Strategies targeting tumor necrosis factor in Crohn's disease

Tumor necrosis factor plays an important role in mediating the inflammation of Crohn's disease. Strategies aimed at reducing tumor necrosis factor in patients with Crohn's disease include the mouse/human chimeric monoclonal antibody infliximab, the humanized monoclonal antibody CDP571, the human recombinant tumor necrosis factor receptor fusion protein etanercept, and the small molecule thalidomide. Infliximab is effective for treating active Crohn's disease, maintaining remission, and closing fistulas. Side effects occurring in patients treated with infliximab include human anti-chimeric antibodies, infusion reactions, formation of autoantibodies, and rarely drug induced lupus. CDP571 is effective for treating active Crohn's disease, steroid sparing, and possibly for closing fistulas and maintaining remission. Side effects occurring in patients treated with CDP571 include anti-idiotype antibodies, infusion reactions, and formation of autoantibodies. Pilot studies have suggested that etanercept and thalidomide may also be beneficial. Anti-tumor necrosis factor therapies are effective for the treatment for Crohn's disease.