Certain medications increase risk of inflammatory bowel disease
Medications that target tumour necrosis factor alpha (TNFα), a protein involved in inflammation, have revolutionized the management of certain autoimmune diseases, but paradoxically, these agents might provoke the development of other autoimmune conditions including inflammatory bowel disease. The study has appeared in the Journal Alimentary Pharmacology & Therapeutics.
The researchers conducted the study to examine whether there is an increased risk of developing Crohn's disease (CD) and ulcerative colitis (UC) while under treatment with anti‐TNFα agents for diseases other than inflammatory bowel disease (IBD).
A nationwide cohort study, based on Danish health registries, of all patients who utilised anti‐TNFα agents for non‐IBD indications. Included were patients, who had diseases for which anti‐TNFα agent is indicated (rheumatoid arthritis, psoriasis/psoriatic arthritis, ankylosing spondylitis, others). The observation period for the development of de novo IBD started in 2004. Exposed patients had received at least one dose of anti‐TNFα.
In a study of 17,018 individuals with autoimmune diseases who were treated with anti-TNFα medications--mostly infliximab, etanercept, and adalimumab--and 63,308 individuals who were not, treatment with etanercept, but not other anti? TNFα agents was linked with an elevated risk of developing inflammatory bowel disease: a twofold increased risk of Crohn's disease and a twofold increased risk of ulcerative colitis.
"This study established that there is an increased risk of developing inflammatory bowel disease in individuals taking etanercept. Recognition of this phenomenon is important for clinicians taking care of these patients," said lead author Joshua Korzenik, MD, of Brigham and Women's Hospital, in Boston. "Perhaps more importantly, this study suggests that inflammatory bowel disease may be one of the auto-immune diseases that can be provoked by anti-TNFα agents. This suggests that there may be a common mechanism of immune dysregulation underpinning these diseases."This finding has relevance to clinical care and insights into common mechanisms of the pathophysiology of these diseases.
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