinal inflammation. Patients presenting with atypical gastrointestinal disease and/or failure to respond to conventional therapy should be evaluated for an underlying primary immune disorder in order to initiate appropriate treatment, such as immunoglobulin or in more severe cases bone marrow transplantation, to prevent long term complications. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21033">
<title>Salmonella septic arthritis in a patient with Crohn&#x27;s disease on infliximab</title>
<link>http://dx.doi.org/10.1002%2Fibd.21033</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21005">
<title>Acute lymphoid leukemia in a Crohn&#x27;s disease patient during treatment with adalimumab after a prolonged treatment with azathioprine and steroids</title>
<link>http://dx.doi.org/10.1002%2Fibd.21005</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21072">
<title>Granulocyte-macrophage colony-stimulating factor elicits bone marrow-derived cells that promote efficient colonic mucosal healing</title>
<link>http://dx.doi.org/10.1002%2Fibd.21072</link>
<description><![CDATA[Granulocyte-macrophage colony-stimulating factor (GM-CSF) therapy is effective in treating some Crohn's disease (CD) patients and protects mice from colitis induced by dextran sulfate sodium (DSS) administration. However, its mechanisms of action remain elusive. We hypothesized that GM-CSF affects intestinal mucosal repair.DSS colitic mice were treated with daily pegylated GM-CSF or saline and clinical, histological, and inflammatory parameters were kinetically evaluated. Further, the role of bone marrow-derived cells in the impact of GM-CSF therapy on DSS colitis was addressed using cell transfers.GM-CSF therapy reduced clinical signs of colitis and the release of inflammatory mediators. GM-CSF therapy improved mucosal repair, with faster ulcer reepithelialization, accelerated hyperproliferative response of epithelial cells in ulcer-adjacent crypts, and lower colonoscopic ulceration scores in GM-CSF-administered mice relative to untreated mice. We observed that GM-CSF-induced promotion of mucosal repair is timely associated with a reduction in neutrophil numbers and increased accumulation of CD11b+ monocytic cells in colon tissues. Importantly, transfer of splenic GM-CSF-induced CD11b+ myeloid cells into DSS-exposed mice improved colitis, and lethally irradiated GM-CSF receptor-deficient mice reconstituted with wildtype bone marrow cells were protected from DSS-induced colitis upon GM-CSF therapy. Lastly, GM-CSF-induced CD11b+ myeloid cells were shown to promote in vitro wound repair.Our study shows that GM-CSF-dependent stimulation of bone marrow-derived cells during DSS-induced colitis accelerates colonic tissue repair. These data provide a putative mechanism for the observed beneficial effects of GM-CSF therapy in Crohn's disease. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21009">
<title>Severe sporotrichoid fishtank granuloma following infliximab therapy for Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21009</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20998">
<title>Splenic tuberculosis in a patient with Crohn&#x27;s disease on infliximab: Case report</title>
<link>http://dx.doi.org/10.1002%2Fibd.20998</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21020">
<title>Sterile seroma after surgical drainage of purulent psoas abscess in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21020</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21017">
<title>Potential for amino acids supplementation during inflammatory bowel diseases</title>
<link>http://dx.doi.org/10.1002%2Fibd.21017</link>
<description><![CDATA[The pathophysiology of inflammatory bowel diseases (IBDs) is multifactorial and involves interactions of gut luminal content with mucosal barrier and especially immune cells. Malnutrition is a frequent issue during IBD flares, especially in Crohn's disease (CD) patients, and nutritional support is frequently used to treat malnutrition but also in an attempt to modulate intestinal inflammation. The use of oral or enteral nutrition intervention in IBDs may be effective, alone or in combination with drugs, to achieve and maintain remission. However, standard diets are less effective than new-generation biotherapies and could be improved by supplementation with specific immunomodulatory amino acids. Experimental studies evaluating glutamine, the preferential substrate for enterocytes, are promising. Some clinical studies with oral glutamine in CD are until now disappointing, but new formulations and targeting could enhance glutamine efficacy at the site of mucosal lesions. The role of arginine, involved in nitric oxide and polyamines synthesis, still remains debated. However, the effects of these amino acids in IBD have been poorly documented in humans. Other candidates like glycine, cysteine, histidine, or taurine should also be evaluated in the future. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20996">
<title>Cerebral venous thrombosis in inflammatory bowel diseases</title>
<link>http://dx.doi.org/10.1002%2Fibd.20996</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21015">
<title>Does methotrexate induce mucosal healing in Crohn&#x27;s disease?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21015</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21006">
<title>Atrioventricular block associated with Crohn&#x27;s relapsing colitis in a 12-year-old child</title>
<link>http://dx.doi.org/10.1002%2Fibd.21006</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20982">
<title>Elevated serum chromogranin A in irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD): A shared model for pathogenesis?</title>
<link>http://dx.doi.org/10.1002%2Fibd.20982</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20981">
<title>Current smoking, not duration of remission, delays Crohn&#x27;s disease relapse following azathioprine withdrawal</title>
<link>http://dx.doi.org/10.1002%2Fibd.20981</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20980">
<title>Varicella pneumonia in an immunocompromised inflammatory bowel disease patient</title>
<link>http://dx.doi.org/10.1002%2Fibd.20980</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20779">
<title>Endoscopic healing should be a goal for everyone with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20779</link>
<description><![CDATA[No abstract.]]></description>
</item>

</rdf:RDF>