Volume 51, Number 2

Rheumatic Manifestations of Gastrointestinal Diseases

Ibrahim S. Alghafeer, MD
Fellow, Division of Rheumatology 
University of Medicine and Dentistry of New Jersey 
New Brunswick, NJ 

Leonard H. Sigal, MD 
Professor and Chief, Division of Rheumatology 
University of Medicine and Dentistry of New Jersey 
New Brunswick, NJ

Gastrointestinal Pathophysiology
The gut has multiple mechanisms to regulate the efficient absorption of nutrients while excluding bacterial and dietary antigens. Impairment of the gastrointestinal barrier function can be observed in several diseases including inflammatory bowel disease (IBD) and other spondyloarthropathies, and this defect may play a role in the pathogenesis of arthropathies.

Illeocolonoscopy and multiple biopsies were carried out in 96 patients with seronegative spondyloarthropathy, 17 patients with osteoarthritis taking nonsteroidal anti-inflammatory drugs (NSAIDs), and 19 patients with chronic abdominal discomfort. Inflammatory gut lesions were detected in two thirds of the patients with spondyloarthropathy, 12.5% of patients with osteoarthritis, and 16% of patients with abdominal discomfort. More recently, an Italian study confirmed microscopical mucosal inflammation on biopsy in 15 people with psoriatic arthritis but without bowel symptoms, 6 of whom had normal appearing mucosa by colonoscopy (2).

Altered gut permeability may also play a role in the pathogenesis of arthropathies. Permeability may be measured by oral feeding of different tracers (eg, 51Cr-labeled EDTA, lactoglobulin, lactalbumin, polyethylene glycol particles, lactulose, or mannitol) followed by urine analysis of excretion. Increased intestinal permeability was found in all subtypes of juvenile chronic arthritis with correlation between abnormalities in lactulose/mannitol test and the histopathological features of the gut mucosa (3). Another study showed an increase in the 24-hour urine excretion of 51Cr-EDTA in 34 patients with Behcet’s syndrome and 10 patients with ankylosing spondylitis (AS), when compared with 15 healthy controls (4).

Because the results obtained from such studies are entirely dependent on normal gastric emptying, normal renal function, and an accurate urine collection, they should be interpreted carefully. Also, the results may be altered by possible effect of the NSAIDs on prostaglandin synthesis and gut permeability.

Most recently, Salmi et al concluded that different leukocyte populations derived from inflamed gut of patients with IBD bind avidly to synovial vessels using a distinct repertoire of adhesion molecules, suggesting that their recirculation may contribute to the development of reactive arthritis in inflammatory bowel diseases (5). This study is the first experimental support of the homing of lymphocytes from the gut mucosa to joint tissue in enteropathic arthritis.