Tumor necrosis factor (TNF)-α is a cytokine that plays a well-established, key role as a central mediator of inflammation and immune regulation. TNF-α and its receptors are suggested to play a critical role in a number of chronic inflammatory diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis (AS), juvenile chronic arthritis, and inflammatory bowel disease (IBD). TNF-α inhibitors are currently used in the treatment of these diseases. We report a 29-year-old male with AS who developed Crohn's disease while taking etanercept. Etanercept treatment was interrupted and a switch to a monoclonal antibody-based anti-TNF treatment using adalimumab was started, which induced a prompt improvement of the gastrointestinal symptoms. We indicate the immunodysregulatory and proinflammatory effects of etanercept and discuss the potential pathogenic mechanisms of the paradoxical effect of TNF-α inhibitors. We also review the related literature on new-onset IBD following anti-TNF treatment for AS.
Keywords: Ankylosing spondylitis; Crohn’s disease; Etanercept; Mechanism of action; Tumor necrosis factor-alpha inhibitors.