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Clinical manifestations and diagnosis of arthritis associated with inflammatory bowel disease and other gastrointestinal diseases

Author
Robert D Inman, MD, FRCPC, FACP, FRCP Edin
Section Editor
Joachim Sieper, MD
Deputy Editor
Paul L Romain, MD

INTRODUCTION

Arthritis is a recognized extraintestinal manifestation of several illnesses and conditions, including inflammatory bowel disease (IBD), bacterial infections of the gut, gluten-sensitive enteropathy (celiac disease), various parasitic infections, pseudomembranous colitis, and Whipple’s disease, as well as following intestinal bypass surgery. Other illnesses also have a propensity for causing inflammation of joints and the gut.

The clinical manifestations, and diagnosis of arthritis associated with IBD are presented here. Other disorders associated with both gastrointestinal disease and joint involvement are discussed here briefly, particularly in the context of the differential diagnosis of patients with these symptoms and findings. The treatment of IBD-associated arthritis; and the pathogenesis, other clinical manifestations, diagnosis, and management of inflammatory bowel disease, including Crohn disease and ulcerative colitis, are reviewed in detail separately. (See "Treatment of arthritis associated with inflammatory bowel disease" and "Immune and microbial mechanisms in the pathogenesis of inflammatory bowel disease" and "Clinical manifestations, diagnosis and prognosis of Crohn disease in adults" and "Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults" and "Management of severe ulcerative colitis in adults" and "Overview of the medical management of mild to moderate Crohn disease in adults".)

PATHOGENESIS

There are several mechanisms which may underlie concurrent inflammation in the gut and the joint, but the precise pathogenic pathways remain to be defined. A disturbance of the gut barrier is postulated as the first and primary process for most of these proposed mechanisms. An alternative suggestion is that shared genetic or environmental factors predispose individuals to various organ manifestations of these inflammatory conditions, such as gut or joint involvement [1]. In addition, there may be a role for translocation of pathogens, as occurs in parasitic rheumatism, in which case effective antihelminthic treatment resolves the arthritis. There may also be circulating microbial elements, as proposed for post-Yersinia reactive arthritis, in which case the pathogen cannot be cultured from the synovial fluid.

Both human leukocyte antigen (HLA) and non-HLA genes have been associated with different articular phenotypes, with an increase in HLA-B27 in patients with spondylitis/sacroiliitis (see 'Laboratory findings' below). Molecular mimicry, in which an immune response to a gut-derived antigen cross-reacts with normal host protein, has been invoked to explain the role of human leukocyte antigen (HLA)-B27 in post-dysenteric reactive arthritis, but this mechanism has proved difficult to confirm definitively in either the clinical setting or in experimental models of colitis. Circulating immune complexes, initiated by an immune response to gut microbes, have been implicated in the arthritis following intestinal bypass surgery.

The concept of distinctive trafficking of gut-derived immunocompetent cells has been supported by studies of the integrins which direct the homing patterns of circulating lymphocytes. Cells such as mucosa-associated invariant T cells (MAITS) can be recovered from the synovial fluid of patients with ankylosing spondylitis [2]. Integrins, such as alpha4-beta7 integrin, are thought to have a role in mediating trafficking of lymphocytes to gut and joint tissues.

                       
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Literature review current through: Sep 2017. | This topic last updated: Mar 10, 2017.
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