Inflammatory bowel disease (IBD)
Crohn’s disease and ulcerative colitis (UC) are associated with a number of extra-intestinal inflammatory conditions. Arthritis, the most common of these manifestations, occurs more commonly in patients with large bowel inflammation.
The arthritis may develop prior to, during, or after the onset of bowel inflammation. Generally the arthritis will parallel bowel disease activity. IBD-associated arthritis may either affect the spine or peripheral joints. When affecting the spine it is often associated with the HLA-B27 genetic marker. This is termed spondylitis or sacroiliitis and occurs in only 2-7% of IBD patients.
There are two general classifications for IBD-associated peripheral arthritis. Type 1 is typically self-limited, and develops fewer than 5 joints, and parallels bowel disease activity. Whereas type 2 often involves more than 5 joints and does not follow the course of bowel inflammation
There may be a genetic or immunologic predisposition to development type 1 or 2 arthritis, however more research on this matter is necessary.
Management of IBD-associated arthritisrelies on control of the underlying inflammatory bowel disease. Medications that modify the immune system, wuch as sulfasalazine, azathioprine, glucocorticoids, and methotrexate are widely used. More recently, tumor necrosis factor-alpha blocking agents (Infliximab – Remicade, Humira – Adalimumab, and Enbrel – Etanercept) have been approved for the treatment of IBD, which has similarly resulted in a significant improvement of axial and peripheral arthritis symptoms.
Other IBD-associated concerns
Low bone mineral density is a recognized complication of IBD. Risk factors for the development of osteopenia or osteoporosis were identified as advanced age, cumulative glucocorticoid doses, prior use of 6-mercaptopurine, increased erythrocyte sedimentation rate, and low osteocalcin level. Patients with IBD should be advised to consume adequate calcium and vitamin D and to participate in a regular weight-bearing exercise program. Therapy with bisphosphonates may also be necessary.
Prevention of decreased bone mineral density includes regular monitoring with bone densitometry. This will identify those in need of treatment and to monitor the effect of treatment designed to prevent bone loss. The dose of glucocorticoids should be kept to a minimum.
Volume 51, Number 2
Rheumatic Manifestations of Gastrointestinal Diseases
Written by: Ibrahim S. Alghafeer, MD and Leonard H. Sigal, MD