Outcome assessments in rheumatoid arthritis.

Increasing evidence suggests low disease activity or remission is achievable in rheumatoid arthritis (RA). Using a treat to target strategy (T2T) has been shown to achieve these targets of remission or low disease activity in RA. In order to successfully treat to target, rheumatologists need reliable measures of disease activity to switch and/or escalate therapy to achieve or maintain therapeutic targets. Multiple disease-activity measures have been developed for both research and clinical practice. For clinical practice, the American College of Rheumatology (ACR) has recommended the PAS, PAS II, RAPID 3, CDAI, DAS 28, and SDAI for measuring disease activity in rheumatoid arthritis. Each of these measures has strengths and limitations, but they all accurately reflect disease activity, discriminate well between disease states, and are feasible to perform in the clinical setting. Implementation in the clinical setting can be optimized through leveraging technology and systems redesign. Tools such as web-based and smartphone applications have been developed to increase the ease with which these measures can be deployed. Disease-activity measurement in rheumatoid arthritis is included in the rheumatoid arthritis quality measures group in the Centers for Medicare and Medicaid Services' incentive-based Physician Quality Reporting System.

Tumor necrosis factor-alpha inhibitor associated ulcerative colitis.

BACKGROUND: Flares or onset of inflammatory bowel disease in association with immunosuppression has been reported in the literature. METHODS: We studied 4 cases of patients with rheumatic disease who developed or had a flare of ulcerative colitis either after initiation of or while taking a tumor necrosis factor-alpha inhibitor. RESULTS: We identified 4 patients, three male and one female. Two of the male patients had a seronegative spondyloarthropathy and one had rheumatoid arthritis. The female patient had amyopathic dermatomyositis. Two of the 4 patients had ulcerative colitis prior to tumor necrosis factor-alpha treatment. Both of these patients had quiescent ulcerative colitis that flared after they began taking etanercept. Two patients developed de novo ulcerative colitis while taking a tumor necrosis factor-alpha inhibitor. CONCLUSIONS: The data presented in these 4 cases supports a temporal relationship between initiating a tumor necrosis factor-alpha inhibitor and onset or flare of ulcerative colitis. These observations raise the possibility that tumor necrosis factor-alpha inhibitor therapy, which has been used as treatment for inflammatory bowel disease, may rarely be a factor in the development of disease.