<?xml version="1.0" encoding="UTF-8"?>

<rdf:RDF
 xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
 xmlns="http://purl.org/rss/1.0/"
 xmlns:content="http://purl.org/rss/1.0/modules/content/"
 xmlns:taxo="http://purl.org/rss/1.0/modules/taxonomy/"
 xmlns:dc="http://purl.org/dc/elements/1.1/"
 xmlns:syn="http://purl.org/rss/1.0/modules/syndication/"
 xmlns:admin="http://webns.net/mvcb/"
>

<channel rdf:about="http://www.gourt.com/Health/Medicine/Medical-Specialties/Gastroenterology/Journals.html">
<title>Journals RSS : Gourt</title>
<link>http://www.gourt.com/Health/Medicine/Medical-Specialties/Gastroenterology/Journals.html</link>
<description></description>
<dc:language>en-us</dc:language>
<dc:rights>Copyright 2007, Gourt.com</dc:rights>
<dc:date>2009-07-02T18:32+39:00
</dc:date>
<dc:publisher>rtruog@gourt.com</dc:publisher>
<dc:creator>rtruog@gourt.com</dc:creator>
<dc:subject>Journals RSS : Gourt</dc:subject>
<syn:updatePeriod>hourly</syn:updatePeriod>
<syn:updateFrequency>1</syn:updateFrequency>
<syn:updateBase>1901-01-01T00:00+00:00</syn:updateBase>
<items>
 <rdf:Seq>
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1590865809002448&#x26;_version=1&#x26;md5=e5494ec870c718115a59c4861306be4b" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004553&#x26;_version=1&#x26;md5=cc94d074f800586887ff3345f003c025" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004528&#x26;_version=1&#x26;md5=712458fc4564793e80d5ff0d34e83f0a" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004516&#x26;_version=1&#x26;md5=2ae0f8162b096f1a731c65e731a4b6ee" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004504&#x26;_version=1&#x26;md5=016958384993f7f79f8da3eb09bc1d10" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509006004&#x26;_version=1&#x26;md5=2276f6880c4e3eaf2785078f19ee558a" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005990&#x26;_version=1&#x26;md5=3d0e65146b144c7e866986a2609abf79" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005977&#x26;_version=1&#x26;md5=7feacbd79bf7f30d571461bf098c0be0" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005953&#x26;_version=1&#x26;md5=da3880fc1d8b31b78726e0f71d570c58" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S154235650900593X&#x26;_version=1&#x26;md5=8060e5f39c3cb5e7eb15616e4a30bf63" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005916&#x26;_version=1&#x26;md5=f95e76ebe35827ac6cec96d07a8b6131" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004947&#x26;_version=1&#x26;md5=9fa50d7a855ab96def037195b4937cd2" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004959&#x26;_version=1&#x26;md5=120501cab97ef44558b075ced6f27739" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005965&#x26;_version=1&#x26;md5=0bc9e4485021065acacd6ffa3de98ead" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004935&#x26;_version=1&#x26;md5=769b2f6a4fcf200f863cc5f362f0d59e" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005928&#x26;_version=1&#x26;md5=64a22bd7b634cb4902f5b76d176ac839" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509006016&#x26;_version=1&#x26;md5=3d5e4282d7ee814559d6f8eb8ac93f3a" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004923&#x26;_version=1&#x26;md5=badb42a84842a5a0aa3a92e2d9134224" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004911&#x26;_version=1&#x26;md5=f08fce2af0542aa57f4dcb4a6973b689" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005989&#x26;_version=1&#x26;md5=9b54ad6eee21a0cb277085cb92a4220e" />
  <rdf:li rdf:resource="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19563914&#x26;dopt=Abstract" />
  <rdf:li rdf:resource="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19563913&#x26;dopt=Abstract" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.88" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.78" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.74" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.79" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.73" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.75" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.80" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.84" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.82" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.81" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.63" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.83" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.70" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.72" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.69" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.43" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1038/nrgastro.2009.65" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21031" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21029" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21028" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21020" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21017" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21013" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21011" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21007" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21018" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21014" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21003" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20993" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20985" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20977" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20970" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20961" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20949" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20928" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20989" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20919" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20986" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20981" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20976" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20974" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20973" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20968" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20967" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20966" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20965" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20964" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20963" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20954" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20951" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20946" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20943" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20987" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20988" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20978" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20971" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20956" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20950" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20969" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20962" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20960" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20958" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20957" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20955" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20953" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20948" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20947" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20942" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20941" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20939" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20937" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20926" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20925" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20924" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20980" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20940" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20938" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20930" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20929" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20871" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20920" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20911" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20935" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20934" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20927" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20932" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20917" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20921" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20923" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20922" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20916" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20913" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20912" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20910" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20909" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20902" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20918" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20906" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20933" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20931" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20915" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20908" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20905" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20914" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20907" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20904" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20892" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20896" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20903" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20901" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20899" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20898" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20897" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20895" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20889" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20890" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20886" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20887" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20866" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20888" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20891" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20883" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20869" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20884" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20882" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20870" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20874" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20867" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20864" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20861" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20878" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20856" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20823" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20840" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20836" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20834" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20832" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20830" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20841" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20853" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20822" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20802" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20801" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20791" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20795" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20789" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20779" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20775" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20773" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20790" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20796" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20784" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20772" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20769" />
 </rdf:Seq>
</items>
</channel>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1590865809002448&#x26;_version=1&#x26;md5=e5494ec870c718115a59c4861306be4b">
<title>Optical coherence tomography in children with coeliac disease</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1590865809002448&#x26;_version=1&#x26;md5=e5494ec870c718115a59c4861306be4b</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004553&#x26;_version=1&#x26;md5=cc94d074f800586887ff3345f003c025">
<title>The complexities of hepatitis C virus entry?</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004553&#x26;_version=1&#x26;md5=cc94d074f800586887ff3345f003c025</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004528&#x26;_version=1&#x26;md5=712458fc4564793e80d5ff0d34e83f0a">
<title>Forewarned is forearmed?</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004528&#x26;_version=1&#x26;md5=712458fc4564793e80d5ff0d34e83f0a</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004516&#x26;_version=1&#x26;md5=2ae0f8162b096f1a731c65e731a4b6ee">
<title>Infection and inflammation in liver failure: Two sides of the same coin?</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004516&#x26;_version=1&#x26;md5=2ae0f8162b096f1a731c65e731a4b6ee</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004504&#x26;_version=1&#x26;md5=016958384993f7f79f8da3eb09bc1d10">
<title>Coronary artery disease in liver cirrhosis: Does the aetiology of liver disease matter?</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0168827809004504&#x26;_version=1&#x26;md5=016958384993f7f79f8da3eb09bc1d10</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509006004&#x26;_version=1&#x26;md5=2276f6880c4e3eaf2785078f19ee558a">
<title>Reactivation of Hepatitis B with Reappearance of Hepatitis B Surface Antigen After Chemotherapy and Immune Suppression</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509006004&#x26;_version=1&#x26;md5=2276f6880c4e3eaf2785078f19ee558a</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005990&#x26;_version=1&#x26;md5=3d0e65146b144c7e866986a2609abf79">
<title>International Consensus Guidelines for Surgical Resection of Mucinous Neoplasms Cannot Be Applied to All Cystic Lesions of the Pancreas</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005990&#x26;_version=1&#x26;md5=3d0e65146b144c7e866986a2609abf79</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005977&#x26;_version=1&#x26;md5=7feacbd79bf7f30d571461bf098c0be0">
<title>A systematic prospective comparison of non-invasive disease activity indices in ulcerative colitis</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005977&#x26;_version=1&#x26;md5=7feacbd79bf7f30d571461bf098c0be0</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005953&#x26;_version=1&#x26;md5=da3880fc1d8b31b78726e0f71d570c58">
<title>A 38 year old with recurrent colitis. Is it noncompliance?</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005953&#x26;_version=1&#x26;md5=da3880fc1d8b31b78726e0f71d570c58</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S154235650900593X&#x26;_version=1&#x26;md5=8060e5f39c3cb5e7eb15616e4a30bf63">
<title>Response to Lankisch et al</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S154235650900593X&#x26;_version=1&#x26;md5=8060e5f39c3cb5e7eb15616e4a30bf63</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005916&#x26;_version=1&#x26;md5=f95e76ebe35827ac6cec96d07a8b6131">
<title>A randomized controlled trial of enemas in combination with oral laxative therapy for children with chronic constipation</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005916&#x26;_version=1&#x26;md5=f95e76ebe35827ac6cec96d07a8b6131</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004947&#x26;_version=1&#x26;md5=9fa50d7a855ab96def037195b4937cd2">
<title>Copyright Assignment, Authorship Responsibility, NIH Funding, Financial Disclosure, Institutional Review Board/Animal Care Committee Approval, and Sponsorship</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004947&#x26;_version=1&#x26;md5=9fa50d7a855ab96def037195b4937cd2</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004959&#x26;_version=1&#x26;md5=120501cab97ef44558b075ced6f27739">
<title>Information for Authors</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004959&#x26;_version=1&#x26;md5=120501cab97ef44558b075ced6f27739</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005965&#x26;_version=1&#x26;md5=0bc9e4485021065acacd6ffa3de98ead">
<title>Epidemiology of Eosinophilic Esophagitis over 3 Decades in Olmsted County, Minnesota</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005965&#x26;_version=1&#x26;md5=0bc9e4485021065acacd6ffa3de98ead</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004935&#x26;_version=1&#x26;md5=769b2f6a4fcf200f863cc5f362f0d59e">
<title>Information for Authors and Readers</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004935&#x26;_version=1&#x26;md5=769b2f6a4fcf200f863cc5f362f0d59e</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005928&#x26;_version=1&#x26;md5=64a22bd7b634cb4902f5b76d176ac839">
<title>Grievous Disease</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005928&#x26;_version=1&#x26;md5=64a22bd7b634cb4902f5b76d176ac839</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509006016&#x26;_version=1&#x26;md5=3d5e4282d7ee814559d6f8eb8ac93f3a">
<title>The Impact of Narrow Band Imaging in Screening Colonoscopy: A Randomized Controlled Trial</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509006016&#x26;_version=1&#x26;md5=3d5e4282d7ee814559d6f8eb8ac93f3a</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004923&#x26;_version=1&#x26;md5=badb42a84842a5a0aa3a92e2d9134224">
<title>Contents</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004923&#x26;_version=1&#x26;md5=badb42a84842a5a0aa3a92e2d9134224</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004911&#x26;_version=1&#x26;md5=f08fce2af0542aa57f4dcb4a6973b689">
<title>Editorial Board</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509004911&#x26;_version=1&#x26;md5=f08fce2af0542aa57f4dcb4a6973b689</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005989&#x26;_version=1&#x26;md5=9b54ad6eee21a0cb277085cb92a4220e">
<title>Do We Know What Patients Want? The Doctor-Patient communication gap in Functional Gastrointestinal Disorders</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1542356509005989&#x26;_version=1&#x26;md5=9b54ad6eee21a0cb277085cb92a4220e</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=19563914&#x26;dopt=Abstract">
<title>Reply: Persistent Nausea and Abdominal Pain in a Patient with Delayed Gastric Emptying: Shall We Think of Celiac Disease?</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19563914&#x26;dopt=Abstract</link>
<description><![CDATA[
	 Related Articles
        Reply: Persistent Nausea and Abdominal Pain in a Patient with Delayed Gastric Emptying: Shall We Think of Celiac Disease?
        Clin Gastroenterol Hepatol. 2009 Jun 26;
        Authors:  Friedenberg FK, Parkman HP
        
        PMID: 19563914 [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=19563913&#x26;dopt=Abstract">
<title>Reply:</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19563913&#x26;dopt=Abstract</link>
<description><![CDATA[
	 Related Articles
        Reply:
        Clin Gastroenterol Hepatol. 2009 Jun 26;
        Authors:  Ananthakrishnan AN, McGinley EL, Saeian K
        
        PMID: 19563913 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.88">
<title>Keep your cool: burn calories</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.88</link>
<description><![CDATA[The relevance of brown adipose tissue (brown fat) and its potential role in the prevention and management of obesity has been examined in a recent series of articles. That energy intake in excess of energy expenditure leads to the accumulation of adipose tissue is no ]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.78">
<title>Ulcerative colitis: Appendicitis, but not appendectomy, reduces risk of ulcerative colitis</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.78</link>
<description><![CDATA[


Ulcerative colitis: Appendicitis, but not appendectomy, reduces risk of ulcerative colitis

Nature Reviews Gastroenterology &amp; Hepatology 6, 317 (2009). doi:10.1038/nrgastro.2009.78

Author: Susan J. Allison

]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.74">
<title>IBD: Diagnosis by proteasome pattern</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.74</link>
<description><![CDATA[


IBD: Diagnosis by proteasome pattern

Nature Reviews Gastroenterology &amp; Hepatology 6, 318 (2009). doi:10.1038/nrgastro.2009.74

Author: Rachel S. Jones

]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.79">
<title>Esophageal cancer: Hot tea raises risk of cancer</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.79</link>
<description><![CDATA[


Esophageal cancer: Hot tea raises risk of cancer

Nature Reviews Gastroenterology &amp; Hepatology 6, 318 (2009). doi:10.1038/nrgastro.2009.79

Author: Rachel S. Jones

]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.73">
<title>Prediction of recurrent C. difficile infection</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.73</link>
<description><![CDATA[


Prediction of recurrent C. difficile infection

Nature Reviews Gastroenterology &amp; Hepatology 6, 319 (2009). doi:10.1038/nrgastro.2009.73

Author: Susan J. Allison

]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.75">
<title>Liver: Dietary links to NAFLD in nonobese patients</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.75</link>
<description><![CDATA[


Liver: Dietary links to NAFLD in nonobese patients

Nature Reviews Gastroenterology &amp; Hepatology 6, 320 (2009). doi:10.1038/nrgastro.2009.75

Author: Susan J. Allison

]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.80">
<title>Gastrointestinal stromal tumor: Adjuvant imatinib mesylate therapy improves recurrence-free survival</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.80</link>
<description><![CDATA[


Gastrointestinal stromal tumor: Adjuvant imatinib mesylate therapy improves recurrence-free survival

Nature Reviews Gastroenterology &amp; Hepatology 6, 320 (2009). doi:10.1038/nrgastro.2009.80

Author: Rachel S. Jones

]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.84">
<title>Pancreas: Alcoholic pancreatitis&#x2014;it&#x27;s the alcohol, stupid</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.84</link>
<description><![CDATA[The management of alcoholic pancreatitis is mostly reactive; little is done to prevent disease progression. It is time for physicians to pay attention to the root cause of the condition—that is, alcohol—rather than just responding to its effects. This article discusses an important paper that describes the first prospective, randomized, controlled, clinical trial to investigate the effect of brief interventions for alcohol abuse on the progression of alcoholic pancreatitis.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.82">
<title>Rectal cancer: The evolution of laparoscopy&#x2014;what&#x27;s next?</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.82</link>
<description><![CDATA[Despite advances in laparoscopic surgery for colorectal cancer, the role of laparoscopic approaches for rectal cancer remains controversial. A large, single-center study has now demonstrated the safety and feasibility of laparoscopy for rectal cancer, which provides new incentives for prospective clinical trials to rigorously test this surgical approach.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.81">
<title>Motility: Prucalopride for chronic constipation</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.81</link>
<description><![CDATA[Many patients with chronic constipation have a poor quality of life and are dissatisfied with laxative treatment. Findings from a multicenter, randomized, placebo-controlled, phase III study have demonstrated the beneficial effects of the 5-hydroxytryptamine 4 receptor agonist, prucalopride, for chronic constipation and associated symptoms. This drug represents the newest addition to the medical armamentarium for this disorder.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.63">
<title>Hepatitis C: New therapeutic strategies needed for advanced disease</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.63</link>
<description><![CDATA[Approximately 50% of patients with chronic hepatitis C fail to achieve a sustained virological response to standard therapy with pegylated interferon and ribavirin. Progression to advanced liver disease (which may lead to hepatic decompensation, hepatocellular carcinoma, and death) is common in these patients, but can low-dose pegylated interferon maintenance therapy improve outcomes?]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.83">
<title>Surgery: Neoadjuvant chemoradiation and sphincter preservation</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.83</link>
<description><![CDATA[The benefit of preoperative combined chemotherapy and radiotherapy to perform sphincter-preserving surgery for patients with locally advanced distal rectal cancer is not supported by findings from randomized, controlled trials. These findings have, however, now been questioned by a study that supports the prospect of a tailored surgical approach to rectal-cancer treatment on the basis of tumor behavior after neoadjuvant treatment.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.70">
<title>Management of gastric polyps: a pathology-based guide for gastroenterologists</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.70</link>
<description><![CDATA[1–4% of patients who undergo gastric biopsy have gastric polyps. These lesions may be true epithelial polyps, heterotopias, lymphoid tissue, or stromal lesions. Hyperplastic polyps, which arise in patients with underlying gastritis, and fundic-gland polyps, which are associated with PPI therapy, are the most common ]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.72">
<title>Actions and therapeutic pathways of ghrelin for gastrointestinal disorders</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.72</link>
<description><![CDATA[Ghrelin is a peptide hormone that possesses unique orexigenic properties. By acting on the growth-hormone secretagogue receptor 1a, ghrelin induces a short-term increase in food consumption, which ultimately induces a positive energy balance and increases fat deposition. Reduced ghrelin levels have been observed in obese ]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.69">
<title>Capsule endoscopy: progress update and challenges ahead</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.69</link>
<description><![CDATA[Capsule endoscopy (CE) enables remote diagnostic inspection of the gastrointestinal tract without sedation and with minimal discomfort. Initially intended for small-bowel endoscopy, modifications to the original capsule have since been introduced for imaging of the esophagus and the colon. This Review presents a research update ]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.43">
<title>A guide for the diagnosis and management of gastrointestinal stromal cell tumors</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.43</link>
<description><![CDATA[Gastrointestinal stromal cell tumors (GISTs) are the most common mesenchymal neoplasm of the gastrointestinal tract and are frequently detected on routine endoscopy. Although only ∼10–30% of GISTs are clinically malignant, all may have some degree of malignant potential. Preoperative determination of malignancy risk can be ]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1038/nrgastro.2009.65">
<title>Treatment of chronic hepatitis C in a slow responder: a case for extended therapy</title>
<link>http://dx.doi.org/10.1038/nrgastro.2009.65</link>
<description><![CDATA[Background. A 49-year-old white man presented to his primary-care clinic with fatigue and poor concentration. He had an enlarged liver with a minimally tender edge and was subsequently referred to our liver clinic.Investigations. Physical examination, laboratory investigations (including tests for HCV-RNA, antibodies ]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21031">
<title>Epithelial vanin-1 controls inflammation-driven carcinogenesis in the colitis-associated colon cancer model</title>
<link>http://dx.doi.org/10.1002%2Fibd.21031</link>
<description><![CDATA[Vanin-1 is an epithelial pantetheinase that provides cysteamine to tissue and regulates response to stress. Vanin-1 is expressed by enterocytes, and its absence limits intestinal epithelial cell production of proinflammatory signals. A link between chronic active inflammation and cancer is illustrated in patients with ulcerative colitis, who have an augmented risk of developing colorectal cancer. Indeed, sustained inflammation provides advantageous growth conditions to tumors. We examined whether epithelial cells affect tumorigenesis through vanin-1-dependent modulation of colonic inflammation.To vanin-1-/- mice, we applied the colitis-associated cancer (CAC) protocol, which combines injection of azoxymethane (AOM) with repeated administrations of dextran sodium sulfate (DSS). We numbered tumors and quantified macrophage infiltration and molecular markers of cell death and proliferation. We also tested DSS-induced colitis. We scored survival, tissue damages, proinflammatory cytokine production, and tissue regeneration. Finally, we explored activation pathways by biochemical analysis on purified colonic epithelial cells (CECs) and in situ immunofluorescence.Vanin-1-/- mice displayed a drastically reduced incidence of colorectal cancer in the CAC protocol and manifested mild clinical signs of DSS-induced colitis. The early impact of vanin-1 deficiency on tumor induction was directly correlated to the amount of inflammation and subsequent epithelial proliferation rather than cell death rate; all this was linked to the modulation of NF-[kappa]B pathway activation in CECs.These results emphasize the importance of the intestinal epithelium in the control of mucosal inflammation acting as a cofactor in carcinogenesis. This might lead to novel anti-inflammatory strategies useful in cancer therapy. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21029">
<title>Resolvin E1, an endogenous lipid mediator derived from eicosapentaenoic acid, prevents dextran sulfate sodium-induced colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21029</link>
<description><![CDATA[Resolvin E1 (RvE1), an endogenous lipid mediator derived from eicosapentaenoic acid, has been identified in local inflammation during the healing stage. RvE1 reduces inflammation in several types of animal models including peritonitis and retinopathy and blocks human neutrophil transendothelial cell migration. The RvE1 receptor ChemR23 is expressed on myeloid cells such as macrophages and dendritic cells. The aim of this study was to determine whether RvE1 regulates colonic inflammation when the innate immune response of macrophages plays a key role in pathogenesis and tissue damage.The RvE1 receptor ChemR23 was expressed in mouse peritoneal macrophages as defined by flow cytometry. Peritoneal macrophages were pretreated with RvE1, followed by lipopolysaccharide stimulation, whereupon transcriptional levels of proinflammatory cytokines were analyzed.RvE1 treatment led to inhibition of proinflammatory cytokines including TNF-[alpha] and IL-12p40. In HEK293 cells, pretreatment with RvE1 inhibited TNF-[alpha]-induced nuclear translocation of NF-[kappa]B in a ChemR23-dependent manner. These results suggested that RvE1 could regulate proinflammatory responses of macrophages expressing ChemR23. Therefore, we investigated the beneficial effects of RvE1 in dextran sulfate sodium-induced colitis. RvE1 treatment led to amelioration of colonic inflammation.These results indicate that RvE1 suppresses proinflammatory responses of macrophages. RvE1 and its receptor may therefore be useful as therapeutic targets in the treatment of human inflammatory bowel disease and other inflammatory disorders. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21028">
<title>Quality of care in inflammatory bowel disease: A review and discussion</title>
<link>http://dx.doi.org/10.1002%2Fibd.21028</link>
<description><![CDATA[The Institute of Medicine's publications To Err Is Human and Crossing the Quality Chasm publicized the widespread deficits in U.S. health care quality. Emerging studies continue to reveal deficits in the quality of adult and pediatric care, including subspecialty care. The inflammatory bowel diseases (IBD) Crohn's disease and ulcerative colitis require diligent, long-term management and attention to their impact on intestinal and extraintestinal organ systems. Although the quality of IBD care has not been prospectively or comprehensively evaluated in the United States, several small studies have demonstrated significant variation in care. As variation may indicate underuse, overuse, or misuse of medical services, such variation suggests a clear need for translating evidence-based practices into the actual practice and follow-up provided for patients. This article reviews the history, rationale, and methods of quality measurement and improvement and identifies the unique challenges in adapting these general strategies to the care of the inflammatory bowel diseases. Inflamm Bowel Dis 2009]]></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.21013">
<title>MDP-Induced selective tolerance to TLR4 ligands: Impairment in NOD2 mutant Crohn&#x27;s disease patients</title>
<link>http://dx.doi.org/10.1002%2Fibd.21013</link>
<description><![CDATA[Pathogen infection is a complex process in which several pathogen-recognition receptor (PRR) pathways are activated to induce proinflammatory mediators. The activation of multiple PRRs suggests an interaction between Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain-like receptor (NOD) signaling pathways.To understand the modulation induced by NOD2 signals on successive responses to pathogen-associated molecular patterns (PAMPs), we examined how muramyl dipeptide (MDP) pretreatment reprograms the MDP+LPS (lipopolysaccharide) response of monocytes from human peripheral blood.Preexposure to bacterial MDP components induced selective tolerance to a subsequent NOD2+TLR4 stimulation. MDP pretreatment inhibited the production of tumor necrosis factor alpha (TNF[alpha]) and interleuken 10 (IL10), whereas IL6 and IL8 remained unaffected. MDP-induced tolerance was independent of receptor downregulation but was associated with reduced levels of phosphorylated TAK1 and abrogated phosphorylation of the downstream MAPK.Since Nod2 mutations have been associated with susceptibility to develop Crohn's disease (CD), we compared the MDP-induced tolerance in healthy donors and CD patients with compound heterozygous Nod2 mutations (Mut-Nod2) expressing variant NOD2 proteins. MDP-induced tolerance in Mut-Nod2 patients reduced IL10 but not TNF[alpha] production. In contrast with healthy donors, a p38-independent TNF[alpha] production was observed during the kinetics of the MDP+LPS response in Mut-Nod2 patients.Our findings suggest that the selective tolerance induced by MDP in healthy donors was related to the modulation of a convergent nub of NOD2 and TLR4 signaling pathways. This MDP-induced tolerance was impaired in Mut-Nod2 CD patients, resulting in a p38-independent TNF[alpha] production and an imbalance between pro- and antiinflammatory cytokines that could be partly responsible for the pathogenesis of CD. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21011">
<title>Circulating midkine in Crohn&#x27;s disease: Clinical implications</title>
<link>http://dx.doi.org/10.1002%2Fibd.21011</link>
<description><![CDATA[A noninvasive marker facilitating differential diagnosis in Crohn's disease (CD) is sought after. Midkine is a heparin-binding growth factor of angiogenic and chemotactic properties, positively evaluated as a tumor marker, and a possible association with CD has not yet been investigated.Circulating midkine was measured in 91 CD patients and 108 controls and related to disease clinical and biochemical activity, inflammation severity, and angiogenesis. Midkine diagnostic value in comparison with C-reactive protein (CRP) was evaluated by receiver operating characteristic (ROC) analysis.Circulating midkine was elevated both in quiescent and active disease compared to controls (147, 506, and 93 pg/mL, respectively), and corresponded well with disease activity (r = 0.49, P < 0.001). Midkine significantly correlated with inflammatory indices: CRP (r = 0.49), erythrocyte sedimentation rate (r = 0.31), leukocytes (r = 0.48), platelets (r = 0.52), albumin (r = -0.49), transferrin (r = -0.47), and IL-6 (r = 0.54); hematological variables: hemoglobin (r = -0.38), hematocrit (r = -0.43), and iron (r = -0.58); angiogenic factors: vascular endothelial growth factor-A (r = 0.42), fibroblast growth factor-2 (r = 0.54), and platelet-derived growth factor-BB (r = 0.57). Midkine elevation corresponded well (r = -0.41) with the drop in paraoxonase-1 activity - a quorum-quenching factor. Midkine as a marker of active CD had sensitivity and specificity of 86% and 97%, respectively, whereas CRP was 83% and 92%.CD is associated with an elevation of midkine, which corresponds well with disease activity and reflects the severity of inflammatory response and exacerbation of pathological angiogenesis. Midkine performance as a disease marker was slightly better than that of CRP. Its high specificity and likelihood ratios for positive test results might recommend midkine as a possible "ruling in" marker in CD. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21007">
<title>Overall and cause-specific mortality in Crohn&#x27;s disease: A meta-analysis of population-based studies</title>
<link>http://dx.doi.org/10.1002%2Fibd.21007</link>
<description><![CDATA[An overview of mortality risk among unselected patients with Crohn's disease (CD) is lacking. We therefore performed a systematic review and meta-analysis of population-based studies on overall and cause-specific mortality in CD.MEDLINE (January 1965 to February 2008), abstracts from international conferences and reference lists of selected articles were searched systematically. All articles fulfilling the predefined inclusion criteria were scrutinized for data on population size, time of follow-up, gender, age, and observed to expected deaths. STATA meta-analysis software was used to calculate overall and cause-specific pooled standardized mortality ratios (SMR, observed/expected).Nine studies were included with overall SMRs ranging from 0.72-3.2, resulting in a significantly increased pooled SMR of 1.39 (95% confidence interval [CI]: 1.30-1.49). Regarding cause-specific mortality, a significantly increased risk of death from cancer (SMR 1.50, 95% CI: 1.18-1.92), in particular of pulmonary cancer (SMR 2.72, 95% CI: 1.35-5.45), as well as chronic obstructive pulmonary disease (SMR 2.55, 95% CI: 1.19-5.47), gastrointestinal diseases (SMR 6.76, 95% CI: 4.37-10.45), and genitourinary diseases (SMR 3.28, 95% CI: 1.69-6.35) was observed.Among unselected patients with CD, overall mortality was slightly but significantly higher than in the general population - primarily explained by deaths from gastrointestinal, respiratory, and genitourinary diseases. Notably, mortality from colorectal cancer was not increased. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21018">
<title>Genetic dissection of granulomatous enterocolitis and arthritis in the intramural peptidoglycan-polysaccharide-treated rat model of IBD</title>
<link>http://dx.doi.org/10.1002%2Fibd.21018</link>
<description><![CDATA[Inflammatory arthropathies are common extraintestinal manifestations of inflammatory bowel diseases (IBD). As genetic susceptibility plays an important role in the etiology of IBD, we questioned how granulomatous enterocolitis and arthritis are genetically controlled in an experimental animal model displaying both conditions.Chronic intestinal and systemic inflammation was induced by intramural injection of peptidoglycan-polysaccharide (PG-PS) polymers in the ileocecal region of female F2 progeny derived from susceptible LEW and resistant F344 rats. Animals were followed for 24 days after injection and phenotyped by evaluating gross gut lesions, liver weight and granulomas, hematocrit, white blood cell count, and change in rear ankle joint diameters. Coinheritance of the phenotypic parameters with polymorphic DNA markers was analyzed by genome-wide quantitative trait locus (QTL) analysis.Linkage analysis revealed significant QTLs for enterocolitis and/or related phenotypes (liver granulomas, white blood cell count) on chromosomes 8 and 17. The QTL on chromosome 8 also showed suggestive linkage to arthritis. Significant QTLs for arthritis were detected on chromosomes 10, 13, 15, and 17. Analyses of the modes of inheritance showed arthritogenic contributions by both parental genomes. In addition, several other loci with suggestive evidence for linkage to 1 or several phenotypes were found.Susceptibility to PG-PS-induced chronic intestinal and systemic inflammation in rats is under complex multigenic control in which the genetic loci regulating arthritis are largely different from those controlling enterocolitis. Possible candidate genes within these QTL (including Tnfrsf11a/RANK, Gpc5, Il2ra, and Nfrkb) are also implicated in the respective human diseases. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21014">
<title>Disability in IBD: The devil is in the details</title>
<link>http://dx.doi.org/10.1002%2Fibd.21014</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21003">
<title>Endoscopy and MR enteroclysis: Equivalent tools in predicting clinical recurrence in patients with Crohn&#x27;s disease after ileocolic resection</title>
<link>http://dx.doi.org/10.1002%2Fibd.21003</link>
<description><![CDATA[Ileocolonoscopy poses the gold standard in the evaluation of postoperative recurrence of Crohn's disease (CD) at the site of ileocolonic anastomosis. Magnetic resonance enteroclysis (MRE) on the other hand is a promising technique for small bowel imaging. The aim was to compare MRE and ileocolonoscopy for predicting clinical recurrence in CD patients who have undergone ileocolonic resection.We included 29 patients in the study. The median time since index operation was 35 months and between ileocolonoscopy and MRE was 3 days. Patients were followed up for a maximum of 2 years unless clinical recurrence occurred earlier. Endoscopic findings were evaluated on a 5-grade scale (i0-i4), whereas MRE findings on the neoterminal ileum and anastomosis were assessed according to a previously validated 4-grade scale MR score (MR0-MR3).By classifying patients into subgroups of endoscopic severity of postoperative recurrence using as a threshold an endoscopic score of i3, we found that 10% of patients in the i0 to i2 group had a clinical recurrence during the 2-year follow-up period as compared to 52.6% of subjects with i3 to i4 (P = 0.043). The corresponding clinical exacerbation rates in the subgroups based on MRE severity assessment were 12.5% for MR0 to MR1 and 50% for MR2 to MR3 (P = 0.09).Our data suggest that colonoscopy and MR enteroclysis are of similar value to predict the risk of clinical recurrence in postoperative patients with Crohn's disease. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20993">
<title>Alterations of phospholipid concentration and species composition of the intestinal mucus barrier in ulcerative colitis: A clue to pathogenesis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20993</link>
<description><![CDATA[Phospholipids are essential for the normal function of the intestinal mucus barrier. The objective of this study was to systematically investigate phospholipids in the intestinal mucus of humans suffering from inflammatory bowel diseases, where a barrier defect is strongly supposed to be pathogenetic.Optimal mucus recovery was first validated in healthy mice and the method was then transferred to the endoscopic acquisition of ileal and colonic mucus from 21 patients with ulcerative colitis (UC), 10 patients with Crohn's disease (CD), and 29 healthy controls. Nano-electrospray ionization tandem mass spectrometry (ESI-MS/MS) was used to determine phosphatidylcholine (PC), lysophosphatidylcholine (LPC), and sphingomyelin (SM) in lipid extracts of mucus specimens.Human and rodent mucus contained very similar phospholipid species. In the ileal and colonic mucus from patients suffering from UC, the concentration of PC was highly significantly lower (607 ± 147 pmol/100 [mu]g protein and 745 ± 148 pmol/100 [mu]g protein) compared to that of patients with CD (3223 ± 1519 pmol/100 [mu]g protein and 2450 ± 431 pmol/100 [mu]g protein) and to controls (3870 ± 760 pmol/100 [mu]g protein and 2790 ± 354 pmol/100 [mu]g protein); overall, P = 0.0002 for ileal specimens and P < 0.0001 for colonic specimens. Independent of disease activity, patients suffering from UC showed an increased saturation grade of PC fatty acid residues and a higher LPC-to-PC ratio.The intestinal mucus barrier of patients with UC is significantly altered concerning its phospholipid concentration and species composition. These alterations may be very important for the pathogenesis of this disease and underline new therapeutic strategies. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20985">
<title>Familial aggregation and antimicrobial response dose-dependently affect the risk for Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20985</link>
<description><![CDATA[An increased risk of Crohn's disease (CD) has been reported consistently in first-degree relatives of patients. Our aim was to test whether a combination of CD-associated genes involved in innate immunity and/or antibody responses to microbial antigens may be valuable in identifying healthy relatives at risk.We investigated 86 families from Belgium and northern France, 45 with at least 3 first-degree relatives with CD, 24 with a single case, and 17 control families without inflammatory bowel disease (IBD). The cohort consisted of 186 CD patients, 290 healthy relatives, and 142 controls (total 618). Genetic (NOD2, NOD1, TLR4, CARD8) and serologic markers (ASCA, ACMA, ALCA, ACCA, A[Sigma]MA, OmpC, CBir1, I2) were determined in all subjects. All Belgian families were prospectively followed up for 54 months.In multiple-affected families, an increment of affected first-degree relatives and of positive antibodies were additive risks factors for CD (P < 0.0001), independent of NOD2 mutations. When comparing subjects from multiple-affected families, having 3 additional first-degree relatives with CD and 1 additional positive antibody increased the odds for CD to 9.19 (95% confidence interval [CI]: 4.07-20.80). After a follow-up of 54 months among all Belgian families, a total of 4 new diagnoses of IBD were confirmed in the multiple-affected families only, resulting in a 57-fold increase in incidence within multiple-affected families compared to the known incidence of IBD in our region.We found an additive risk increment for CD in subjects from multicase families per additional affected relative and per additional positive antibody, independent of NOD2. Furthermore, a very high disease incidence was observed in these multiple-affected families. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20977">
<title>Defining clinical criteria for clinical remission and disease activity in collagenous colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20977</link>
<description><![CDATA[Collagenous colitis is a chronic inflammatory bowel disease accompanied mainly by nonbloody diarrhea. The objectives of treatment are to alleviate the symptoms and minimize the deleterious effects on health-related quality of life (HRQOL). There is still no generally accepted clinical definition of remission or relapse. The purpose of this study was to analyze the impact of bowel symptoms on HRQOL and accordingly suggest criteria for remission and disease activity based on impact of patient symptoms on HRQOL.The design was a cross-sectional postal survey of 116 patients with collagenous colitis. The main outcome measures were 4 HRQOL questionnaires: the Short Health Scale, the Inflammatory Bowel Disease Questionnaire, the Rating Form of IBD Patient Concerns, and the Psychological General Well-Being Index, and a 1-week symptom diary recording number of stools/day and number of watery stools/day.Severity of bowel symptoms had a deleterious impact on patients' HRQOL. Patients with a mean of [ge]3 stools/day or a mean of [ge]1 watery stool/day had a significantly impaired HRQOL compared to those with <3 stools/day and <1 watery stool/day.We propose that clinical remission in collagenous colitis is defined as a mean of <3 stools/day and a mean of <1 watery stool per day and disease activity to be a daily mean of [ge]3 stools or a mean of [ge]1 watery stool. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20970">
<title>Efficacy of oral tacrolimus on intestinal Behcet&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20970</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20961">
<title>Prevention of TNBS-induced colitis by different Lactobacillus and Bifidobacterium strains is associated with an expansion of [gamma][delta]T and regulatory T cells of intestinal intraepithelial lymphocytes</title>
<link>http://dx.doi.org/10.1002%2Fibd.20961</link>
<description><![CDATA[Probiotics may protect against inflammatory bowel disease through regulation of lamina propria lymphocytes (LPLs) function. Data are lacking on possible involvement of intraepithelial lymphocytes (IELs). The aim of this study was to investigate whether different probiotic mixtures prevented gut inflammatory disease and the role of both IELs and LPLs.BALB/c mice received 2 probiotic mixtures orally for 3 weeks, as Mix1 (Lactobacillus acidophilus and Bifidobacterium longum), or Mix2 (Lactobacillus plantarum, Streptococcus thermophilus, and Bifidobacterium animalis subsp. lactis). Colitis was induced by intrarectal administration of trinitrobenzene sulfonic acid (TNBS). Probiotics in stools were analyzed by real-time polymerase chain reaction (PCR). Colon subpopulations of IELs and LPLs were assayed by flow cytometry. Serum cytokines were measured by cytometric bead array (CBA).All probiotics colonized the intestine. The 2 mixtures prevented the TNBS-induced intestinal damage, and Mix1 was the most effective. The Mix1 protection was associated with a reduction in CD4+ cells of IELs and LPLs, an increase in [gamma][delta]T cells of IELs, and a decrease in [gamma][delta]T cells of LPLs. An expansion of T regulatory (Treg) cells of IELs was induced by Mix1 and Mix2. Both probiotic mixtures inhibited tumor necrosis factor (TNF)-[alpha] and monocyte chemotactic protein (MCP)-1 production and upregulated interleukin (IL)-10. In addition, Mix1 prevented the TNBS-induced increase of IL-12 and interferon (IFN)-[gamma].The 2 probiotic mixtures were able to prevent the TNBS-induced colitis; the L. acidophilus and B. longum mixture was the most effective. Other than an involvement of LPLs, our results report a novel importance of the IELs population in probiotic protection. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20949">
<title>Magnifying colonoscopy used to predict disease relapse in patients with quiescent ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20949</link>
<description><![CDATA[Many patients with quiescent ulcerative colitis (UC) experience relapse. However, clinical and conventional colonoscopic signs are inadequate for predicting relapse. This study's aim was to investigate the effectiveness of magnifying colonoscopy in predicting relapse in patients with quiescent UC and to evaluate the association of the findings of magnifying colonoscopy with the histological findings.Magnifying colonoscopy was performed in 57 patients with clinical and endoscopic inactive UC. Patients were divided into 3 groups according to the findings of magnifying colonoscopy as MR (magnify-regular), MI (magnify-irregular), and MD (magnify-defect). Their subsequent clinical course was compared to assess the clinical usefulness of magnifying observation in predicting relapse. We also compared histological findings according to Riley's criteria to each finding of magnifying colonoscopy.Within 12 months, 1 of 18 patients (6.7%), 10 of 22 patients (45.5%), and 12 of 17 patients (70.6%) with findings of magnifying colonoscopy of MR, MI, and MD, respectively, experienced relapse. The MR group had a significantly low relapse rate compared with the MD and MI groups (P = 0.016, P = 0.002). When histological findings were compared with the findings of magnifying colonoscopy, the mean score of each variable, such as acute inflammatory cell infiltrate, chronic inflammatory cell infiltrate, and crypt architectural irregularities was significantly lower in the MR group than in the MD and MI groups.The findings of magnifying colonoscopy in patients with quiescent UC is useful for predicting relapse and is associated with histological grade of inflammation. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20928">
<title>Pityrosporum folliculitis in a Crohn&#x27;s disease patient receiving infliximab</title>
<link>http://dx.doi.org/10.1002%2Fibd.20928</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20989">
<title>Validity, reliability, and responsiveness of the EQ-5D in inflammatory bowel disease in Germany</title>
<link>http://dx.doi.org/10.1002%2Fibd.20989</link>
<description><![CDATA[The EuroQol (EQ)-5D questionnaire is a generic instrument measuring health-related quality of life. Its validity, reliability, and responsiveness were assessed in a large sample of Crohn's disease (CD) and ulcerative colitis (UC) patients.The EQ-5D was completed initially (270 CD and 232 UC subjects) and after 4 weeks (447 subjects) with a transition question rating health change. Responsiveness of EQ visual analog scale (EQ-VAS) and the United Kingdom (UK-index) and German EQ-5D index (EQ-index) scores to reported changes in health was evaluated by standardized response means (SRM) and meaningful differences (MDs).EQ-VAS and EQ-index scores correlated well with disease activity indices and differed significantly between active disease and remission groups. All scores were reliable in test-retest (ICC: EQ-VAS: 0.89; UK-index: 0.76; German EQ-index: 0.72). According to SRM, EQ-VAS was more responsive for deterioration in health than for improvement in health and was more responsive than index scores. Index scores were most responsive for deterioration in health in subjects in remission and for improved health in subjects with active disease. MDs for improved health (EQ-VAS: 10.9; UK EQ-index: 0.076; German EQ-index: 0.050) and deteriorated health (EQ-VAS: -14.4; UK EQ-index: -0.109; German EQ-index: -0.067) were significant, but MD of EQ-VAS also differed significantly according to disease activity.The EQ-5D generates valid, reliable, and responsive preference-based valuations of health in CD and UC. EQ-VAS scores were more responsive than EQ-5D index scores. Thus, small health differences that are important from the patient's perspective may not be reflected in the EQ-index. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20919">
<title>Strategies to improve quality of life in adolescents with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20919</link>
<description><![CDATA[Inflammatory bowel disease (IBD), which encompasses Crohn's disease (CD) and ulcerative colitis (UC), are chronic and debilitating conditions with unpredictable courses and complicated treatment. Pediatric IBD carries implications that extend beyond the health of the gastrointestinal tract. When these lifelong illnesses are diagnosed during adolescence, a critical developmental period, the transition to adulthood can be even more turbulent. Like other chronic diseases of childhood, patients with IBD are at risk for depression, anxiety, social isolation, and altered self-image, which can all negatively affect health-related quality of life (HRQOL). The review will draw from pertinent adult and pediatric literature about HRQOL over the past 10 years using a PubMed literature search to summarize instruments with which HRQOL is measured, and address factors that affect HRQOL in adolescents and young adults with IBD. Psychosocial interventions that have been utilized to improve quality of life in this population will also be covered. Identifying patients with impaired quality of life is of paramount importance, as is implementing strategies that may improve HRQOL, so that they may have an easier transition to adulthood while living with IBD. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20986">
<title>Ulcerative colitis: Correlation of the Rachmilewitz endoscopic activity index with fecal calprotectin, clinical activity, c-reactive protein, and blood leukocytes</title>
<link>http://dx.doi.org/10.1002%2Fibd.20986</link>
<description><![CDATA[The accuracy of noninvasive markers for the detection of endoscopically active ulcerative colitis (UC) according the Rachmilewitz Score is so far unknown. The aim was to evaluate the correlation between endoscopic disease activity and fecal calprotectin, Clinical Activity Index, C-reactive protein (CRP), and blood leukocytes.UC patients undergoing colonoscopy were prospectively enrolled and scored independently according the endoscopic and clinical part of the Rachmilewitz Index. Patients and controls provided fecal and blood samples for measuring calprotectin, CRP, and leukocytes.Values in UC patients (n = 134) compared to controls (n = 48): calprotectin: 396 ± 351 versus 18.1 ± 5 [mu]g/g, CRP 16 ± 13 versus 3 ± 2 mg/L, blood leukocytes 9.9 ± 3.5 versus 5.4 ± 1.9 g/L (all P < 0.001). Endoscopic disease activity correlated closest with calprotectin (Spearman's rank correlation coefficient r = 0.834), followed by Clinical Activity Index (r = 0.672), CRP (r = 0.503), and leukocytes (r = 0.461). Calprotectin levels were significantly lower in UC patients with inactive disease (endoscopic score 0-3, calprotectin 42 ± 38 [mu]g/g), compared to patients with mild (score 4-6, calprotectin 210 ± 121 [mu]g/g, P < 0.001), moderate (score 7-9, calprotectin 392 ± 246 [mu]g/g, P = 0.002), and severe disease (score 10-12, calprotectin 730 ± 291 [mu]g/g, P < 0.001). The overall accuracy for the detection of endoscopically active disease (score [ge]4) was 89% for calprotectin, 73% for Clinical Activity Index, 62% for elevated CRP, and 60% for leukocytosis.Fecal calprotectin correlated closest with endoscopic disease activity, followed by Clinical Activity Index, CRP, and blood leukocytes. Furthermore, fecal calprotectin was the only marker that reliably discriminated inactive from mild, moderate, and highly active disease, which emphasizes its usefulness for activity monitoring. Inflamm Bowel Dis 2009]]></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.20976">
<title>Quality of web-based information on inflammatory bowel diseases</title>
<link>http://dx.doi.org/10.1002%2Fibd.20976</link>
<description><![CDATA[The Internet is the largest source of health information and is widely used by inflammatory bowel disease (IBD) patients. As information is largely unregulated, our objective was to evaluate the quality, readability, accuracy, and accessibility of the information concerning IBD available on the World Wide Web.The phrases "inflammatory bowel disease," "Crohn's disease," and "Ulcerative Colitis" were entered separately as search terms into the 6 most commonly used search engines. Sites were categorized as institutional, pharmaceutical, nonpharmaceutical commercial sites, charitable, support, or alternative medicine. Websites were evaluated for content quality using the validated DISCERN rating instrument. Readability was graded by the Flesch Reading Ease and the Flesch-Kincaid Grade Level score.Of the 76 websites evaluated by DISCERN, 43% of the sites were rated as excellent to good and 57% as fair to poor. Alternative medicine sites scored significant lower (P > 0.05) than institutional, pharmaceutical, and nonpharmaceutical commercial sites. There was no relation between a rating score and the position of a website on the search engine ranking. The median Flesch Reading Ease Score was 41.65 (range, 2.6-77.7) and 11.85 (range, 6.2-21.1) for the Flesch-Kincaid Grade Level.The quality of websites containing information on IBD varies widely. Most of the online material available is too difficult to comprehend for a substantial portion of the patient population, and good quality information may be beyond reach of the average information seeker. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20974">
<title>Durability of infliximab in Crohn&#x27;s disease: A single-center experience</title>
<link>http://dx.doi.org/10.1002%2Fibd.20974</link>
<description><![CDATA[Infliximab is effective maintenance for moderate to severe Crohn's disease (CD); however, problems with immunogenicity and decreased efficacy often complicate long-term use. Durability of infliximab maintenance therapy over multiple years has not been defined.This was a retrospective, observational study of CD patients who received maintenance infliximab for [ge]1 year with the intention of ongoing maintenance. Patients were categorized into those who either discontinued treatment or continued maintenance therapy. We examined the impact of demographic, clinical characteristics, and prior episodic exposure on long-term durability of infliximab therapy and also examined the reasons for discontinuation of therapy.A total of 153 CD patients received maintenance infliximab treatment beyond 1 year and 42 (27%) ultimately discontinued treatment. The mean duration of maintenance treatment at the time of discontinuation was 42.4 ± 19.1 months compared to a follow-up period of 49.4 ± 19.8 months in the cohort continuing therapy (P = 0.049). The main reasons for discontinuation were allergy/adverse reaction (44.2%) and decreased efficacy (38.2%). Use of concomitant immunosuppression was similar between the 2 groups (78.6% versus 83.8%, P = NS). However, the discontinued group had a higher rate of prior episodic dosing compared to CD patients who continued maintenance (28.8% versus 11.7%, P = 0.025), while there was no difference in the rate of intensified dosing (57.2% versus 50.5%, P = NS).One-quarter of CD patients on long-term infliximab maintenance discontinued treatment. A history of prior episodic dosing was significantly associated with infliximab discontinuation, despite concomitant immunosuppression. These data emphasize the need for optimization of infliximab for successful long-term management. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20973">
<title>Targeting TNF in postoperative recurrence of Crohn&#x27;s disease: Can we extinguish the fire before it starts?</title>
<link>http://dx.doi.org/10.1002%2Fibd.20973</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20968">
<title>Role of diet in the development of inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20968</link>
<description><![CDATA[The inflammatory bowel diseases (IBDs) are a group of heterogeneous disorders characterized by acute and chronic inflammatory changes in the small or large bowel, or in both. Increasing incidence and prevalence figures for IBD both in the developed and developing world indicate that environmental factors are at least as significant in IBD as genetic susceptibility. Of these, diet and the host microbiota are likely to play important but as yet poorly defined roles. The major constituents of a standard "Western" diet may contribute to, or protect against, intestinal inflammation via several mechanisms. These include the effects of insulin resistance and short-chain fatty acids such as butyrate, modification of intestinal permeability, the antiinflammatory role of polyunsaturated fatty acids, and the effect of sulfur compounds from protein on host microbiota. This detailed review critically assesses the evidence for the role of diet in the development of IBD and examines the evidence for obesity as a contributing factor to IBD pathogenesis. Particular attention is focused on methodological issues including suitability of cases and controls, confounders such as smoking, and total energy expenditure. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20967">
<title>Mycobacterium avium subspecies paratuberculosis in children with early-onset Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20967</link>
<description><![CDATA[Mycobacterium avium subspecies paratuberculosis (MAP) is the most enduring infectious candidate that may be associated with inflammatory bowel disease (IBD). It is possible that the inconsistencies in the prevalence studies of MAP in adults reflect clinical differences in adult patients studied, including duration of disease and treatment regimens, and also in lack of specificity of some of the assays used. The aim was to determine the presence of MAP in children with symptoms of Crohn's disease (CD) and ulcerative colitis (UC), using gut biopsy tissue and peripheral blood mononuclear cells (PBMC) collected at initial endoscopic examination prior to clinical treatment.Mucosal biopsies and/or PBMC specimens were collected from a total of 142 children, comprising 62 with CD, 26 with UC, and 54 with non-IBD. MAP-specific IS900 polymerase chain reaction (PCR) analysis was performed on all biopsies and PBMC specimens. Conventional MAP culture technique was performed on a subset of 10 CD, 2 UC, and 4 non-IBD patients to isolate MAP.MAP was identified by IS900 PCR significantly more often in mucosal biopsies from CD 39% (22/56) than from non-IBD 15% (6/39) patients (P < 0.05), and in PBMC from CD 16% (8/50) than from non-IBD 0% (0/31) patients (P < 0.05). Viable MAP were cultured from mucosal biopsies from 4/10 CD, 0/2 UC, and 0/4 non-IBD patients, but were not cultured from PBMC specimens.This unique study on the occurrence of MAP in gut tissue and blood from pediatric IBD patients suggests the possible involvement of MAP in the early stages of development of CD in children. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20966">
<title>Phylogenetic analysis of inflammatory bowel disease associated Escherichia coli and the fimH virulence determinant</title>
<link>http://dx.doi.org/10.1002%2Fibd.20966</link>
<description><![CDATA[Evidence supports the role of adherent invasive Escherichia coli (AIEC) in the pathogenesis of inflammatory bowel disease (IBD). However, little is known about the phylogenetic structure and origin of this group of bacteria. Multi-locus sequence typing (MLST), and fimH sequence analysis were performed to elucidate the phylogenetic relationships between E. coli strains isolated from IBD tissue.Thirty-six E. coli isolated from IBD patients and healthy individuals were used. MLST analysis of the adk, fumC, gyrB, icd, mdh, purA, and recA housekeeping genes was performed. The fimH gene was also sequenced and phylogenetically analyzed. Biochemical profiling of strains were performed using the API 20 E system.MLST analysis distinguished 9 new alleles and 11 new sequence types, nearly all of which belonged to IBD isolates. E. coli isolated from IBD patients were more likely to be grouped into separate clonal clusters by eBURST analysis of allelic profiles (P = 0.02). Sequencing of fimH placed putative AIEC strains into the same cluster with the uro-pathogenic E. coli CFT073 and the avian-pathogenic E. coli O1:K1:H7.MLST analysis suggested that E. coli isolated from IBD patients did not evolve from a unique ancestral background. Together with the fimH sequence we conclude that AIEC represent a group of bacteria that have been able to take advantage of an "IBD microenvironment" and likely shares common genes with extraintestinal pathogens like uro-pathogenic CFT073 and avian-pathogenic O1:K1:H7 E. coli. Future research should focus on genes that are unique to AIEC. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20965">
<title>Infliximab for postsurgical endoscopic recurrence of Crohn&#x27;s disease: No trumpets yet</title>
<link>http://dx.doi.org/10.1002%2Fibd.20965</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20964">
<title>Thyroid disorders and inflammatory bowel diseases: Retrospective evaluation of 909 patients from an Italian Referral Center</title>
<link>http://dx.doi.org/10.1002%2Fibd.20964</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20963">
<title>PepT1 oligopeptide transporter (SLC15A1) gene polymorphism in inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20963</link>
<description><![CDATA[Human polymorphisms affecting gut epithelial barrier and interactions with bacteria predispose to the inflammatory bowel diseases (IBD) Crohn's disease (CD) and ulcerative colitis (UC). The intestinal transporter PepT1, encoded by the SLC15A1 gene, mediates intracellular uptake of bacterial products that can induce inflammation and NF-[kappa]B activation upon binding to NOD2, a protein often mutated in CD. Hence, we tested SLC15A1 polymorphisms for association with IBD.Twelve SLC15A1 single nucleotide polymorphisms (SNPs) were genotyped in 1783 individuals from 2 cohorts of Swedish and Finnish IBD patients and controls. An in vitro system was set up to evaluate the potential impact of SLC15A1 polymorphism on PepT1 transporter function by quantification of NOD2-mediated activation of NF-[kappa]B.The common allele (C) of a coding polymorphism (rs2297322, Ser117Asn) was associated with CD susceptibility both in Sweden and in Finland, but with genetic effects in opposite directions (risk and protection, respectively). The best evidence of association was found in both populations when the analysis was performed on individuals not carrying NOD2 common risk alleles (Sweden allelic P = 0.0007, OR 1.97, 95% confidence interval [CI] 1.34-2.92; Finland genotype P = 0.0013, OR 0.63, 95% CI 0.44-0.90). The PepT1 variant encoded by the C allele (PepT1-Ser117) was associated with reduced signaling downstream of NOD2 (P < 0.0001 compared to Pept1-Asn117).A functional polymorphism in the SLC15A1 gene might be of relevance to inflammation and antibacterial responses in IBD. Whether this polymorphism truly contributes to disease susceptibility needs to be further addressed, and should stimulate additional studies in other populations. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20954">
<title>Adalimumab-induced psoriasis of the scalp with diffuse alopecia: A severe potentially irreversible cutaneous side effect of TNF-alpha blockers</title>
<link>http://dx.doi.org/10.1002%2Fibd.20954</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20951">
<title>Role of TNF receptors, TNFR1 and TNFR2, in dextran sodium sulfate-induced colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20951</link>
<description><![CDATA[In this study we determined the consequence of the absence of each TNF receptor, TNFR1 or TNFR2, in the dextran sulfate sodium (DSS) model of colitis.Wildtype (WT), TNFR1-/- and TNFR2-/- mice were fed 3% w/v DSS in drinking water for 5 days followed by 2 (day 7) or 7 (day 12) days of tap water.The colons from untreated TNFR1-/- and TNFR2-/- mice were histologically normal. Following DSS, all strains became inflamed. TNFR1-/- mice had a more severe clinical score at days 8 and 9 compared to WT and TNFR2-/- mice despite similar histopathological damage in their colons. The more severe clinical score was associated with a reduced macrophage infiltration into the colonic mucosa. TNFR2-/- mice showed increased indicators of disease including increased colon weight, a shrunken cecum, and an increased number of ulcers compared to TNFR1-/- and WT strains at day 7. Mucosal levels of TNFR2 were elevated in colitic mice compared to uninflamed controls, with no difference between strains on day 7 but on day 12, unlike WT mice, levels were reduced in TNFR1-/- mice. There was no difference in the number of TUNEL-positive apoptotic colonic epithelial cells between strains, nor in total cleaved caspase 3 levels between strains, measured by Western blot of colon homogenates.While deficiency of either receptor contributes to some measures of DSS colitis, the histopathological scores are similar, indicating that TNF receptors either do not play a major role or are redundant in the pathology associated with DSS colitis. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20946">
<title>Fecal dimeric M2-pyruvate kinase (tumor M2-PK) in the differential diagnosis of functional and organic bowel disorders</title>
<link>http://dx.doi.org/10.1002%2Fibd.20946</link>
<description><![CDATA[Fecal inflammatory markers have been shown to be useful as noninvasive screening tools to differentiate patients with functional from organic bowel pathology. Of these markers calprotectin has been the most intensively studied. More recently, the dimeric isoform of M2-pyruvate kinase (tumor M2-PK) has been suggested as a marker of gastrointestinal inflammation. The aim of this study was to investigate fecal tumor M2-PK in the differentiation of functional from organic bowel disease.Fecal calprotectin and tumor M2-PK were measured in 94 controls and 105 gastroenterology outpatients with a possible diagnosis of organic bowel disease. The diagnosis was made by clinical, endoscopic, and radiological criteria.Organic bowel disease was diagnosed in 14 patients (13%). Median calprotectin and tumor M2-PK concentrations were 24.5 [mu]g/g and 1 U/mL in controls, 23 [mu]g/g and 1 U/mL in functional, and 227.5 [mu]g/g and 12.6 U/mL in organic bowel disease. Sensitivity, specificity, and positive and negative likelihood ratios for diagnosis of organic bowel disease were 93%, 92%, 11.6, and 0.07 for calprotectin and 67%, 88% 5.6, and 0.18 for tumor M2-PK, respectively. Calprotectin in combination with tumor M2-PK gave a sensitivity of 64%, specificity of 98%, and likelihood ratios of 32 and 0.03. Elevated calprotectin or tumor M2-PK decreased specificity to 87%, but increased sensitivity to 100%.Tumor M2-PK is able to differentiate organic from functional bowel disease but has a lower sensitivity, specificity, and predictive value than calprotectin. Further studies are required, alone or in combination with other markers, before its usefulness in this setting can be recommended. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20943">
<title>Vaccination strategies for patients with inflammatory bowel disease on immunomodulators and biologics</title>
<link>http://dx.doi.org/10.1002%2Fibd.20943</link>
<description><![CDATA[The treatment of Crohn's disease and ulcerative colitis frequently includes potent immunomodulator and biologic therapy to reduce intestinal inflammation, heal fistulae, limit complications, and improve quality of life. These medications may increase susceptibility to and severity of infections, many of which are preventable by preemptive immunizations. Conversely, live-virus vaccines are generally contraindicated in patients receiving immunosuppressive regimens due to risks of vaccine-associated infection. While most patients on immunosuppressive therapies develop immune responses after vaccinations, these may be impaired relative to their nonimmunosuppressed counterparts. This review discusses the rationale for currently recommended vaccinations, as well as issues pertaining to vaccine safety and immunogenicity in immunosuppressed patients with inflammatory bowel disease and their household contacts. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20987">
<title>Is it time for increased pap performance? Cervical cancer and pap testing in women with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20987</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20988">
<title>Barriers to adherence among adolescents with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20988</link>
<description><![CDATA[The purpose of this study was to describe barriers to adherence among adolescents with inflammatory bowel disease (IBD) and to examine demographic, disease-related, and treatment regimen-related correlates of adherence barriers using a multimethod reporting strategy. A final goal was to examine relationships between the frequencies of barriers and levels of nonadherence.In all, 64 adolescents (ages 11-18) participated, along with 61 mothers and 25 fathers. Barriers to adherence and ratings of medication adherence were assessed via patient and parent reports. Disease activity ratings were provided by pediatric gastroenterologists.Lack of time and medication side effects were commonly reported barriers across adolescent, mother, and father reports. Other adolescent-reported barriers included missing medication due to feeling well or discontinuing medication based on the belief that the medication was not working. The prevalence of adherence barriers was not consistently associated with adolescent age, sex, time since diagnosis, or disease activity. Adolescents whose regimen involved more than 1 daily medication administration had more adherence barriers based on adolescent and maternal report than did those whose regimen involved 1 or less than 1 daily medication administration. Finally, adherence barriers were significantly higher among families reporting imperfect adherence as compared to those reporting perfect adherence.Barriers to medication adherence do exist among adolescents with IBD and may have negative implications for medication adherence. Systematic assessment of barriers during routine medical appointments may help to identify and modify these barriers and ultimately improve adherence. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20978">
<title>Clustering in time of familial IBD separates ulcerative colitis from Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20978</link>
<description><![CDATA[The aim was to compare clustering of time at diagnosis and phenotype of inflammatory bowel disease (IBD) between affected parents and children and to explore generational differences in age at diagnosis (AAD) as well as the concordance of clinical characteristics.Eighty-four affected pairs from 45 families were included from 5 counties in southeastern Norway between August 2003 and December 2006; 43 were sib-sib pairs and 39 parent-child pairs. Clinical data were obtained by phone interviews and by hospital records.The difference in median AAD was 17.0 years (P < 0.001) and 2.0 years (P = 0.29) in parent-child and sib-sib pairs, respectively. When the time interval between diagnosis in parent and child was split into 2 groups, below and above 5 years, 64% of pairs with ulcerative colitis (UC) offspring were diagnosed within 5 years, compared to 24% of pairs with Crohn's disease (CD) offspring (odds ratio [OR] = 5.7, 95% confidence interval [CI]: 1.4, 23.8). Concordance for smoking habits was low in 26 pairs with mixed disease ([kappa] = 0.15), whereas patients with CD tended to be current smokers.Most of the children acquire their disease at an earlier time in life compared to their parents, suggesting genetic anticipation. The time interval between diagnosis of the parents and offspring was lower when the offspring developed UC compared to CD, which might reflect the influence of shared environment on the generational difference in AAD in UC families. This study confirmed the effect of smoking habits on IBD phenotype. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20971">
<title>Solitary rectal ulcer syndrome in association with ulcerative colitis: A case report</title>
<link>http://dx.doi.org/10.1002%2Fibd.20971</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20956">
<title>Adalimumab safety in global clinical trials of patients with Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20956</link>
<description><![CDATA[Adalimumab, a fully human anti-tumor necrosis factor (anti-TNF) monoclonal antibody, is approved for the treatment of Crohn's disease (CD) in adults. We evaluated the overall safety profile of adalimumab in global clinical trials in patients with CD. Patients who participated in these trials, which included randomized induction and maintenance trials, Phase IIIb trials, and open-label extension studies, had moderately to severely active CD and were evaluated for safety at regular intervals.Rates of adverse events of interest were assessed per 100-patient-years of adalimumab exposure. Standardized mortality rates and standardized incidence rates (for malignancies) were calculated using population-matched data. As of April 15, 2008, 3160 patients with CD had been treated with adalimumab in clinical trials, representing 3401.9 patient-years of adalimumab exposure.Serious infection was the most frequently reported serious adverse event of interest in the CD trials; abscess (intraabdominal and gastrointestinal related) was the most common serious infection. Low incidences of malignancies, lymphomas, opportunistic infections (including tuberculosis), demyelinating disorders, and lupus-like disorders were reported in the CD trials. The standardized mortality rate for adalimumab-treated patients with CD, 0.44 (95% confidence interval [CI], 0.12-1.12), is less than the rate of 1.52 (95% CI, 1.32-1.74) reported in a recent meta-analysis of patients with CD.The safety profile of adalimumab in patients with CD was similar to that of other TNF antagonists in CD populations, and the rates of adverse events were comparable to other approved indications for adalimumab spanning >10 years of clinical observation. No new safety signals were identified. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20950">
<title>Pediatric Crohn&#x27;s disease activity at diagnosis, its influence on pediatrician&#x27;s prescribing behavior, and clinical outcome 5 years later</title>
<link>http://dx.doi.org/10.1002%2Fibd.20950</link>
<description><![CDATA[No studies have been performed in which therapeutic regimens have been compared between mild and moderate-to-severe pediatric Crohn's disease (CD) at diagnosis. The aim was to analyze pediatric CD activity at diagnosis, its influence on pediatrician's prescribing behavior, and clinical outcome 5 years later.In a retrospective multicenter study we divided pediatric CD patients at diagnosis into mild or moderate-severe disease. We compared initial therapies, duration of first remission, number of exacerbations, height-for-age and weight-for-height evolvement, and cumulative duration of systemic steroid use in a 5-year follow-up period.Forty-three children were included (25 with mild and 18 with moderate-severe disease). Aminosalicylate monotherapy was more frequently prescribed in the mild group (40% versus 17%; P < 0.01). The median duration of systemic steroid use was 18.3 months in the mild group and 10.4 months in the moderate-severe group (P = 0.09). Duration of first remission was 15.0 months in the mild group and 23.4 months in the moderate-severe group (P = 0.16). The mean number of exacerbations was 2.2 in the mild group and 1.8 in the moderate-severe group (P = 0.28).CD patients with mild disease were treated with aminosalicylate monotherapy more frequently. These patients, however, tend to have more exacerbations, shorter duration of first remission, and longer total duration of systemic steroid use. Our data support the concept that severity of disease at diagnosis does not reliably predict subsequent clinical course. This study suggests that there is no indication that children with mild CD should be treated differently compared to children with moderate-severe disease. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20969">
<title>Stress in the ER leads to inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20969</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20962">
<title>Low bone mineral density in children and adolescents with inflammatory bowel disease: A population-based study from western Sweden</title>
<link>http://dx.doi.org/10.1002%2Fibd.20962</link>
<description><![CDATA[Low bone mineral density (BMD) has been recognized as a potential problem in children with inflammatory bowel disease (IBD). The aim of the study was to investigate BMD in Swedish children and adolescents with IBD and to evaluate possible factors affecting BMD.To evaluate BMD, all patients (n = 144) underwent a dual-energy X-ray absorptiometry (DXA) of the whole body and the spine. BMD values were expressed as Z-scores using normative pediatric data from Lunar (GE Medical Systems).In this population-based study, the lowest BMD values were found in the lumbar spine. The entire IBD group showed significantly lower BMD Z-scores of the lumbar spine (L2-L4) in comparison to healthy references (-0.8 standard deviation [SD], range -5.9 to 3.7 SD, P < 0.001). Decreased BMD with a Z-score < -1 SD occurred in 46.7% of the individuals with Crohn's disease (CD) and in 47.0% of those with ulcerative colitis (UC). Low BMD with a Z-score [le] -2 SD was present in 26.7% of the patients with CD and in 24.1% of the UC patients. In a multiple regression model with BMD lumbar spine as the depending variable, possible factors associated with lower BMD were male gender, low body mass index (BMI), and treatment with azathioprine.Low BMD is prevalent in Swedish pediatric patients with IBD. Possible risk factors for lower BMD are male gender, low BMI, and treatment with azathioprine, as a probable marker of disease course severity. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20960">
<title>Activation of the cannabinoid 2 receptor (CB2) protects against experimental colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20960</link>
<description><![CDATA[Activation of cannabinoid (CB)1 receptors results in attenuation of experimental colitis. Our aim was to examine the role of CB2 receptors in experimental colitis using agonists (JWH133, AM1241) and an antagonist (AM630) in trinitrobenzene sulfonic acid (TNBS)-induced colitis in wildtype and CB2 receptor-deficient (CB2-/-) mice.Mice were treated with TNBS to induce colitis and then given intraperitoneal injections of the CB2 receptor agonists JWH133, AM1241, or the CB2 receptor antagonist AM630. Additionally, CB2-/- mice were treated with TNBS and injected with JWH133 or AM1241. Animals were examined 3 days after the induction of colitis. The colons were removed for macroscopic and microscopic evaluation, as well as the determination of myeloperoxidase activity. Quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) for CB2 receptor was also performed in animals with TNBS and dextran sodium sulfate colitis.Intracolonic installation of TNBS caused severe colitis. CB2 mRNA expression was significantly increased during the course of experimental colitis. Three-day treatment with JWH133 or AM1241 significantly reduced colitis; AM630 exacerbated colitis. The effect of JWH133 was abolished when animals were pretreated with AM630. Neither JWH133 nor AM1241 had effects in CB2-/- mice.We show that activation of the CB2 receptor protects against experimental colitis in mice. Increased expression of CB2 receptor mRNA and aggravation of colitis by AM630 suggests a role for this receptor in normally limiting the development of colitis. These results support the idea that the CB2 receptor may be a possible novel therapeutic target in inflammatory bowel disease. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20958">
<title>Adalimumab as therapy for fistulizing orofacial Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20958</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20957">
<title>Cervical neoplasia risk in IBD: Truth or hysteria?</title>
<link>http://dx.doi.org/10.1002%2Fibd.20957</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20955">
<title>Physicians may inadequately address Sexuality in women with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20955</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20953">
<title>Clostridium difficile-associated diarrhea in Crohn&#x27;s disease patients with Ostomy</title>
<link>http://dx.doi.org/10.1002%2Fibd.20953</link>
<description><![CDATA[No Abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20948">
<title>Severity of postoperative recurrence in crohn&#x27;s disease: Correlation between endoscopic and sonographic findings</title>
<link>http://dx.doi.org/10.1002%2Fibd.20948</link>
<description><![CDATA[Crohn's disease (CD) recurrence is currently assessed by ileocolonoscopy. Small intestine contrast ultrasonography (SICUS) visualizes the small bowel lesions in CD, although its role after curative resection is undefined. We aimed to investigate the accuracy of SICUS in assessing CD recurrence after ileocolonic resection when using ileocolonoscopy as a gold standard. The correlation between the bowel wall thickness (BWT) measured by SICUS and the endoscopic score of recurrence was also assessed.The analysis included 72 CD patients with ileocolonic resection requiring ileocolonoscopy, undergoing SICUS within 6 months. Recurrence was assessed by ileocolonoscopy using the Rutgeerts' score. SICUS was performed after PEG ingestion and findings compatible with recurrence included: increased BWT (>3 mm), bowel dilation (>25 mm) or stricture (<10 mm).Ileocolonoscopy detected recurrence in 67/72 (93%) patients. SICUS detected findings compatible with recurrence in 62/72 (86%) patients (5 false negative (FN), 4 false positive (FP), 1 true negative (TN), 62 true positive (TP)), showing a 92.5% sensitivity, 20% specificity, and 87.5% accuracy for detecting CD recurrence. The BWT detected by SICUS was correlated with the Rutgeerts' score (P = 0.0001; r = 0.67). The median BWT, the extent of the ileal lesions, and the prestenotic dilation were higher in patients with an endoscopic degree of recurrence [ge]3 versus [le]2 (P < 0.001) and the lumen diameter was lower in patients with a Rutgeerts' score [ge]3 versus [le]2 (P < 0.0001).Although SICUS and ileocolonoscopy provide different views of the small bowel, SICUS shows a significant correlation with the endoscopic findings. SICUS may represent an alternative noninvasive technique for assessing CD recurrence after ileocolonic resection. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20947">
<title>Comparison of the effects of 1,25 dihydroxyvitamin D and 25 hydroxyvitamin D on bone pathology and disease activity in Crohn&#x27;s disease patients</title>
<link>http://dx.doi.org/10.1002%2Fibd.20947</link>
<description><![CDATA[Vitamin D is essential for osteopenia therapy in Crohn's disease (CD). The active form of vitamin-D (aVD) is the 1,25(OH)2D. There are no data available whether aVD or plain vitamin-D (pVD) has any advantage in managing osteoporosis in CD or has any effect on the activity of the disease itself. Our work is a prospective study to compare the effects of aVD and pVD on bone metabolism and the clinical course of CD.In all, 37 inactive CD patients were involved in the study and divided into 2 age-, gender-, and t-score-matched groups. Group A was treated with aVD while group B received pVD. Osteocalcin, beta-CrossLaps, osteoprotegerin, and receptor activator nuclear factor kappa-B ligand concentrations were estimated at the start of the study and at 6 weeks and 3 and 12 months. The activity of CD was also measured clinically and by laboratory parameters.At week 6 the Crohn's Disease Activity Index (CDAI) scores and concentration of C-reactive protein decreased (69.44 ± 58.6 versus 57.0 ± 54.89 and 15.8 ± 23.57 mmol/L versus 7.81 ± 3.91 mmol/L, respectively, P < 0.05) parallel with markers of bone turnover (beta-CrossLaps: 0.46 ± 0.21 ng/mL versus 0.40 ± 0.25 ng/mL, and osteocalcin: 32.29 ± 15.3 ng/mL versus 29.98 ± 14.14 ng/mL, P < 0.05); however, osteoprotegerin concentration (marker of osteoblast activity) increased (3.96 ± 2.1 pg/mL versus 4.58 ± 2.19 pg/mL) in group A, but did not change in group B. Osteocalcin and beta-CrossLaps concentrations changed more significantly by the 3rd month; however, these changes disappeared by the 12th month.According to our study, aVD has a more prominent short-term beneficial effect on bone metabolism and disease activity in CD compared with pVD. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20942">
<title>Musculoskeletal manifestations of inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20942</link>
<description><![CDATA[Extraintestinal manifestations develop in [ap]25% of patients with inflammatory bowel disease (IBD). Musculoskeletal symptoms are the most common extraintestinal manifestations of IBD, often associated with colonic involvement, and present as either articular (arthritis) or periarticular inflammation including enthesitis, myositis, or soft tissue rheumatism (fibromyalgia). Musculoskeletal manifestations can precede or be synchronous with the development of bowel disease or develop following the diagnosis of IBD. Their clinical course often correlates with IBD activity but it can also be independent of the activity of bowel disease. Controlling intestinal inflammation remains the cornerstone therapeutic approach for the musculoskeletal manifestations of IBD. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20941">
<title>Immunizations in patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20941</link>
<description><![CDATA[Abstract: Patients receiving immunosuppressive therapies may be at increased risk for complications of vaccine preventable diseases, including influenza, varicella, and pneumococcus. However, studies suggest that patients with chronic illness may be inadequately immunized. In part, this is because of a paucity of formal vaccine studies in immune compromised populations. This review discusses the methods one uses to assess vaccine efficacy and provides an update on currently known data on the vaccine antibody responses in immune compromised hosts. Currently published studies suggest that influenza vaccine can be safely administered to patients with IBD on immunosuppression, and is effective in the majority of patients. Further formal studies with other inactivated vaccines (e.g., pneumococcal vaccine, meningitis vaccine) should be conducted. While some studies in immune compromised hosts suggest the live attenuated varicella vaccine can be given without adverse events, administration of this vaccine in patients on immunosuppression remains controversial. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20939">
<title>Resource use and societal costs for Crohn&#x27;s disease in Sweden</title>
<link>http://dx.doi.org/10.1002%2Fibd.20939</link>
<description><![CDATA[The usual onset of Crohn's disease (CD) is between 15 and 30 years of age, thus affecting people during their most economically productive period in life.This study intended to estimate societal costs and health-related quality of life (HRQoL) in Swedish patients in different stages of CD. Cross-sectional data on disease activity (measured with the Harvey-Bradshaw Index [HBI]), direct medical resource use, work productivity, and HRQoL (assessed using the 15D instrument) were collected for 420 patients by questionnaires to patients, to the treating physician, and from medical records. Based on HBI, current treatment, and response to treatment, patients were classified into the following disease states: Remission, Response, Active, Refractory, and Surgery.The average 4-week cost per patient in 2007 was estimated at [euro]721 (USD 988), of which 64% was due to lost productivity. The total 4-week cost of care was [euro]255 (USD 349) in Remission, [euro]831 (USD 1138) in Response, [euro]891 (USD 1220) in Active, [euro]1360 (USD 1864) in Refractory, and [euro]16984 (USD 23269) in Surgery. HBI was the most important predictor of costs of care - a 1-point increase in HBI increased total costs by 25% (P < 0.001). HRQoL differed between the disease states: 0.92 in Remission, 0.90 in Response, 0.82 in Active, 0.81 in Refractory, and 0.77 in Surgery.Patients in remission have the lowest costs and the highest HRQoL. Patients responding to treatment have lower costs of care than patients with high disease activity who are not treated or do not respond to treatment. Thus, total costs of care might be reduced by efficient treatment. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20937">
<title>Adipokine signaling in inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20937</link>
<description><![CDATA[While the incidence of inflammatory bowel disease (IBD) is still increasing, the etiology has not finally been dissected. The main hypothesis suggests that the mucosal immune system is hyperresponsive to dietary factors and commensal bacteria in genetically predisposed individuals. Burrill Crohn himself described a local hypertrophy of the mesenteric fat tissue adjacent to the segments of inflamed intestine. In addition, more recent data indicate altered local expression and serum levels of some adipocyte-derived mediators (adipokines) with immune-modulating capacities in IBD. This review focuses on the role of adipose tissue and adipokines in the immune system, with particular focus on the mucosal immune system. The available data will serve to establish a working hypothesis on how the mesenteric fat tissue contributes to the pathogenesis of Crohn's disease. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20926">
<title>Filaggrin loss-of-function variants are associated with atopic comorbidity in pediatric inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20926</link>
<description><![CDATA[Pediatric inflammatory bowel disease (IBD) has a high prevalence of coexistent atopy. Filaggrin (FLG) loss-of-function variants (null-alleles) are associated with eczema and asthma in association with eczema. The aim was to assess the contribution of FLG null-alleles to pediatric IBD susceptibility and to coexistent atopy (eczema, asthma, allergic rhinitis, or food allergy).FLG variants (R501X and 2282del4) were genotyped in 403 children with IBD, 683 parents, and 996 population controls.In all, 11% of IBD patients carried at least 1 FLG null-allele compared to 11% of population controls (P > 0.4). Carriage of 1 or more null-alleles in patients with atopy (present in 52% of IBD patients) differed from IBD patients without atopy (14% versus 6%, P = 0.01; odds ratio [OR] 2.4, 95% confidence interval [CI] 1.2-5.1). The effect of FLG null-alleles was strongest for eczema (19% versus 7%, P = 0.0003; OR 3.3, 95% CI 1.7-6.6) and food allergy (28% versus 8%, P = 0.0001; OR 4.5, 95% CI 2.0-10.0). The presence of more than 1 atopic disease tended to increase the associated OR: eczema + asthma (23% versus 7%, P = 0.001; OR 3.9, 95% CI 1.6-9.1), eczema + asthma + allergic rhinitis (29% versus 7%, P = 0.0006; OR 5.4, 95% CI 1.9-15.4) and eczema + asthma + allergic rhinitis + food allergy (45% versus 6%, P < 10-4; OR 12.2, 95% CI 3.2-46.3). Logistic regression analysis of IBD cases confirmed the association of carriage of an FLG null-allele with atopy (P = 0.01; OR 2.4, 95% CI 1.2-5.1) and co-occurrence of different forms of atopy (P = 0.003; OR 3.5, 95% CI 1.5-8.1).Filaggrin null-alleles have no effect on IBD susceptibility but contribute to coexistent eczema and food allergy. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20925">
<title>Oral and intravenous iron treatment in inflammatory bowel disease: Hematological response and quality of life improvement</title>
<link>http://dx.doi.org/10.1002%2Fibd.20925</link>
<description><![CDATA[The aim was to evaluate the efficacy and tolerance of oral and intravenous iron treatment in anemic inflammatory bowel disease (IBD) patients, considering both hematological and quality-of-life outcomes.We performed a prospective multicenter study in IBD patients with iron deficiency anemia. Patients having hemoglobin >10 g/dL were prescribed oral ferrous sulfate. If hemoglobin <10 g/dL, intravenous (sucrose) iron was administered. Oral iron-intolerant patients were changed to intravenous treatment. Clinical (Truelove/Harvey-Bradshaw), hematological (response defined as hemoglobin normalization), and quality-of-life (shortened CCVEII-9 questionnaire) evaluations were performed at baseline and at 3 and 6 months.100 IBD patients (59 Crohn's disease, 41 ulcerative colitis) were included. Mean basal hemoglobin levels were 10.8 ± 1.3 g/dL (range, 6.6-12.9). Seventy-eight patients received oral treatment and 22 intravenous iron. Hemoglobin normalization was achieved in 86% of patients: 89% with oral, and 77% with intravenous iron. An IBD activity increase was not demonstrated in any patient. Four patients (5.1%) showed oral iron intolerance leading to discontinuation of treatment. No adverse events were reported for intravenous iron. Hemoglobin correlated with CCVEII-9 (P < 0.001). The CCVEII-9 score increased in patients who normalized hemoglobin levels in 3 months (from 58 ± 9 to 73 ± 10) or 6 months (54 ± 9, 68 ± 12, and 74 ± 10) (P < 0.001).Oral iron treatment is effective and well tolerated in most IBD patients, and does not exacerbate the symptoms of the underlying IBD. Intravenous iron, on the other hand, is an effective and safe alternative treatment for iron deficiency anemia in more severely anemic or intolerant patients. Anemia correction with iron treatment is associated with a relevant improvement in the patients' quality of life. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20924">
<title>Open-label study of adalimumab in patients with ulcerative colitis including those with prior loss of response or intolerance to infliximab</title>
<link>http://dx.doi.org/10.1002%2Fibd.20924</link>
<description><![CDATA[The aim of this study was to assess the clinical benefit and tolerability of adalimumab, a fully human monoclonal antibody to tumor necrosis factor (TNF), in patients with ulcerative colitis (UC).Patients with active UC, including those who had lost response or developed intolerance to the chimeric anti-TNF antibody infliximab, were enrolled in a 24-week uncontrolled trial. Patients were treated with subcutaneous adalimumab 160 mg at week 0, 80 mg at week 2, and 40 mg every other week starting at week 4. After week 8 the dose could be escalated to 40 mg weekly for incomplete response. Outcome measures included clinical response and remission and mucosal healing.Twenty patients were enrolled, of whom 13 had previously received infliximab. Seven patients had dose escalation of adalimumab between weeks 8 and 16, from 40 mg every other week to 40 mg weekly, due to incomplete response. The rates of clinical response were 25% at week 8 and 50% at week 24. The rates of clinical remission were 5% at week 8 and 20% at week 24. The rate of mucosal healing was 30% at week 8. The rates of clinical response and remission and mucosal healing were similar in infliximab-naïve and previously exposed patients. None of the patients experienced hypersensitivity reactions during treatment with adalimumab.Adalimumab is well tolerated and appears to be a clinically beneficial option for patients with UC, including those who have previously lost their response to or cannot tolerate infliximab. (Inflamm Bowel Dis 2009)]]></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.20940">
<title>Obestatin/ghrelin ratio: A new activity index in inflammatory bowel diseases</title>
<link>http://dx.doi.org/10.1002%2Fibd.20940</link>
<description><![CDATA[The aim was to determine obestatin and ghrelin serum levels and their ratio in inflammatory bowel disease (IBD) patients.We measured the ghrelin and obestatin levels of 31 Crohn's disease patients and 22 patients with ulcerative colitis using a radioimmunoassay method. Circulating levels of the 2 hormones and their ratio were correlated with the disease type and activity, disease localization, and treatment.The mean ghrelin value was statistically significantly higher in patients with active disease (402.4 ± 462.6 pg/mL) than in patients in remission (148.2 ± 59.6 pg/mL) P = 0.0290, [alpha] = 0.05, whereas obestatin mean values were not (217.4 ± 59.8 pg/mL in active disease and 189.0 ± 46.8 pg/mL in patients with inactive disease P = 0.0607). When we evaluated the obestatin/ghrelin ratio between active and inactive disease, it was found that the ratio in active disease was statistically significantly lower (0.8 ± 0.3) than in patients in remission (1.4 ± 0.3) P < 0.001, [alpha] = 0.05. There is also a statistically significantly correlation between obestatin/ghrelin ratio and disease activity (P < 0,001).Ghrelin and obestatin seem to play a significant role in IBD pathogenesis. Further studies are needed to elucidate the role of these hormones as new biological markers of activity of IBD. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20938">
<title>Probiotics and their derivatives as treatments for inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20938</link>
<description><![CDATA[Inflammatory bowel disease (IBD) is a chronic relapsing disorder that is increasing in prevalence in Western society and has been linked to the development of colorectal cancer. There remains no definitive treatment for IBD, hence recent investigations have focused on the development of new therapeutics, including probiotics, which can reduce intestinal inflammation and restore balance to the gastrointestinal microbiota. Probiotics are currently being studied in greater detail, albeit predominantly in animal models of IBD. Clinical studies have yielded promising findings and justify further investigation. Furthermore, the use of inactivated probiotics as well as the soluble products produced by these bacteria has demonstrated therapeutic potential, and may in fact be more suitable, as there is no risk of sepsis associated with their administration and they can be manufactured with greater quality control. Further research is essential to define the mechanism and source of probiotic action, and to identify more efficacious strains, while future clinical trials must focus on determining whether the bacterial and genetic profiles of IBD patients influence the effectiveness of treatment. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20930">
<title>Bacteria-free solution derived from lactobacillus plantarum inhibits multiple NF-kappaB pathways and inhibits proteasome function</title>
<link>http://dx.doi.org/10.1002%2Fibd.20930</link>
<description><![CDATA[Bacteria play a role in inflammatory bowel disease and other forms of intestinal inflammation. Although much attention has focused on the search for a pathogen or inciting inflammatory bacteria, another possibility is a lack of beneficial bacteria that normally confer anti-inflammatory properties in the gut. The purpose of this study was to determine whether normal commensal bacteria could inhibit inflammatory pathways important in intestinal inflammation.Conditioned media from Lactobacillus plantarum (Lp-CM) and other gut bacteria was used to treat intestinal epithelial cell (YAMC) and macrophage (RAW 264.7) or primary culture murine dendritic cells. NF-[kappa]B was activated through TNF-Receptor, MyD88-dependent and -independent pathways and effects of Lp-CM on the NF-[kappa]B pathway were assessed. NF-[kappa]B binding activity was measured using ELISA and EMSA. 1[kappa]B expression was assessed by Western blot analysis, and proteasome activity determined using fluorescence-based proteasome assays. MCP-1 release was determined by ELISA.Lp-CM inhibited NF-[kappa]B binding activity, degradation of I[kappa]B[alpha] and the chymotrypsin-like activity of the proteasome. Moreover, Lp-CM directly inhibited the activity of purified mouse proteasomes. This effect was specific, since conditioned media from other bacteria had no inhibitory effect. Unlike other proteasome inhibitors, Lp-CM was not toxic in cell death assays. Lp-CM inhibited MCP-1 release in all cell types tested.These studies confirm, and provide a mechanism for, the anti-inflammatory effects of the probiotic and commensal bacterium Lactobacillus plantarum. The use of bacteria-free Lp-CM provides a novel strategy for treatment of intestinal inflammation which would eliminate the risk of bacteremia reported with conventional probiotics. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20929">
<title>Prepouch ileitis, myth or reality? The first case with acute abdomen</title>
<link>http://dx.doi.org/10.1002%2Fibd.20929</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20871">
<title>Women with inflammatory bowel disease may infrequently rely on their physicians as a source of disease-specific information</title>
<link>http://dx.doi.org/10.1002%2Fibd.20871</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20920">
<title>Questions and answers on the role of fecal lactoferrin as a biological marker in inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20920</link>
<description><![CDATA[Among the available fecal biomarkers for the diagnosis and monitoring of inflammatory bowel disease (IBD), only calprotectin and lactoferrin have translated into useful clinical tools. Lactoferrin can be detected using simple and cheap techniques and it has excellent stability in feces over a long period of time. Fecal lactoferrin has a good diagnostic precision for separating organic and functional intestinal disease. However, a negative fecal lactoferrin test should be interpreted merely as the absence of significant neutrophilic intestinal inflammation. The mean sensitivity and specificity of the fecal lactoferrin determination for the diagnosis of IBD is 80% and 82%, respectively. Some studies have suggested a lower accuracy of lactoferrin when compared with calprotectin for the diagnosis of IBD, indicating that more studies on this topic are necessary. A parallel between fecal lactoferrin levels and IBD activity estimated with clinical, endoscopic, and histological parameters has been confirmed. However, this correlation seems to be lower in Crohn's disease than in ulcerative colitis, mainly when Crohn's disease patients with purely ileal disease are considered. Fecal lactoferrin determination may be useful in predicting impending clinical relapse in IBD patients. Fecal lactoferrin may be a helpful noninvasive diagnostic tool for monitoring therapeutic efficacy, mainly on mucosal healing, as a decreasing concentration of lactoferrin can be interpreted as a marker of therapeutic response. Finally, in patients with Crohn's disease who have undergone ileocolonic resection, those with higher lactoferrin fecal levels might be more prone to postsurgical recurrence.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20911">
<title>Volvulus of an ileal J-pouch</title>
<link>http://dx.doi.org/10.1002%2Fibd.20911</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20935">
<title>Differential expression of leukocyte functions associated antigen-1 (LFA-1) on peripheral blood mononuclear cells in patients with Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20935</link>
<description><![CDATA[The leukocyte function associated antigen-1 (LFA-1) intracellular adhesion molecule-1 pathway is presumed to play a pivotal role in the perpetuation of inflammatory bowel disease. We aimed to elucidate the effect of 2 different therapies on LFA-1 expression in patients with Crohn's disease (CD) and correlate LFA-1 expression with disease activity.In all, 30 patients with active CD were recruited for the present investigation. Eleven patients were treated with infliximab and 19 patients with total parenteral nutrition. The clinical activity and the expression of LFA-1 in peripheral blood mononuclear cells were assessed prior to and 4 weeks after treatment. Clinical activity was determined by measuring the Crohn's Disease Activity Index and LFA-1 expression was measured by mean fluorescence intensity (MFI) under fluorescence-activated cell sorter analysis.In each treatment group the clinical disease activity index decreased significantly 4 weeks after treatment. In patients treated with infliximab, LFA-1 expression decreased significantly (mean MFI decreased from 1983 to 1487, P  0.05).The mechanism of therapeutic action on CD is different between infliximab and total parenteral nutrition. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20934">
<title>Retinoic acid contributes to the induction of IL-12-hypoproducing dendritic cells</title>
<link>http://dx.doi.org/10.1002%2Fibd.20934</link>
<description><![CDATA[Vitamin A is an important regulator of the human immune system, especially in the gut. Recent studies have revealed that retinoic acid (RA) in gut-associated dendritic cells (DCs) enhances the transforming growth factor (TGF)-[beta]-dependent conversion of naïve T cells into regulatory T (Treg) cells. Thus, RA produced by DCs contributes to immune tolerance mechanisms in the gut. In the present study we focused on the effect of RA on the differentiation of the DC, and tried to clarify the role of DCs induced by RA in a murine colitis model.Human peripheral blood CD14+ monocytes were cultured with granulocyte-macrophage colony stimulation factor and interleukin (IL)-4, with or without synthetic RA, Am80. Differentiated DCs cultured with Am80 (Am-DCs) were compared with conventional monocyte-derived DCs (cDCs).Am-DCs showed macrophage (M[phis])-like adherent phenotypes, and lacked the expression of the typical DC marker CD1a. Am-DCs produced less IL-12p70 and revealed less polarizing ability toward type 1 helper T cells (Th1) by allogeneic mixed lymphocyte reaction with naïve T cells. In addition, Am80 treatment ameliorated macro- and microscopic damage in dextran sodium sulfate-induced colitis in mice, and suppressed the colitis-induced elevation of IL-12 in the intestinal lamina propria.RA might play an important role in gut immune tolerances via local generation of IL-12 hypoproductive DCs. RA may be a useful clinical treatment for Th1-mediated inflammatory diseases, especially those such as Crohn's disease occurring in the gut. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20927">
<title>Mucosal healing predicts long-term outcome of maintenance therapy with infliximab in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20927</link>
<description><![CDATA[Infliximab (IFX) treatment induces mucosal healing (MH) in patients with Crohn's disease (CD) but the impact of MH on the long-term outcome of IFX treatment in CD is still debated.We studied MH during long-term treatment with IFX in 214 CD patients. A total of 183 patients (85.5%) responded to induction therapy and 31 patients (14.5%) were primary nonresponders. They underwent lower gastrointestinal (GI) endoscopy within a median of 0.7 months (interquartile range [IQR] 0.1-6.8) prior to first IFX and after a median of 6.7 months (IQR 1.4-24.6) after start of IFX and were further analyzed. The relationship between the outcome of IFX treatment long-term and MH was studied.MH was observed in 67.8% of the 183 initial responders (n = 124), with 83 patients having complete healing (45.4%) and 41 having partial healing (22.4%). Scheduled IFX treatment from the start resulted in MH more frequently (76.9% MH rate) than episodic treatment (61.0% MH rate; P = 0.0222, odds ratio [OR] 2.14, 95% confidence interval [CI] 1.11-4.12). Concomitant treatment with corticosteroids (CS) had a negative impact on MH (37.9% in patients with CS versus 63.2% in patients without CS; P = 0.021, OR 0.36, 95% CI 0.16-0.80). MH was associated with a significantly lower need for major abdominal surgery (MAS) during long-term follow-up (14.1% of patients with MH needed MAS versus 38.4% of patients without MH; P < 0.0001).MH induced by long-term maintenance IFX treatment is associated with an improved long-term outcome of the disease especially with a lower need for major abdominal surgeries. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20932">
<title>Predictive value and clinical significance of myenteric plexitis in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20932</link>
<description><![CDATA[Recurrence of Crohn's disease (CD) after ileal or colonic resection is common. Myenteric plexitis in the proximal resection margin of an ileocolonic CD resection specimen may indicate ongoing pathology that relates to disease recurrence. We assessed risk factors for myenteric plexitis, the effect of plexitis on clinical recurrence, and whether preoperative medical therapies affect the intensity of plexitis.Ileocolonic resection specimens from 99 patients with CD were histologically scored for the presence and severity of plexitis. Myenteric plexitis was correlated with immunosuppressive therapy before index surgery. Univariate and multivariate analyses were performed to identify predictive factors for plexitis.Myenteric plexitis was present in 43% and 85% of cases in the proximal resection margin and the affected resected segments of CD, respectively. Patients with a previous resection were more likely to have plexitis than those with no previous resection (odds ratio [OR] 3.5, 95% confidence interval [CI] 1.21-10.15, P = 0.02), and those with a greater duration of disease were less likely to have plexitis in the proximal resection margin (OR 0.68, 95% CI 0.48-0.96, P = 0.03). Preoperative immunosuppressive therapy was not associated with a lesser incidence of plexitis. Twelve of 40 (30%) patients with plexitis and 9 of 54 (16%) patients without plexitis in the proximal resection margin subsequently developed clinical recurrence (median 10 months; P = 0.17).Previous resections and shorter disease duration are associated with plexitis in proximal resection margin of CD. The prognostic value of plexitis in postoperative disease recurrence and risk stratification remain to be prospectively established.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20917">
<title>3,3[prime]-diindolylmethane attenuates colonic inflammation and tumorigenesis in mice</title>
<link>http://dx.doi.org/10.1002%2Fibd.20917</link>
<description><![CDATA[Background: 3,3-Diindolylmethane (DIM) is a major in vivo product of acid-catalyzed oligomerization of indole-3-carbinol (I3C) derived from Brassica food plants. Although DIM is known as a chemopreventive and chemotherapeutic phytochemical, the effects of DIM on inflammation in vivo are still unknown. In the present study we investigated the antiinflammatory effects of DIM on experimental colitis and colitis-associated colorectal carcinogenesis.Methods: To determine if DIM has an antiinflammatory effect in vivo, we examined the therapeutic effects of DIM in dextran sodium sulfate (DSS)-induced experimental colitis and colitis-associated colon carcinogenesis induced by azoxymethane (AOM)/DSS in BALB/c mice.Results: Treatment with DIM significantly attenuated loss of body weight, shortening of the colon, and severe clinical signs in a colitis model. This was associated with a remarkable amelioration of the disruption of the colonic architecture and a significant reduction in colonic myeloperoxidase activity and production of prostaglandin E2, nitric oxide, and proinflammatory cytokines. Further, DIM administration dramatically decreased the number of colon tumors in AOM/DSS mice.Conclusions: These results suggest that DIM-mediated antiinflammatory action at colorectal sites may be therapeutic in the setting of inflammatory bowel disease and colitis-associated colon cancer.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20921">
<title>Contribution of IL23R but not ATG16L1 to Crohn&#x27;s disease susceptibility in Koreans</title>
<link>http://dx.doi.org/10.1002%2Fibd.20921</link>
<description><![CDATA[Background: Recent genome-wide association studies in Caucasian populations identified IL23R and ATG16L1 as susceptibility genes to Crohn's disease (CD). We tested 5 IL23R single nucleotide polymorphisms (SNPs) and 12 ATG16L1 SNPs in Korean patients to determine whether these genes are associated with susceptibility to CD in a non-Caucasian population.Methods: We analyzed 5 IL23R SNPs and 12 ATG16L1 SNPs in 380 patients with CD and 380 healthy controls.Results: Two IL23R gene variants, an intronic SNP rs1004819 and intergenic SNP rs1495465, showed significant associations with CD; the adjusted odds ratio (aOR) for rs1004819 was 1.822 (95% confidence interval [CI] = 1.164-2.852, P = 0.009) and aOR for rs1495965 was 1.650 (95% CI = 1.102-2.471, P = 0.015). The genotype-phenotype analysis showed subphenotype specificity to stricturing and penetrating behaviors. On the other hand, none of the 12 ATG16L1 SNPs showed any positive association with CD in Koreans. The contribution of IL23R variants in Korean CD patients overall is low in comparison with studies of Caucasian.Conclusions: Our data in Koreans support the previous Caucasian reports of an association of the IL23R gene with CD.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20923">
<title>Il-21 enhances NK cell activation and cytolytic activity and induces Th17 cell differentiation in inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20923</link>
<description><![CDATA[Background: Interleukin-21 (IL-21) is involved in T and NK cell activation and effector response and promotes Th17 cell differentiation. Here we investigated IL-21 receptor (IL-21R) expression in inflamed mucosa of inflammatory bowel disease (IBD) and evaluated its role in the induction of NK cell cytotoxicity and activation as well as Th17 differentiation.Methods: Expression of IL-21R was performed by immunohistochemistry and flow cytometry. NK cell cytotoxicity was detected by a standard 51Cr-release assay. Cytokine levels were analyzed by enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (PCR).Results: IL-21R-positive cells were significantly increased in inflamed mucosa of IBD compared with controls, and mainly expressed in freshly isolated peripheral blood (PB)- and lamina propria (LP)-CD4+, CD8+ T, B, and NK cells. PB-NK cells from IBD patients produced higher levels of interferon gamma (IFN-[gamma]) and tumor necrosis factor (TNF) than controls when stimulated with immobilized human IgG and IL-21. IL-21-primed IBD NK cells showed a more potent antitumor cytotoxicity to NK-sensitive K562 cells than controls. Moreover, PB-T and LP-T cells from IBD patients produced large amounts of proinflammatory cytokines (e.g., TNF, IFN-[gamma]) than controls when stimulated with IL-21 and anti-CD3. Importantly, IL-21 facilitated IBD CD4+ T cell to differentiate into Th17 cells, characterized by increased expression of IL-17A and ROR[gamma]t.Conclusions: IL-21 enhances IBD NK cell cytotoxic response, triggers T cells to produce proinflammatory cytokines, and induces IBD CD4+ T cells to differentiate into Th17 cells, suggesting that IL-21 is involved in the pathogenesis of IBD and that blocking IL-21R signaling may have a therapeutic potential in IBD.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20922">
<title>Established genetic risk factors do not distinguish early and later onset Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20922</link>
<description><![CDATA[Background: Early-onset disease is frequently examined in genetic studies because it is presumed to contain a more severe subset of patients under a higher influence of genetic effects. In light of the dramatic success of Crohn's disease (CD) gene discovery efforts, we aimed to characterize the contribution of established common risk variants to pediatric CD.Methods: Using 35 confirmed CD risk alleles, we genotyped 384 parent-child trios (mean age of onset 11.7 years) along with 321 healthy controls. We performed association tests on the independent pediatric cohort and compared results to those previously published. We also computed a weighted CD genetic risk score for each affected person. Six variants not previously validated in children (at 5q33, 1q24, 7p12, 12q12, 8q24, and 1q32) were significantly associated with pediatric CD (P < 0.03).Results: We detected no significant association between risk score and age at onset through age 30. This analysis illustrates that the genetic effect of established CD risk variants is similar in early and later onset CD.Conclusions: These results motivate joint analyses of genome-wide association data in early and late onset cohorts and suggest that, rather than established risk variants, independent variants or environmental exposures should be sought as modulators of age of onset.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20916">
<title>Increased number and activation of colonic macrophages in pediatric patients with untreated Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20916</link>
<description><![CDATA[Background: Pediatric inflammatory bowel disease (IBD) may be phenotypically different from adult IBD. In IBD lesions, macrophages are overactivated, suggesting involvement of innate immunity in the pathogenesis. Here, mucosal macrophages were studied in selected untreated pediatric patients compared with adults from a population-based Norwegian cohort of IBD patients. Age-matched non-IBD controls were also included.Methods: Untreated children (<18 years) and adults ([ge]18 years) were included at diagnosis with colonic and ileal biopsies. Controls were symptomatic non-IBD patients with histologically normal gut. Frozen mucosal sections were examined by immunohistochemistry for cellular expression of the pan-macrophage marker CD68 and the costimulatory molecule CD40. Two-color immunofluorescence staining in situ was performed to identify CD40+ macrophages.Results: Non-IBD adults had significantly higher mucosal density of colonic CD68+ macrophages than non-IBD children. In pediatric Crohn's disease (CD), macrophages were significantly increased in the colon (but not in the ileum) compared with controls. Their mucosal density in pediatric CD was significantly higher than in pediatric ulcerative colitis. The number of CD40+ (activated) macrophages was significantly elevated in both histologically inflamed and uninflamed colon and ileum of IBD children.Conclusions: Histologically normal colon mucosa contains fewer macrophages in children than in adults. However, in colon of children with untreated CD the mucosal macrophage density is increased. Activated mucosal macrophages are increased in untreated pediatric IBD regardless of inflammatory grade. Such upregulated innate mucosal immune activation may contribute to the colonic phenotype of childhood CD.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20913">
<title>Ulcerative colitis and primary sclerosing cholangitis as part of autoimmune polyglandular syndrome type III</title>
<link>http://dx.doi.org/10.1002%2Fibd.20913</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20912">
<title>Chronic granulomatous disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20912</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20910">
<title>Indoleamine 2,3-dioxygenase in intestinal immunity and inflammation</title>
<link>http://dx.doi.org/10.1002%2Fibd.20910</link>
<description><![CDATA[Indoleamine 2,3-dioxygenase (IDO) is a tryptophan catabolizing enzyme that has a number of immunoregulatory effects. It is expressed at high levels in the gastrointestinal tract, particularly in the small intestine, and has been implicated in the control of intestinal inflammation. However, its precise role in intestinal immunity is not well understood. This review will summarize the current state of knowledge about IDO function, particularly as it pertains to inflammatory responses in the gut.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20909">
<title>Management and prevention of postoperative Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20909</link>
<description><![CDATA[Postoperative Crohn's disease (CD) recurrence is a common occurrence after intestinal resection. Currently, the optimal management of patients who have undergone surgical resection is unknown and treatment remains subjective. Clinicians in conjunction with patients must balance the risks of recurrence against the potential risks associated with treatment. For those at very low risk of recurrence, no therapy may be needed; however, for patients at moderate risk immunomodulators should be considered. For those at highest risk of recurrence, biologic therapy, specifically antitumor necrosis factor agents, have emerged as appropriate treatment. Any postoperative management strategy should include a colonoscopy 6-12 months after surgery to identify recurrence. This review discusses current evidence for various pharmacologic approaches in the prevention of postoperative recurrence and provides guidance for clarifying patient risk.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20902">
<title>Blockage of the neurokinin 1 receptor and capsaicin-induced ablation of the enteric afferent nerves protect SCID mice against T-cell-induced chronic colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20902</link>
<description><![CDATA[Background: The neurotransmitter substance P (SP) released by, and the transient receptor potential vanilloid (TRPV1), expressed by afferent nerves, have been implicated in mucosal neuro-immune-regulation. To test if enteric afferent nerves are of importance for the development of chronic colitis, we examined antagonists for the high-affinity neurokinin 1 (NK-1) SP receptor and the TRPV1 receptor agonist capsaicin in a T-cell transfer model for chronic colitis.Methods: Chronic colitis was induced in SCID mice by injection of CD4+CD25- T cells. The importance of NK-1 signaling and TRPV1 expressing afferent nerves for disease development was studied in recipient SCID mice systemically treated with either high-affinity NK-1 receptor antagonists or neurotoxic doses of capsaicin. In addition, we studied the colitis-inducing effect of NK-1 receptor deleted CD4+CD25- T cells.Results: Treatment with the NK-1 receptor antagonist CAM 4092 reduced the severity of colitis, but colitis was induced by NK-1 receptor-deleted T cells, suggesting that SP in colitis targets the recipient mouse cells and not the colitogenic donor T cells. Capsaicin-induced depletion of nociceptive afferent nerves prior to CD4+CD25- T-cell transfer completely inhibited the development of colitis.Conclusions: Our data demonstrate the importance of an intact enteric afferent nerve system and NK-1 signaling in mucosal inflammation and may suggest new treatment modalities for patients suffering from inflammatory bowel disease.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20918">
<title>Positioning biologic agents in the treatment of Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20918</link>
<description><![CDATA[One decade after the emergence of biologic therapy for Crohn's disease (CD), our treatment algorithms are beginning to change. Once reserved for patients with refractory disease, disease unresponsive to conventional therapies, or those requiring multiple courses of corticosteroids, there is increasing evidence that early, aggressive interventions with immunosuppressants or biologic therapies targeting tumor necrosis factor-[alpha] or [alpha]-4 integrins can alter the natural history of CD by reducing the transmural complications of structuring and fistulization and the nearly inevitable requisite for surgical resections. More recent trials are beginning to suggest that intervention with combination therapy for selected patients with a poor prognosis may modify the long-term course of CD. Selection of patients with features predicting a complex or progressive course and early, combined intervention is now possible. Future studies are still needed to best identify predictors of response to individual agents with differing mechanisms of action, as well as to optimize the risk-benefit of long-term maintenance therapy.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20906">
<title>Assessment and validation of the new capsule endoscopy Crohn&#x27;s disease activity index (CECDAI): What difference does it make?</title>
<link>http://dx.doi.org/10.1002%2Fibd.20906</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20933">
<title>Fecal calprotectin and lactoferrin for the prediction of inflammatory bowel disease relapse</title>
<link>http://dx.doi.org/10.1002%2Fibd.20933</link>
<description><![CDATA[The purpose of the study was to determine the role of fecal calprotectin and lactoferrin in the prediction of inflammatory bowel disease relapses, both in patients with ulcerative colitis (UC) and Crohn's disease (CD), in a large, long-term, follow-up study.The prospective multicenter study included CD and UC patients who had been in clinical remission for 6 months. At baseline, patients provided a single stool sample for calprotectin and lactoferrin determination. Follow-up was 12 months in patients showing no relapse and until activity flare in relapsing patients.In all, 163 patients (89 CD, 74 UC) were included. Twenty-six patients (16%) relapsed during follow-up. Calprotectin concentrations in patients who suffered a relapse were higher than in nonrelapsing patients (239 ± 150 versus 136 ± 158 [mu]g/g; P 150 [mu]g/g) calprotectin concentrations (30% versus 7.8%; P 150 [mu]g/g) sensitivity and specificity to predict relapse were 69% and 69%, respectively. Corresponding values for lactoferrin were 62% and 65%, respectively. The area under the receiver operating characteristic curve to predict relapse using calprotectin determination was 0.73 (0.69 for UC and 0.77 for CD). Better results were obtained when only colonic CD disease or only relapses during the first 3 months were considered (100% sensitivity). High fecal calprotectin levels or lactoferrin positivity was associated with clinical relapse in Kaplan-Meier survival analysis, and both fecal tests were associated with relapse in the multivariate analysis.Fecal calprotectin and lactoferrin determination may be useful in predicting impending clinical relapse - especially during the following 3 months - in both CD and UC patients. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20931">
<title>Effects of infliximab therapy on abdominal fat and metabolic profile in patients with Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20931</link>
<description><![CDATA[Tumor necrosis factor is an adipocytokine possessing a well-established lipolytic effect. In Crohn's disease (CD) patients, infliximab therapy may thus result in visceral fat accumulation, which is associated with an increased risk of metabolic syndrome.A total of 132 CD patients were investigated. In a first prospective study, magnetic resonance imaging (MRI) quantification of subcutaneous and visceral abdominal fat was performed before and 8 weeks after initiation of infliximab induction therapy (5 mg/kg at weeks 0, 2, and 6) in 21 responding patients treated for perianal disease. In a second prospective study, fasting glycemia, glycated hemoglobin (HbA1c), HDL, LDL, and total cholesterol and triglyceride levels were assessed in 111 responding patients receiving infliximab infusions every 8 weeks, with a mean follow-up of 41 weeks.A significant homogeneous 18% increase in total abdominal fat was observed in the 21 CD patients after infliximab induction therapy (P = 0.027), independently of body mass index evolution. Infliximab maintenance therapy was associated with a decrease in glycemia (P < 0.0001) and HbA1c (P = 0.0005) concentrations, together with an increase in both total cholesterol (P = 0.02) and HDL cholesterol (P = 0.008) concentrations. All glycemic and lipid parameters remained within the normal range throughout the study.Infliximab induction therapy is associated with a significant increase in abdominal fat tissue in CD patients. Infliximab maintenance therapy has no deleterious effects on lipid profile and is accompanied by a decrease in glycemia and HbA1c concentrations, probably by reversing the impairment of tumor necrosis factor-induced insulin-mediated glucose uptake. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20915">
<title>Impact of infliximab therapy after early endoscopic recurrence following ileocolonic resection of Crohn&#x27;s disease: A prospective pilot study</title>
<link>http://dx.doi.org/10.1002%2Fibd.20915</link>
<description><![CDATA[Background: The efficacy of infliximab for endoscopic recurrence after resection of Crohn's disease (CD) has not yet been reported. The aim of this prospective study was to investigate the impact of infliximab on early endoscopic lesions after resection for CD.Methods: Twenty-six patients maintaining clinical remission (CD activity index [CDAI] score <150) with mesalamine (3 g/day) after resection showed endoscopic recurrence in the neoterminal ileum at 6 months postoperatively (=baseline). Over the following 6 months, 10 patients were treated with continuous mesalamine (3 g/day), 8 patients were treated with azathioprine therapy (50 mg/day), and the other 8 patients were treated with infliximab therapy (5 mg/kg, every 8 weeks). During ileocolonoscopy at baseline and 6 months later, mucosal biopsies were taken for cytokine assays.Results: During 6-month observation, no patients in the infliximab group, 3 (38%) in the azathioprine group, and 7 (70%) in the mesalamine group developed clinical recurrence (CDAI [ge]150) (P = 0.01). At 6 months, endoscopic inflammation was improved in 75% of patients in the infliximab group, 38% in the azathioprine group, and 0% in the mesalamine group (P = 0.006). The mucosal interleukin (IL)-1[beta], IL-6, and tumor necrosis factor-[alpha] levels significantly decreased in the infliximab group, while they significantly increased in the mesalamine group, and they did not change significantly in the azathioprine group.Conclusions: Infliximab therapy showed clear suppressive effects on clinical and endoscopic disease activity, and mucosal cytokine production in patients with early endoscopic lesions after resection. To confirm our conclusions, randomized controlled trials with a larger number of patients are necessary.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20908">
<title>Lactobacillus fermentum CECT 5716 prevents and reverts intestinal damage on TNBS-induced colitis in mice</title>
<link>http://dx.doi.org/10.1002%2Fibd.20908</link>
<description><![CDATA[Background: Probiotics attenuate gut inflammation when administered before experimental colitis, but data on their effect after colitis induction are scarce. We aimed to evaluate the effects of Lactobacillus fermentum CECT 5716 on gut injury when administered either before or after trinitrobencene sulfonic acid (TNBS) colitis in Balb/c mice.Methods: In a preventive study, probiotic or vehicle was administered for 2 weeks before colitis. Then mice were allocated to: probiotic + TNBS, probiotic + sham, vehicle + TNBS, or vehicle + sham, and sacrificed 72 hours later. In a therapeutic study, mice were allocated into the same groups as before. Probiotic or vehicle were administered for 3 weeks. Mice were sacrificed at weeks 1, 2, and 3 after TNBS. Histological score, myeloperoxidase activity, and eicosanoid and cytokine production in colonic explant cultures were measured. Immunohistochemistry for nitrotyrosine and MyD88 was also performed.Results: In the preventive study, colitis was milder with probiotic than with vehicle (P = 0.041). This was associated with increased PGE2, IL-2, and IL-4 production, as well as attenuated nitrotyrosine staining in the former. In the therapeutic study, histological score at week 1 post-TNBS was higher in probiotic than in vehicle fed mice (P = 0.018). However, at weeks 2 and 3 the histological score was significantly lower - with decreased IL-6 production and increased MyD88 staining - in mice receiving the probiotic.Conclusions: Pretreatment with L. fermentum CECT 5716 attenuates TNBS colitis, an effect that seems to be due to its antioxidant abilities. When administered after TNBS, this probiotic is also effective in accelerating colitis recovery, and this is associated with an enhanced Toll-like receptor function.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20905">
<title>Likelihood ratio for Crohn&#x27;s disease as a function of Anti-Saccharomyces cerevisiae antibody concentration</title>
<link>http://dx.doi.org/10.1002%2Fibd.20905</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20914">
<title>Minimally invasive total proctocolectomy with Brooke ileostomy for ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20914</link>
<description><![CDATA[Background: Total proctocolectomy with Brooke ileostomy remains the optimal surgical procedure for select ulcerative colitis patients. However, few studies describe outcomes of minimally invasive total proctocolectomy with Brooke ileostomy. Our aim was to describe the safety and feasibility of these procedures by examining short-term (30-day) outcomes.Methods: Using a prospective database, we identified a cohort of patients who underwent laparoscopic total proctocolectomy with Brooke ileostomy at our institution from 2000-2007. Results are reported as median (range) or frequency (proportion).Results: Forty-four patients were included; age 65 years (54-73), 24 were male (55%), body mass index was 26.5 (22.1-30.2) kg/m2. Colitis duration was 66 months (24-240), and 40% had prior surgery. The indication for surgery was refractory colitis (82%) and neoplasia (18%). Factors influencing choice of total proctocolectomy with permanent ileostomy were advanced age in 18 (41%), lifestyle in 13 (30%), medical comorbidities in 11 (25%), fecal incontinence in 10 (23%), oncologic reasons in 3 (6.8%), and obesity in 3 (6.8%). Twenty-three (52%) operations were hand-assisted laparoscopic surgery, 13 (30%) were laparoscopic-assisted, and 8 (18%) were "laparoscopic-incisionless" with transanal specimen extraction. Two laparoscopic-assisted cases (4.6%) were converted. Operative time was 329 (272-402) minutes, and length of stay 5 () days. Major post-operative complications occurred in 4 (9%); there were no perioperative mortalities.Conclusions: Minimally invasive total proctocolectomy with Brooke ileostomy is a safe, feasible option for the surgical treatment of chronic ulcerative colitis, and is the procedure of choice for select patients.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20907">
<title>Activation of NOD2-mediated intestinal pathway in a pediatric population with Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20907</link>
<description><![CDATA[Background: NOD2 is an intracellular protein involved in host recognition of specific bacterial molecules and is genetically associated with several inflammatory diseases, including Crohn's disease (CD). NOD2 stimulation activates the transcription factor, NF-[kappa]B, through RIP2, a caspase-recruitment domain-containing kinase. NOD2/RIP2 signaling also mediates the activation of antimicrobial peptides such as human [alpha]-defensin 5 (HD-5) and human [alpha]-defensin 6 (HD-6), both produced by Paneth cells. The present study is aimed at describing the downstream events triggered specifically by NOD2 induction in order to demonstrate that the protein, other than overexpressed, is also physiologically associated with RIP2 and Erbin in the bioptic intestinal inflamed specimens of children affected by CD.Methods: Fifteen children with CD and 10 children used as controls were entered in the study. Mucosal biopsy specimens were taken during endoscopy and mRNA and protein expressions were detected by using real-time polymerase chain reaction and Western blot.Results: NOD2 is able to form an immunocomplex with the kinase RIP2. As compared to controls, in the inflamed mucosa of patients both mRNA and protein expression levels of RIP2 are increased, and its active phosphorylated form is overexpressed.Conclusions: In this study we provide for the first time ex vivo evidence of physiologically relevant protein interactions with NOD2, which are able to trigger the innate immune response in intestinal mucosal specimens of children with CD.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20904">
<title>Gastroenterologists&#x27; prescribing of infliximab for Crohn&#x27;s disease: A national survey</title>
<link>http://dx.doi.org/10.1002%2Fibd.20904</link>
<description><![CDATA[Background: Practice guidelines suggest that immunomodulators (IMs) be given prior to infliximab (IFX) in patients with Crohn's disease (CD). The package insert for IFX recommends that maintenance therapy be prescribed for patients who respond to induction therapy. Our aim was to determine the extent to which gastroenterologists (GIs) are utilizing IM prior to IFX and prescribing maintenance IFX when treating patients with CD.Methods: An 18-item questionnaire was developed and validated. The survey was sent to 4515 GIs who are members of the American Gastroenterology Association. Bivariate and multivariate analyses were performed.Results: In all, 305 GIs responded; 70% use an IM prior to IFX, 86% prescribe maintenance IFX, and 62% reported both use of IM prior to IFX and use of maintenance IFX. Academic GIs, Midwest GIs, and GIs prescribing IFX a few times per year were more likely to report both use of an IM prior to IFX and use of maintenance IFX (odds ratio [OR] = 4.56, 2.18, and 2.25, respectively). GIs demonstrated awareness of the risk of reactivation of tuberculosis when initiating IFX and appropriately manage infusion reactions. GIs were unable to rank serious adverse reactions associated with IFX.Conclusions: A total of 38% of GIs did not report the use of IM prior to IFX and/or did not use maintenance IFX. GIs practicing outside the Midwest and those in nonacademic settings may need additional training regarding prescribing IFX.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20892">
<title>Phenotypic associations of Crohn&#x27;s disease with antibodies to flagellins A4-Fla2 and Fla-X, ASCA, p-ANCA, PAB, and NOD2 mutations in a swiss cohort</title>
<link>http://dx.doi.org/10.1002%2Fibd.20892</link>
<description><![CDATA[Background: Distinct Crohn's disease (CD) phenotypes correlate with antibody reactivity to microbial antigens. We examined the association between antibody response to 2 new flagellins called A4-Fla2 and Fla-X, anti-Saccharomyces cerevisiae antibodies (ASCA), anti-neutrophil cytoplasmic antibodies (p-ANCA), anti-pancreas antibodies (PAB), NOD2 mutations (R702W, G908R, and L1007fsinsC), and clinical CD phenotypes (according to Vienna criteria).Methods: All the above-mentioned antibodies as well as NOD2 mutations were determined in 252 CD patients, 53 with ulcerative colitis (UC), and 43 healthy controls (HC) and correlated with clinical data.Results: A seroreactivity for A4-Fla2/Fla-X/ASCA/p-ANCA/PAB (in percent) was found in 59/57/62/12/22 of CD patients, 6/6/4/51/0 of UC patients, and 0/2/5/0/0 of healthy controls. CD behavior: 37% B1, 36% B2, and 27% B3. In multivariate logistic regression, antibodies to A4-Fla2, Fla-X, and ASCA were significantly associated with stricturing phenotype (P = 0.027, P = 0.041, P < 0.001), negative associations were found with inflammatory phenotype (P = 0.001, P = 0.005, P < 0.001). Antibodies to A4-Fla2, Fla-X, ASCA, and NOD2 mutations were significantly associated with small bowel disease (P = 0.013, P = 0.01, P < 0.001, P = 0.04), whereas ASCA was correlated with fistulizing disease (P = 0.007), and small bowel surgery (P = 0.009). Multiple antibody responses against microbial antigens were associated with stricturing (P < 0.001), fistulizing disease (P = 0.002), and small bowel surgery (P = 0.002).Conclusions: Anti-flagellin antibodies and ASCA are strongly associated with complicated CD phenotypes. CD patients with serum reactivity against multiple microbes have the greatest frequency of strictures, perforations, and small bowel surgery. Further prospective longitudinal studies are needed to show that antibody-based risk stratification improves the clinical outcome of CD patients.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20896">
<title>Inflammatory bowel disease: A paradigm for the link between coagulation and inflammation</title>
<link>http://dx.doi.org/10.1002%2Fibd.20896</link>
<description><![CDATA[Inflammatory bowel diseases (IBDs) are associated with platelet activation and an increased risk for thromboembolism. While the mechanisms that underlie the altered platelet function and hypercoagulable state in IBD remain poorly understood, emerging evidence indicates that inflammation and coagulation are interdependent processes that can initiate a vicious cycle wherein each process propagates and intensifies the other. This review addresses the mechanisms that may account for the mutual activation of coagulation and inflammation during inflammation and summarizes evidence that implicates a role for platelets and the coagulation system in the pathogenesis of human and experimental IBD. The proposed link between inflammation and coagulation raises the possibility of targeting the inflammation-coagulation interface to reduce the morbidity and mortality associated with IBD.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20903">
<title>Low counts of Faecalibacterium prausnitzii in colitis microbiota</title>
<link>http://dx.doi.org/10.1002%2Fibd.20903</link>
<description><![CDATA[Background: The intestinal microbiota is suspected to play a role in colitis and particularly in inflammatory bowel disease (IBD) pathogenesis. The aim was to compare the fecal microbiota composition of patients with colitis to that of healthy subjects (HS).Methods: fecal samples from 22 active Crohn's disease (A-CD) patients, 10 CD patients in remission (R-CD), 13 active ulcerative colitis (A-UC) patients, 4 UC patients in remission (R-UC), 8 infectious colitis (IC) patients, and 27 HS were analyzed by quantitative real-time polymerase chain reaction (PCR) targeting the 16S rRNA gene. Bacterial counts were transformed to logarithms (Log10 CFU) for statistical analysis.Results: Bacteria of the phylum Firmicutes (Clostridium leptum and Clostridium coccoides groups) were less represented in A-IBD patients (9.7; P = 0.004) and IC (9.4; P = 0.02), compared to HS (10.8). Faecalibacterium prausnitzii species (a major representative of the C. leptum group) had lower counts in A-IBD and IC patients compared to HS (8.8 and 8.3 versus 10.4; P = 0.0004 and P = 0.003). The Firmicutes/Bacteroidetes ratio was lower in A-IBD (1.3; P = 0.0001) and IC patients (0.4; P = 0.002). Compared to HS, Bifidobacteria were less represented in A-IBD and IC (7.9 and 7.7 versus 9.2; P = 0.001 and P = 0.01).Conclusions: The fecal microbiota of patients with IBD differs from that of HS. The phylum Firmicutes and particularly the species F. prausnitzii, are underrepresented in A-IBD patients as well as in IC patients. These bacteria could be crucial to gut homeostasis since lower counts of F. prausnitzii are consistently associated with a reduced protection of the gut mucosa.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20901">
<title>Crohn&#x27;s disease in a southern European country: Montreal classification and clinical activity</title>
<link>http://dx.doi.org/10.1002%2Fibd.20901</link>
<description><![CDATA[Background: Given the heterogeneous nature of Crohn's disease (CD), our aim was to apply the Montreal Classification to a large cohort of Portuguese patients with CD in order to identify potential predictive regarding the need for medical and/or surgical treatment.Methods: A cross-sectional study was used based on data from an on-line registry of patients with CD.Results: Of the 1692 patients with 5 or more years of disease, 747 (44%) were male and 945 (56%) female. On multivariate analysis the A2 group was an independent risk factor of the need for steroids (odds ratio [OR] 1.6, 95% confidence interval [CI] 1.1-2.3) and the A1 and A2 groups for immunosuppressants (OR 2.2; CI 1.2-3.8; OR 1.4; CI 1.0-2.0, respectively). An L3+L34 and L4 location were risk factors for immunosuppression (OR 1.9; CI 1.5-2.4), whereas an L1 location was significantly associated with the need for abdominal surgery (P < 0.001). After 20 years of disease, less than 10% of patients persisted without steroids, immunosuppression, or surgery. The Montreal Classification allowed us to identify different groups of disease severity: A1 were more immunosuppressed without surgery, most of A2 patients were submitted to surgery, and 52% of L1+L14 patients were operated without immunosuppressants.Conclusions: Stratifying patients according to the Montreal Classification may prove useful in identifying different phenotypes with different therapies and severity. Most of our patients have severe disease.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20899">
<title>Incidence and clinical significance of immunogenicity to infliximab in Crohn&#x27;s disease: A critical systematic review</title>
<link>http://dx.doi.org/10.1002%2Fibd.20899</link>
<description><![CDATA[Background: Infliximab (IFX) is a chimeric (mouse/human) anti-TNF-alpha monoclonal antibody approved for the treatment of refractory luminal and fistulizing Crohn's disease (CD). It is a source of potential immunogenicity for humans, with the occurrence of anti-infliximab antibodies (ATIs), which are thought to interfere with the pharmacodynamics and/or pharmacokinetics of the compound. It remains unclear whether ATIs have any clinical importance for drug efficacy or safety. We review studies specifically evaluating the incidence of ATIs in CD and their impact on the efficacy and safety of IFX.Methods: A systematic review was undertaken by electronic searches of the PubMed and SCOPUS databases from earliest records to October 2008, as well as reference lists of all relevant articles and relevant abstracts from meetings.Results: The biological and clinical mechanisms of ATI development are poorly understood. The incidence of ATIs in vivo depends on multiple analytical and clinical factors, both patient- and treatment-related. The presence of ATIs is weakly and variably associated with clinical response or infusion reactions, but not with reactions relevant to clinical decision-making. Enormous variation in the methods of reporting ATIs and immunogenicity of IFX make almost any interpretation possible from different studies, but few have clinical relevance.Conclusions: There is no clear evidence that ATIs have an impact on efficacy or safety, nor a need to measure or prevent them in clinical practice. Circulating drug concentration may be a more relevant measure of immunogenicity.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20898">
<title>Inflammatory bowel disease in the setting of autoimmune pancreatitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20898</link>
<description><![CDATA[Background: Despite scattered case reports, the prevalence of inflammatory bowel disease (IBD) in patients with autoimmune pancreatitis (AIP) is unknown. We sought to better characterize the putative association between the conditions.Methods: Medical records of 71 patients meeting accepted criteria for AIP were reviewed to identify those with endoscopic and histological evidence of IBD. Colon samples in patients with both AIP and IBD were immunostained to identify IgG4-positive cells.Results: Four patients with AIP (5.6%) had a diagnosis of IBD: 3 had ulcerative colitis (UC) and 1 had Crohn's disease (CD). The diagnosis of IBD preceded or was simultaneous to that of AIP. Two AIP-UC patients treated for AIP with prednisone had a recurrence of AIP, and 1 required 6-mercaptopurine for long-term corticosteroid-sparing treatment. Two AIP-IBD patients underwent Whipple resections, and 1 had recurrent AIP. All 3 patients with UC presented with pancolitis, and 2 required colectomy. Colon samples from 1 patient with UC and 1 patient with CD were available for review. Increased numbers of IgG4-positive cells (10 per high-power field) were noted on the colon sample from the patient with UC.Conclusions: Almost 6% of patients with proven AIP had a diagnosis of IBD, compared to a prevalence of [ap]0.4%-0.5% in the general population, potentially implying a 12-15-fold increase in risk. Patients with both AIP and IBD may have increased extent and severity of IBD. The finding of IgG4-positive cells on colon biopsy suggests that IBD may represent an extrapancreatic manifestation of AIP.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20897">
<title>Risk factors and characteristics of extent progression in ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20897</link>
<description><![CDATA[Background: The main objective was to identify risk factors for extent progression in distal ulcerative colitis. The secondary objective was to determine clinical characteristics of disease at the time of progression.Methods: Data were obtained from a prospective database. Distal colitis was defined as disease limited to rectum and sigmoid colon (n = 178), extensive colitis as involvement of at least the descending colon (n = 179), and colitis with progression when there was a change of category from distal to extensive (n = 63). To study clinical characteristics at the time of progression, a nested case-control study was performed.Results: Compared to distal colitis, colitis with progression was associated to significantly higher prevalence of extraintestinal manifestations (42.9% versus 15.5%) steroid-refractory course (28.0% versus 2.2%), requirement of thiopurines (44.3% versus 17.3%), cyclosporine (25.4% versus 1.9%), infliximab (9.5% versus 1.2%), surgery (20.6% versus 0.6%), and incidence of neoplasia (6.3% versus 0%). However, these differences appeared after disease progression. Regression analysis demonstrated that preexisting independent predictive factors for progression were younger age at diagnosis (hazard ratio [HR] 0.979 95% confidence interval [CI] 0.959-0.999) and presence of sclerosing cholangitis (HR 12.83, 95% CI 1.36-121.10). The nested case-control study showed that at the time of progression the flare was more severe in cases than in matched controls, with significant differences in markers of disease severity, therapeutic requirements, hospitalizations, and surgery.Conclusions: Patients with distal ulcerative colitis diagnosed at a younger age or with associated sclerosing cholangitis are at higher risk for progression. Disease flare associated with progression follows a severe course with high therapeutic requirements.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20895">
<title>FcRL3 gene promoter variant is associated with peripheral arthritis in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20895</link>
<description><![CDATA[Background: The mechanisms responsible for the pathogenesis of peripheral arthropathies (PA) in Crohn's disease (CD) are largely unknown, although many studies indicate that genetic and environmental factors are likely to contribute to risk.Methods: Because variants in the Fc receptor-like 3 (FcRL3) gene have recently been associated with rheumatoid arthritis and several other autoimmune diseases, we tested 2 FcRL3 promoter variants (-169 C>T and -110 G>A) for association with PA in Spanish CD patients that were recruited from a single center and followed for at least 4 years (mean follow-up time, 11 years).Results: Among the 342 CD patients evaluated, there were 88 cases of peripheral arthropathy; 31 were classified as arthritis and 57 were classified as arthralgia. We used contingency tables and logistic regression to test for association between PA or either subtype and FcRL3 and other factors that have previously been associated with extraintestinal manifestations in CD.Conclusions: We found that female sex, colonic involvement, and the AA genotype at -110 G>A were associated with increased risk of both subtypes of PA, although the association appears to be stronger for arthritis than for arthralgia.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20889">
<title>Digging out Crohn&#x27;s disease genes</title>
<link>http://dx.doi.org/10.1002%2Fibd.20889</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20890">
<title>CD68 expression is markedly different in Crohn&#x27;s disease and the colitis associated with chronic granulomatous disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20890</link>
<description><![CDATA[Background: Chronic granulomatous disease (CGD) is a rare inherited immunodeficiency disorder characterized by inability of phagocytes to kill certain bacteria and fungi. Histology from colon biopsies of CGD patients have shown the presence of inflammation and granulomas, almost indistinguishable from the findings seen in Crohn's disease. We sought to determine if there were any differences in the cell types that comprise the inflammatory infiltrates in inflamed colon specimens between the 2 diseases. The objective was to determine whether the pattern of inflammatory cell composition could be used to distinguish CGD-associated colitis from Crohn's colitis.Methods: Biopsies from 6 patients with Crohn's disease, 6 patients with CGD, and 6 control patients were stained with antibodies to CD3, CD4, CD8, CD68, CD79, CD163, and Foxp3. Positively staining cells per mm2 of lamina propria were calculated for each antibody, with the exception of CD163, in which a percent area of lamina propria stained was calculated.Results: There was a marked difference in the average CD68+ cells per mm2 of lamina propria between the 2 groups (Crohn's: 1104.2 cells/mm2; CGD: 242.3 cells/mm2, P < 0.0004) and a significant difference between the CGD group and control group (Control: 565.4 cells/mm2, CGD: 242.3 cells/mm2, P = 0.0072). There were no significant differences between Crohn's and CGD biopsies in the other cell types.Conclusions: This phenomenon provides physicians with a simple and valuable tool to identify CGD in patients with colonic inflammation.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20886">
<title>More right-sided IBD-associated colorectal cancer in patients with primary sclerosing cholangitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20886</link>
<description><![CDATA[Background: Patients with inflammatory bowel disease (IBD) and concurrent primary sclerosing cholangitis (PSC) have a higher risk of developing colorectal cancer (CRC) than IBD patients without PSC. The aim of this study was to investigate potential clinical differences between patients with CRC in IBD and those with CRC in IBD and PSC, as this may lead to improved knowledge of underlying pathophysiological mechanisms of CRC development.Methods: The retrospective study from 1980-2006 involved 7 Dutch university medical centers. Clinical data were retrieved from cases identified using the national pathology database (PALGA).Results: In total, 27 IBD-CRC patients with PSC (70% male) and 127 IBD-CRC patients without PSC (59% male) were included. CRC-related mortality was not different between groups (30% versus 19%, P = 0.32); however, survival for cases with PSC after diagnosing CRC was lower (5-year survival: 40% versus 75% P = 0.001). Right-sided tumors were more prevalent in the PSC group (67% versus 36%, P = 0.006); adjusted for age, sex, and extent of IBD, this difference remained significant (odds ratio: 4.8, 95% confidence interval [CI] 2.0-11.8). In addition, tumors in individuals with PSC were significantly more advanced.Conclusions: The right colon is the predilection site for development of colonic malignancies in patients with PSC and IBD. When such patients are diagnosed with cancer they tend to have more advanced tumors than patients with IBD without concurrent PSC, and the overall prognosis is worse. Furthermore, the higher frequency of right-sided tumors in patients with PSC suggests a different pathogenesis between patients with PSC and IBD and those with IBD alone.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20887">
<title>Honey, I shrunk the telomere: UC speeds aging</title>
<link>http://dx.doi.org/10.1002%2Fibd.20887</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20866">
<title>Severe Legionella pneumophila pneumonia following infliximab therapy in a patient with Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20866</link>
<description><![CDATA[Background: Immunosuppressive therapy with anti-TNF-[alpha] antibodies is effective in patients with inflammatory bowel disease (IBD). However, there is an increased risk for infections associated with this therapy.Methods: Here, we report the case of a 58-year-old patient with Crohn's disease (CD) treated with steroids and azathioprine who developed severe Legionella pneumophila pneumonia after 3 infusions of infliximab. The patient presented at our IBD department with severe active CD complicated by inflammatory small bowel stenoses and entero-enteral fistulas despite long-term high-dose steroid therapy. To achieve steroid tapering and control of disease activity, immunosuppressive therapy with azathioprine was initiated. Due to persistent symptoms, infusion therapy with the anti-TNF-[alpha] antibody infliximab was started, subsequently leading to significant clinical improvement. However, after the third infliximab infusion the patient was hospitalized with fever, severe fatigue, and syncope.Results: Laboratory findings and chest X-ray revealed left-sided pneumonia; cultural analysis showed L. pneumophila serogroup 1 leading to respiratory insufficiency, which required mechanical ventilation for 2 weeks in the intensive care unit. After discontinuation of all immunosuppressive agents and immediate antibiotic therapy the patient recovered completely.Conclusions: To our knowledge, this is the third case of L. pneumophila pneumonia in an IBD patient treated with infliximab. Similar to other published cases, concomitant treatment of immunosuppressives and anti-TNF agents is a major risk factor for the development of L. pneumophila infection, which should be ruled out in all cases of pneumonia in patients with such a therapeutic regimen. Appropriate prevention strategies should be provided in these patients.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20888">
<title>Big risk, small risk: Small bowel cancer in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20888</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20891">
<title>In flux on infliximab: Conflicting studies on surgical outcomes</title>
<link>http://dx.doi.org/10.1002%2Fibd.20891</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20883">
<title>Patient trust-in-physician and race are predictors of adherence to medical management in inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20883</link>
<description><![CDATA[Background: Adherence plays an important role in the therapeutic effectiveness of medical therapy in inflammatory bowel disease (IBD). We assessed whether trust-in-physician and Black race were predictors of adherence.Methods: We performed a cross-sectional study of Black (n = 120) and White (n = 115) IBD patients recruited from an outpatient IBD clinic. Self-reported adherence to taking medication and keeping appointments, trust-in-physician, and health-related quality of life were measured using the validated instruments, the modified Hill-Bone Compliance Scale (HBCS), the Trust-in-Physician Scale (TIPS), and the Short IBD Questionnaire (SIBDQ), respectively.Results: Overall adherence was 65%. Higher adherence correlated with greater trust-in-physician (r = -0.30; P < 0.0001), increasing age (r = -0.19; P = 0.01), and worsening health-related quality of life (r = -0.18; P = 0.01). Adherence was also higher among White IBD patients compared to Blacks (HBSC: 15.6 versus 14.0, P < 0.0001). Trust-in-physician, race, and age remained predictors of adherence to medical management after adjustment for employment, income, health insurance, marital and socioeconomic status, and immunomodulator therapy. The adjusted odds ratio for adherence in Blacks compared to Whites was 0.29 (95% confidence interval: 0.13-0.64). Every half standard deviation increase in trust-in-physician and every incremental decade in age were associated with 36% and 47% higher likelihood of adherence, respectively.Conclusions: Trust-in-physician is a potentially modifiable predictor of adherence to IBD medical therapy. Black IBD patients exhibited lower adherence compared to their White counterparts. Understanding the mechanisms of these racial differences may lead to better optimization of therapeutic effectiveness.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20869">
<title>Intestinal Beh&#xE7;et&#x27;s disease: Maintenance of remission with adalimumab monotherapy</title>
<link>http://dx.doi.org/10.1002%2Fibd.20869</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20884">
<title>Effects of active and passive smoking on disease course of Crohn&#x27;s disease and ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20884</link>
<description><![CDATA[Background: Smoking is a remarkable risk factor for inflammatory bowel disease (IBD), aggravating Crohn's disease (CD) while having beneficial effects on ulcerative colitis (UC). We studied the effects of active and passive smoking in Dutch IBD patients.Methods: A questionnaire focusing on cigarette smoke exposure was sent to 820 IBD patients. Returned questionnaires were incorporated into a retrospective chart review, containing details about disease behavior and received therapy.Results: In all, 675 IBD patients (380 [56%] CD and 295 [44%] UC) responded. At diagnosis there were 52% smokers in CD, 41% in the general population, and 28% in UC. The number of present smokers in CD is lower than in the general population (26% versus 35%). No detrimental effects of active smoking on CD were observed, but passive smokers needed immunosuppressants and infliximab more frequently than nonpassive smokers. Active smoking had beneficial effects on UC, indicated by reduced rates of colectomy, primary sclerosing cholangitis, and backwash-ileitis in active smokers compared to never smokers, and higher daily cigarette dose correlated with less extensive colitis and a lower need for therapy. Furthermore, smoking cessation after diagnosis was detrimental for UC patients, indicated by increased needs for steroids and hospitalizations for patients that stopped smoking after compared to before the diagnosis.Conclusions: Active smoking is a risk factor for CD, but does not affect the outcome; passive smoking is detrimental for the outcome of CD patients. In UC, active smoking shows dose-dependent beneficial effects. Our data suggest that passive smoking is a novel risk factor for CD.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20882">
<title>Surgical treatment of complex enterocutaneous fistulas in IBD patients using human acellular dermal matrix</title>
<link>http://dx.doi.org/10.1002%2Fibd.20882</link>
<description><![CDATA[Background: Inflammatory bowel disease (IBD) patients represent a high-risk group for enterocutaneous fistula (ECF) formation, related to both their disease process and the need for multiple surgeries. Often the abdominal wall is significantly involved with the ECF and requires partial resection. The use of synthetic prosthetic material to reconstruct the abdominal wall after ECF surgery is associated with increased risk of infection and recurrent fistulas. Herein we report the use human acellular dermal matrix (hADM) in the surgical treatment and reconstruction of the abdominal wall in 11 consecutive IBD patients with complex and medically refractory ECF.Methods: After resection of the involved bowel segment and the overlying abdominal wall, a single sheet of hADM was used to reconstruct the defect. Pre- and perioperative risk factors were reviewed and patients were followed prospectively for a year (360 ± 118 days).Results: Operative mortality was nil. Three patients (27%) developed subcutaneous seroma and there were 2 cases (18%) of superficial wound infection, all of which resolved with conservative management. The mean length of hospital stay was 13.5 (±7.2) days and all patients were tolerating an oral diet at the time of dismissal. There were no recurrences. One patient with Crohn's disease developed a new ECF from a separate bowel site on postoperative day 145, which was treated with the same surgical approach. No further complications have occurred.Conclusions: Our results indicate that in a high-risk IBD patient population with multiple perioperative risk factors the use of hADM during ECF takedown is an effective and well-tolerated treatment option.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20870">
<title>Peripheral neuropathy with infliximab therapy in inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20870</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20874">
<title>Guide to endoscopy of the ileo-anal pouch following restorative proctocolectomy with ileal pouch-anal anastomosis; indications, technique, and management of common findings</title>
<link>http://dx.doi.org/10.1002%2Fibd.20874</link>
<description><![CDATA[Restorative proctocolectomy (RPC) with ileal pouch-anal anastomosis is the surgical procedure of choice for patients with ulcerative colitis (UC). It is also performed in selected patients with familial adenomatous polyposis (FAP). A significant proportion of patients will develop pouch dysfunction. Flexible pouchoscopy is the most important initial investigation in patients with dysfunction. It is also important in UC and FAP surveillance. The aim is to provide gastroenterologists with a clear understanding of the technique, indications, and diagnostic pitfalls when investigating RPC patients with flexible pouchoscopy. Flexible pouchoscopy for the investigation of RPC patients with pouch dysfunction has a high diagnostic yield, with most causes of pouch dysfunction identifiable during this procedure. The risk of developing dysplasia following RPC is low. Surveillance pouchoscopy is only recommended in those with FAP, those with a previous history of dysplasia or carcinoma, primary sclerosing cholangitis, those with a retained rectal cuff, and those with Type C histological changes. Flexible pouchoscopy is a useful first-line investigation in patients with pouch dysfunction. It can be performed without sedation and has a high diagnostic yield; it is also important as part of surveillance in FAP and selected UC patients.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20867">
<title>Appraisal of the pediatric ulcerative colitis activity index (PUCAI)</title>
<link>http://dx.doi.org/10.1002%2Fibd.20867</link>
<description><![CDATA[Background: We evaluated the psychometric performance of the Pediatric Ulcerative Colitis Activity Index (PUCAI) in a real-life cohort from the Pediatric IBD Collaborative Research Group.Methods: Two consecutive visits of 215 children with ulcerative colitis (UC) were included (mean age 11.2 ± 3.6 years; 112 (52%) males; 63 (29%) newly diagnosed and the others after disease duration of 24 ± 15.6 months). Validity was assessed using several constructs of disease activity. Distributional and anchor-based strategies were used to assess the responsiveness of the PUCAI to change over time following treatment.Results: Reflecting feasibility, 97.6% of 770 eligible registry visits had a completed PUCAI score versus only 47.6% for a contemporaneously collected Pediatric Crohn's Disease Activity Index (odds ratio = 45.8, 95% confidence interval [CI] 28.6-73.5) obtained for children with Crohn's disease accessioned into the same database. The PUCAI score was significantly higher in patients requiring escalation of medical therapy (45 points [interquartile range, IQR, 30-60]) versus those who did not, (0 points [IQR 0-10]; P < 0.001), and was highly correlated with physician's global assessment of disease activity (r = 0.9, P < 0.001). The best cutoff to differentiate remission from active disease was 10 points (area under receiver operating characteristic curve [AUC] 0.94; 95% CI 0.90-0.97). Test-retest reliability was excellent (intraclass correlation coefficient = 0.89; 95% CI 0.84-0.92, P < 0.001) as well as responsiveness to change (AUC 0.96 [0.92-0.99]; standardized response mean 2.66).Conclusion: This study on real-life, prospectively obtained data confirms that the PUCAI is highly feasible by virtue of the noninvasiveness, valid, and responsive index. The PUCAI can be used as a primary outcome measure to reflect disease activity in pediatric UC.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20864">
<title>Impact of perceived stigma on inflammatory bowel disease patient outcomes</title>
<link>http://dx.doi.org/10.1002%2Fibd.20864</link>
<description><![CDATA[Background: Perceived stigma has been linked to disease outcome in several chronic illnesses. Stigmatization of illness often leads to increased psychological distress and poorer quality of life. While body stigma has been identified as a specific inflammatory bowel disease (IBD) patient concern, no study to date has systematically investigated the presence of stigma in IBD or its effects on disease course and management.Methods: Participants were recruited online and through the Illinois chapter of the Crohn's & Colitis Foundation of America. A screening measure was used to identify an established IBD diagnosis. Patients completed the Perceived Stigma Scale in IBS, Inflammatory Bowel Disease Questionnaire, Rosenberg Self-Esteem Scale, General Self-Efficacy Scale, the Brief Symptom Inventory, and the Rating Form of IBD Patient Concerns.Results: A total of 211 patients (156 CD, 55 UC) with a confirmed diagnosis for a minimum of 6 months completed the study. Eighty-four percent of participants reported perceived stigma. Hierarchical regression demonstrated that perceived stigma accounted for 10%-22% of the variance in health-related quality of life scores, 4%-16% for psychological distress, 5% for medication adherence, 19% for self-esteem, and 8% for self-efficacy. Effect sizes were small, but comparable with more traditionally evaluated patient variables.Conclusions: The majority of IBD patients report some perceived stigmatization. These results suggest that perceived stigma is a significant predictor of poorer outcomes in patients with IBD when controlling for illness and demographic variables. Perceived stigma is a potentially important psychosocial factor in IBD patient care and warrants further investigation.(Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20861">
<title>Upregulation of T-bet and tight junction molecules by Bifidobactrium longum improves colonic inflammation of ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20861</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20878">
<title>Cervical dysplasia in immunosuppressed IBD women</title>
<link>http://dx.doi.org/10.1002%2Fibd.20878</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20856">
<title>Cholestatic hepatitis, acute acalculous cholecystitis, and hemolytic anemia: primary Epstein-Barr virus infection under azathioprine</title>
<link>http://dx.doi.org/10.1002%2Fibd.20856</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20823">
<title>Epstein-Barr virus-associated lymphoproliferation awareness in hemophagocytic syndrome complicating thiopurine treatment for Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20823</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20840">
<title>Acute hemorrhagic Crohn&#x27;s disease controlled with infliximab</title>
<link>http://dx.doi.org/10.1002%2Fibd.20840</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20836">
<title>Crohn&#x27;s disease and radiation exposure: It&#x27;s time we got our act together?</title>
<link>http://dx.doi.org/10.1002%2Fibd.20836</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20834">
<title>A lump of coal for perianal fistulae?</title>
<link>http://dx.doi.org/10.1002%2Fibd.20834</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20832">
<title>Diffuse colitis cystica profunda in a patient with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20832</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20830">
<title>Fibrosing colonopathy associated with treatment with enteric-coated mesalazine pills</title>
<link>http://dx.doi.org/10.1002%2Fibd.20830</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20841">
<title>Are inflammatory bowel disease (IBD) and pouchitis a reactive enteropathy to group D streptococci (Enterococci)?</title>
<link>http://dx.doi.org/10.1002%2Fibd.20841</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20853">
<title>Successful use of adalimumab in treating cutaneous metastatic Crohn&#x27;s Disease: Report of a Case</title>
<link>http://dx.doi.org/10.1002%2Fibd.20853</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20822">
<title>Endocarditis in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20822</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20802">
<title>Crohn&#x27;s disease, hepatosplenic T-cell lymphoma and no biological therapy: Are we barking up the wrong tree?</title>
<link>http://dx.doi.org/10.1002%2Fibd.20802</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20801">
<title>Bilateral parotidomegaly following anaphylaxis to infliximab</title>
<link>http://dx.doi.org/10.1002%2Fibd.20801</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20791">
<title>Development of de novo celiac disease after restorative proctocolectomy and ileal pouch-anal anastomosism</title>
<link>http://dx.doi.org/10.1002%2Fibd.20791</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20795">
<title>Case of linear IgA bullous dermatosis-involved ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20795</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20789">
<title>Clinical course of late-onset Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20789</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>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20775">
<title>Girls connect: Effects of a support group for teenage girls with inflammatory bowel disease and their mothers</title>
<link>http://dx.doi.org/10.1002%2Fibd.20775</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20773">
<title>Severe case of genital and perianal cutaneous Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20773</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20790">
<title>Association of &#x22;ulcerative appendicitis&#x22; and appendiceal adenocarcinoma</title>
<link>http://dx.doi.org/10.1002%2Fibd.20790</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20796">
<title>Infliximab-induced reactivated Langerhan&#x27;s cell histiocytosis in a patient with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20796</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20784">
<title>Mesenteric ischemia is a cause of resistance to treatment in IBD</title>
<link>http://dx.doi.org/10.1002%2Fibd.20784</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20772">
<title>Preliminary results obtained with cefoperazone plus corticosteroids in the treatment of active Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20772</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20769">
<title>Esophageal ulcer of Crohn&#x27;s disease: Disappearance in 1 week with infliximab</title>
<link>http://dx.doi.org/10.1002%2Fibd.20769</link>
<description><![CDATA[No abstract.]]></description>
</item>

</rdf:RDF>