Rheumatology, a subspecialty of internal medicine, is devoted to the diagnosis and treatment of rheumatic diseases. The term originates from the Greek rheuma, meaning "that which flows as a river or stream" and the suffix -ology, meaning "the study of". Rheumatologists mainly deal with problems involving the muscles and/or joints.

Diseases

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Diseases diagnosed or managed by the rheumatologist include:

• rheumatoid arthritis
• lupus erythematosus
• Sjögren's syndrome
• scleroderma (systemic sclerosis)
• dermatomyositis
• polychondritis
• polymyositis
• polymyalgia rheumatica
• osteoarthritis
• septic arthritis
• gout, pseudogout
• spondyloarthropathies
  • ankylosing spondylitis
  • reactive arthritis (Reiter's syndrome)
  • psoriatic arthropathy
  • enteropathic spondylitis
  • reactive arthropathy
• vasculitis
  • polyarteritis nodosa
  • Henoch-Schönlein purpura
  • serum sickness
  • Wegener's granulomatosis
  • giant cell arteritis
  • temporal arteritis
  • Takayasu's arteritis
  • Behçet's syndrome
  • Kawasaki's disease (mucocutaneous lymph node syndrome)
  • Buerger's disease (thromboangiitis obliterans)

More on [ Rheumatology ]

Permanent Rheumatology Jobs

Southern Academic Pediatric Rheumatology,One of the South’s Top Children’s Hospitals,#5611 :: Mississippi :: Timeline Recruiting
Tue, 09 Feb 2010 09:51:02 -0500
As the only childrens hospital in the state, our more than 100 pediatric medical faculty provide outstanding medical services to millions of patients in our draw area. We are part of the Southeast
Rheumatology Physician Jobs in Eastern North Carolina. :: North Carolina :: MedPro Search - Recruiting For Physician Jobs
Tue, 09 Feb 2010 09:51:02 -0500
Rheumatology Physician Jobs in Eastern North Carolina. Our Rheumatology division has an immediate opening. We currently have three board certified rheumatologists. MRI, CT, nuclear, BMD, x-ray, ultrasound,
Rheumatology Physician Job for Coastal North Carolina :: North Carolina :: MedPro Search - Recruiting For Physician Jobs
Tue, 09 Feb 2010 09:51:02 -0500
Med Pro Search is seeking a Rheumatologist (Rheum) to join a Rheumatology Division with a premier multi-specialty group in Eastern North Carolina. We now have more than 50 providers and our new; state

Arthritis Research & Therapy - Latest Articles

Regulation of microsomal prostaglandin E2 synthase-1 and 5-lipoxygenase-activating protein/5-lipoxygenase by 4-hydroxynonenal in human osteoarthritic chondrocytes
Shu-Huang ChenHassan FahmiQin ShiMohamed Benderdour Tue, 09 Feb 2010 00:00:00 -0000
IntroductionThis study aimed to investigate whether hydroxynonenal (HNE) depletion is responsible for the switch from cyclooxygenase-2 (COX-2) and microsomal prostaglandin E2 synthase-1 (mPGES-1) to 5-lipoxygenase-activating protein (FLAP) and 5-lipoxygenase (5-LOX). Methods: For COX-2 and mPGES-1 studies, human osteoarthritic (OA) chondrocytes were stimulated at different incubation times (up to 24 hours) with a single or repetitive addition of 10 microM HNE to the cultures at 2 hour intervals, up to 14 hours. For 5-LOX and FLAP studies, cells were treated with a single addition of 10 microM HNE for 24 hours, 48 hours, and 72 hours in the presence or absence of naproxen (a nonspecific COX-2 inhibitor) or antibody anti-transforming growth factor-beta 1 (TGF-beta1. The protein levels of COX-2, mPGES-1 and early growth response factor-1 (Egr-1) transcription factor were evaluated by Western blot and that of prostaglandin E2 (PGE2), leukotriene B4 (LTB4) and TGF-beta1were determined with commercial kits. The levels of mPGES-1, FLAP and 5-LOX mRNA were measured by real-time RT-PCR. Transient transfection was performed to determine promoter activities of mPGES-1 and 5-LOX. Results: Single addition of 10 microM HNE to cultured chondrocytes induced PGE2 release as well as COX-2 and mPGES-1 expression at the protein and mRNA levels, with a plateau reached respectively at 8 and 16 hours of incubation, followed by a subsequent decline. However, repeated treatments with HNE prevented the decline of COX-2 and mPGES-1 expression that occurred with a single aldehyde addition. HNE induced mPGES-1 promoter activity, possibly through transcription factor Egr-1 activation. After 48 hours, when COX-2 expression decreased, LTB4 level rose through 5-LOX and FLAP up-regulation. The addition of naproxen to cultured chondrocytes revealed that FLAP and 5-LOX regulation by HNE required PGE2 production. Furthermore, our data showed that HNE significantly induced TGF-beta1 production. The addition of anti-TGF-beta1 antibody reduced HNE-induced 5-LOX and FLAP expression by 40%, indicating the partial involvement of a TGF-beta1-dependent mechanism. Conclusions: Our data demonstrate that the shunt to the FLAP and 5-LOX pathway in HNE-induced human OA chondrocytes is attributed to COX-2 and mPGES-1 inhibition, probably due to HNE depletion. PGE2 and TGF-beta1 are suggested to be involved in this regulation.
Local leptin production in osteoarthritis subchondral osteoblasts may be responsible for their abnormal phenotypic expression
Marie-Solange MutabarukaMohamed Aoulad AissaAline DelalandreMartin LavigneDaniel Lajeunesse Mon, 08 Feb 2010 00:00:00 -0000
IntroductionLeptin is a peptide hormone with a role in bone metabolism and rheumatic diseases. The subchondral bone tissue plays a prominent role in the pathophysiology of osteoarthritis (OA), related to abnormal osteoblast (Ob) differentiation. Although leptin promotes the differentiation of Ob under normal condition, a role for leptin in OA Ob has not been demonstrated. Here we determined if endogenous leptin produced by OA Ob could be responsible for the expression of the abnormal phenotypic biomarkers observed in OA Ob. Methods: We prepared primary normal and OA Ob from subchondral bone of tibial plateaus removed for knee surgery of OA patients or at autopsy. We determined the production of leptin and of the long, biologically active, leptin receptors (OB-Rb) using RT-PCR, ELISA and Western blot analysis. We determined the effect of leptin on cell proliferation by BrdU incorporation and MTT assays, and we determined by Western blot analysis phospho 42/44 MAPK (p42/44 Erk1/2) and phospho p38 levels. We then determined the effect of the addition of exogenous leptin, leptin receptor antagonists, inhibitors of leptin signaling or siRNA techniques on the phenotypic features of OA Ob. Phenotypic features of Ob were determined by measuring alkaline phosphatase activity (ALP), osteocalcin release (OC), collagen type 1 production (CICP) and of Transforming growth factor-beta1 (TGF-beta1). Results: Leptin expression was increased ~5-fold and protein levels ~2-fold in OA Ob compared to normal. Leptin stimulated its own expression and the expression of OB-Rb in OA Ob. Leptin dose-dependently stimulated cell proliferation of OA Ob and also increased phosphorylated p42/44 Erk1/2 and p38 levels. Inactivating antibodies against leptin reduced ALP, OC, CICP and TGF-beta1 levels in OA Ob. Tyrphostin (AG490) and piceatannol (Pce), inhibitors of leptin signaling, reproduced this effect. Inhibition of endogenous leptin levels using siRNA for leptin or inhibiting leptin signaling using siRNA for OB-Rb expression both reduced ALP and OC about 60%. Exogenous leptin addition stimulated ALP, yet this failed to further increase OC or CICP. Conclusions: These results suggest that abnormal production of leptin by OA Ob could be responsible, in part, for the elevated levels of ALP, OC, collagen type 1 and TGF-beta1 observed in these cells compared to normal. Leptin also stimulated cell proliferation, and Erk 1/2 and p38 signaling. Taken together, these data suggest leptin could contribute to abnormal osteoblast function in OA.
Is Phytalgic(R) a goldmine for osteoarthritis patients or is there something fishy about this nutraceutical? A summary of findings and risk of bias assessment
Robin ChristensenHenning Bliddal Mon, 08 Feb 2010 00:00:00 -0000
A food supplement containing fish oils, urtica dioica, Zinc, and Vitamin E (Phytalgic(R)) for osteoarthritis (OA) has now been tested in a placebo-controlled trial for three months and according to the authors has a very large clinical effect, considerably larger than any other known product. Even experts endorsing nutraceuticals for OA symptoms would probably agree that a nutraceutical with an effect size above .5 is rarely seen. Despite our concern about the trial registration taking place after the study was completed, and the likelihood that patients would note the taste of fish, thus leading to detection bias, we consider these data promising although with a high risk of bias.
Autophagy induction and CHOP under-expression promotes survival of fibroblasts from rheumatoid arthritis patients under endoplasmic reticulum stress
Yong-Joo ShinSong-Hee HanDo-Sung KimGeum-Hwa LeeWan-Hee YooYong-Mo KangJe-Yong ChoiYong Chul LeeSeong Ju ParkSeul-Ki JeongHyung-Tae KimSoo-Wan ChaeHyun-Ja JeongHyung-Ryong KimHan-Jung Chae Mon, 01 Feb 2010 00:00:00 -0000
IntroductionSynovial fibroblasts from rheumatoid arthritis show resistance to apoptotic stimuli, indicating they may be difficult to treat. To clearly understand these mechanisms of resistance, rheumatoid and osteoarthritis synovial fibroblasts (RASF and OASF) were exposed to endoplasmic reticulum (ER) stress such as thapsigargin, Ca2+-ATPase inhibitor. Methods: Fibroblasts were assessed microscopically for cell viability by trypan blue exclusion and for autophagic cells by LC-3II formation. Caspase-3 activity was measured as aminomethyl-coumarin (AMC) liberated from AC-DEVD-AMC. Immunoblotting was performed to compare protein expression in OASF and RASF. Results: ER stress caused cell death in OASF but not in RASF. Thapsigargin, a Ca2+-ATPase inhibitor, did not change the expression of GRP78, an ER chaperone in OASF and RASF, but induced another ER stress protein, CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP) differently, showing high levels in OASF and low levels in RASF. Thapsigargin increased the autophagy response in RASF, with autophagosome formation, beclin expression, and LC3-II conversion. Transfection with beclin siRNA inhibited autophagy and increased the susceptibility to ER stress-induced cell death. On the other hand, CHOP siRNA increased autophagy and improved cell survival, especially in RASF, indicating that CHOP is involved in regulation of autophagy and cell death, but that low expression of CHOP protects RASF from apoptosis. Conclusions: Autophagy induction and CHOP under-expression increases cell resistance against ER stress-induced cell death in fibroblasts from rheumatoid arthritis patients.
From the item to the outcome: the promising prospects of PROMIS
Daniel Aletaha Mon, 01 Feb 2010 00:00:00 -0000
Evaluation of patient reported outcomes, and in particular physical function, have gained increasing importance in research and therapy of patients with rheumatic diseases. Most instruments that are used for that purpose are rigid and suffer from floor and ceiling effects when used in patients whose physical function differs from the average. A new approach to the assessment of physical function uses computerised adaptive testing, by which precision and reliability of the measurement can be achieved for most patients, while even requiring less time for the assessment. Well calibrated and tested item and large item data banks are a prerequisite for this purpose, a process that is summarised in the present report by Bruce and colleagues.
A role for age-related changes in TGF-beta signalling in aberrant chondrocyte differentiation and osteoarthritis.
Peter van der KraanEsmeralda Blaney DavidsonWim van den Berg Fri, 29 Jan 2010 00:00:00 -0000
Transforming growth factor beta (TGFβ) is a growth factor with many faces. In our osteoarthritis (OA) research we have found that TGFβ can be protective as well as deleterious for articular cartilage. We postulate that the dual effects of TGFβ on chondrocytes can be explained by the fact that TGFβ can signal via different receptors and related Smad signaling routes. On chondrocytes, TGFβ not only signals via the canonical type I receptor ALK5 but also via the ALK1 receptor. Notably, signaling via ALK5 (Smad2/3 route) results in markedly different chondrocyte responses than ALK1 signaling (Smad1/5/8), and we postulate that the balance between ALK5 and ALK1 expression on chondrocytes will determine the overall effect of TGFβ on these cells. Importantly, signaling via ALK1, but not ALK5, stimulates MMP-13 expression by chondrocytes. In cartilage of ageing mice and in experimental OA models we have found that the ALK1/ALK5 ratio is significantly increased, favoring TGFβ signaling via the Smad1/5/8 route, changes in chondrocyte differentiation and MMP-13 expression. Moreover, human OA cartilage showed a significant correlation between ALK1 and MMP-13 expression. In this paper we summarize concepts in OA, its link with ageing and disturbed growth factor responses, and a potential role of TGFβ signaling in OA development.

Annals of the Rheumatic Diseases current issue

Rheumatoid arthritis and pregnancy; not only for rheumatologists interested in female health issues
Dolhain, R. J E M
Anti-endothelial cell antibodies in systemic sclerosis
Mihai, C, Tervaert, J W C Anti-endothelial cell antibodies (AECA) are a heterogeneous class of antibodies whose role in the pathogenesis of autoimmune diseases with vascular involvement has been extensively studied. Systemic sclerosis (SSc) is one of the systemic autoimmune diseases in which endothelial dysfunction is well defined and important in the development of the disease. AECA are present in the serum samples of many patients with SSc. Depending on the detection method and on patient selection, 22–86% of patients test positive for AECA. Among the demonstrated clinical associations, lung and peripheral vascular involvement are the most common. In this paper, the methods of detection, various molecular specificities and the possible pathogenic mechanisms of AECA in SSc are reviewed.
EULAR evidence-based recommendations for cardiovascular risk management in patients with rheumatoid arthritis and other forms of inflammatory arthritis
Peters, M J L, Symmons, D P M, McCarey, D, Dijkmans, B A C, Nicola, P, Kvien, T K, McInnes, I B, Haentzschel, H, Gonzalez-Gay, M A, Provan, S, Semb, A, Sidiropoulos, P, Kitas, G, Smulders, Y M, Soubrier, M, Szekanecz, Z, Sattar, N, Nurmohamed, M T Objectives: To develop evidence-based EULAR recommendations for cardiovascular (CV) risk management in patients with rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA). Methods: A multidisciplinary expert committee was convened as a task force of the EULAR Standing Committee for Clinical Affairs (ESCCA), comprising 18 members including rheumatologists, cardiologists, internists and epidemiologists, representing nine European countries. Problem areas and related keywords for systematic literature research were identified. A systematic literature research was performed using MedLine, Embase and the Cochrane library through to May 2008. Based on this literature review and in accordance with the EULAR’s "standardised operating procedures", the multidisciplinary steering committee formulated evidence-based and expert opinion-based recommendations for CV risk screening and management in patients with inflammatory arthritis. Results: Annual CV risk assessment using national guidelines is recommended for all patients with RA and should be considered for all patients with AS and PsA. Any CV risk factors identified should be managed according to local guidelines. If no local guidelines are available, CV risk management should be carried out according to the SCORE function. In addition to appropriate CV risk management, aggressive suppression of the inflammatory process is recommended to further lower the CV risk. Conclusions: Ten recommendations were made for CV risk management in patients with RA, AS and PsA. The strength of the recommendations differed between RA on the one hand, and AS and PsA, on the other, as evidence for an increased CV risk is most compelling for RA.
Postpartum onset of rheumatoid arthritis and other chronic arthritides: results from a patient register linked to a medical birth registry
Wallenius, M, Skomsvoll, J F, Irgens, L M, Salvesen, K A, Koldingsnes, W, Mikkelsen, K, Kaufmann, C, Kvien, T K Background: It is known that onset of rheumatoid arthritis (RA) is increased post partum. Objective: To compare incidence rates between RA and other chronic arthritides (OCA) 0–24 months after delivery, and to compare the incidence rates within each group 0–24 versus 25–48 months post partum. Methods: Premenopausal women from a Norwegian patient register were linked with the Medical Birth Registry of Norway to study the interval between delivery and time of diagnosis. Cox regression analysis with adjustments for age at delivery and birth order was applied to compare proportions of incident cases of RA and OCA with onset 0–24 months post partum. Poisson regression analysis with adjustment for the population at risk was applied to estimate the incidence rate ratio (IRR) 0–24 versus 25–48 months post partum. Results: Of 183 RA and 110 patients with OCA diagnosed after delivery, 69 (37.7%) had RA and 31 (28.2%) OCA during the first 24 months post partum (p = 0.09). The IRR (95% CI) for diagnosis during 0–24 months versus 25–48 months was 1.73 (1.11 to 2.70) (p = 0.01) for RA, 1.05 (0.59 to 1.84) (p = 0.86) for OCA. The IRR was 2.23 (1.06 to 4.70) and 1.87 (0.67 to 5.21), respectively, when only considering diagnoses after the first pregnancy. Clinical characteristics were similar within each diagnostic group. Conclusion: The proportions of incident cases with onset 0–24 months after delivery were not different between RA and OCA. A peak in incidence during 0–24 months was seen in the RA group, both when considering all pregnancies and only the first pregnancy.
Correction

Does anti-mutated citrullinated vimentin have additional value as a serological marker in the diagnostic and prognostic investigation of patients with rheumatoid arthritis? A systematic review
Luime, J J, Colin, E M, Hazes, J M W, Lubberts, E Objective: To review the diagnostic and prognostic value of anti-mutated citrullinated vimentin (MCV) in rheumatoid arthritis, taking into account the already available serology. Methods: Medline was searched via PubMed (1966 to May 2008) for anti-MCV and related terms, arthritis and arthropathies. Studies with anti-MCV, arthritis/arthropathy, and primary data on diagnosis and/or prognosis were included. Their methodological quality was assessed using the Quality Assessment of Diagnostic Accuracy Studies (QUADAS) instrument for diagnostic studies and the modified Hayden list for prognostic studies. Results: Of 14 eligible studies, 11 included diagnostic data and 3 included prognostic data. No study evaluated anti-MCV as an added diagnostic test to the already available anti-cyclic citrullinated peptide (CCP) and rheumatoid factor serology. One study included the optimal patient spectrum resulting in a sensitivity of 0.59 and specificity of 0.98. A total of 10 diagnostic case-control studies using the same anti-MCV kit showed a sensitivity of 0.64–0.84 and a specificity of 0.79–0.96. This almost equalled the performance of anti-CCP in the same studies. The prognostic evaluation of anti-MCV was limited by differences in study methodology, outcome and statistical modelling. Individual studies showed moderate associations for anti-MCV and radiological progression with the strength of the association comparable to that of anti-CCP. Conclusions: Study heterogeneity, choice of study population and methodological limitations limited overall conclusions about the true diagnostic and prognostic test performance of anti-MCV. Evidence from the diagnostic case-control studies suggests that anti-MCV may be used as an alternative for anti-CCP.

Arthritis Care & Research

The child, grown, becomes independent
Patricia P. Katz, Edward H. Yelin, Michael D. Lockshin Mon, 30 Nov 2009 12:54:00 -0000
No abstract.
Getting them even earlier: Identifying individuals before clinical presentation with rheumatoid arthritis
Katherine P. Liao, Karen H. Costenbader Mon, 30 Nov 2009 12:54:00 -0000
No abstract.
Each measure of patient-reported change provides useful information and is susceptible to bias: The need to combine methods to assess their relative validity
Pythia T. Nieuwkerk, Mirjam A. G. Sprangers Mon, 30 Nov 2009 12:54:00 -0000
No abstract.

Arthritis & Rheumatism

In this issue
Thu, 28 Jan 2010 12:43:00 -0000
No abstract.
Shaping our own future
Sherine E. Gabriel Thu, 07 Jan 2010 12:22:00 -0000

Lawrence E. Shulman, MD, PhD, 1919-2009
Bevra H. Hahn, Michael D. Lockshin Thu, 07 Jan 2010 12:22:00 -0000
No abstract.

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