Tumor necrosis factor-α (TNF-α) is an inflammatory cytokine that plays a major role during the initiation and perpetuation of inflammatory bowel disease (IBD). Anti-TNF-α agents are the most widely used biologics that specifically target either or both circulating and membrane-bound TNF-α, thus preventing its pro-inflammatory activity. Despite their efficacy, one third of the patients receiving anti-TNF-α agents are primary non-responders and nearly half of the patients that initially respond may subsequently lose response (secondary loss of response). Many of these cases can be explained by immunogenicity, which can lead to lower drug levels associated with reduced response and serious adverse effects that cause patients to withdraw from treatment. New treatment algorithms instruct practitioners to check drug and antibody levels when there is loss of response, and then provide guidance towards either dose optimization and/or change in the biologic agent or class to help regain efficacy.
Keywords: Anti-drug antibody; Crohn’s disease; Immunosuppression; Tumor necrosis factor; Ulcerative colitis.