COMMENTARY

Colitis and Arthritis: What's the Connection?

Stephen Paget, MD

Disclosures

July 08, 2013

In This Article

Shared Immunology and Genetics of IBD and Spondyloarthropathies

IBD and SpA: Shared Pathogenetic Mechanisms

Although at first glance, the overlap between arthritis and SpA might seem to reflect the coexistence of 2 common disorders, the fact is that they share many pathogenetic mechanisms: genetic susceptibility to abnormal antigen presentation, aberrant recognition of self, autoantibodies against specific antigens shared by the colon and other extracolonic tissues, increased intestinal permeability, and an infectious trigger.

The immunologic alterations shared by patients with IBD and SpA (as well as other conditions) include:

E-cadherin expressed highly in gut of patients with IBD and SpA;

Th1, Th17, and Treg cells active in the intestinal mucosa of patients with IBD and synovial fluid of those with ankylosing spondylitis and SpA;

Tumor necrosis factor (TNF) alpha is a dominant cytokine in IBD and SpA;

Interaction of antigen-presenting cells with microorganisms;

Toll-like receptors TLR-2 and TLR-4; and

HLA-B27+ and IgA anti-saccharomyces cerevisiae antibodies in CD.

In addition, HLA-B27 transgenic rats develop IBD, psoriasis, enthesitis (inflammation at the sites where tendons or ligaments attach to bone), synovitis, and epididymitis.

The Connection of Arthritis With Other Types of IBD

The bowel is one of the largest immune organs in the body; therefore, it is not unexpected that various type of bowel inflammation can lead to arthritis. This includes 10% of patients with celiac disease whose peripheral and spine arthritis responds to a gluten-free diet; Whipple disease, in which peripheral and axial (spine) arthritis improve with antibiotics; Behçet disease colitis that is controlled with immunosuppressive drugs; intestinal bypass arthritis that is cured with bowel reconnection; arthritis associated with parasitic disease, such as Strongyloides stercoralis that responds to antimicrobials; and reactive arthritis caused by Clostridium difficile that is cleared by antibiotics.

Modern Treatment Concepts and Options

Thankfully, our knowledge of the genetics and immunology of UC and CD, as well as spondyloarthritides, has expanded in an extraordinary way, and from that, sophisticated biologic drugs have been developed that have transformed the lives of patients with both disorders. In summary, the general treatment concepts are as follow:

Treating the underlying disease helps the arthritis but not necessarily the uveitis, pyoderma gangrenosum, and spondylitis.

Nonsteroidal anti-inflammatory drugs can exacerbate colitis.

Methotrexate, sulfasalazine, and 5´-acetylsalicylic acid drugs can help to control colitis but probably will not help spondylitis.

Anti-TNF medications -- primarily the monoclonal antibodies, such as infliximab, certolizumab, and golimumab -- can profoundly control both the colitis and the spondylitis.

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