Key result
Mesalazine therapy linked to acute myopericarditis that resolves one month after drug discontinuation.
Why the study?
Mesalazine, a cornerstone therapy for ulcerative colitis, can rarely cause immune-mediated cardiotoxicity such as myopericarditis, which requires prompt diagnosis and management.
Case Report (n=1)
Mesalazine can cause immune-mediated myopericarditis in patients with ulcerative colitis, which resolves upon drug discontinuation and can be effectively diagnosed and monitored using CMR and troponin.
Prompts vigilance for pericarditis in mesalazine-treated colitis patients; extends sparse case reports of 5-ASA cardiotoxicity.
Introduction Mesalazine (5–ASA) is a cornerstone therapy for ulcerative colitis (UC), but rarely can cause immune–mediated cardiotoxicity (myocarditis/pericarditis/myopericarditis), usually within weeks of starting induction. CMR is pivotal to confirm myocardial/pericardial involvement and guide follow–up. Case A 28–year–old man with UC presented with acute pericarditic chest pain (worse supine/deep inspiration, better upright), without syncope, palpitations, or relevant dyspnea. One week earlier, he had been discharged after an intestinal flare and started mesalazine 3 g/day plus systemic steroids (tapering). He also reported a recent febrile rhinitis episode. Initial work–up Hemodynamically stable, afebrile, no heart failure signs. ECG was normal (no ST elevation or PR depression). Labs showed isolated troponin elevation (200 pg/mL) with normal CRP/ESR. Differential included viral myocarditis, extra–intestinal IBD involvement, and 5–ASA adverse reaction. Echo/CMR: Transthoracic echo showed a small pericardial effusion, no tamponade, preserved systolic function. Acute CMR confirmed preserved biventricular function, small effusion, myocardial edema (T2/T2–mapping) and a non–ischemic LGE pattern (subepicardial, inferolateral, non–coronary distribution) with associated pericardial enhancement—consistent with acute myopericarditis. Management and outcome Given the compatible timing, lack of systemic inflammation, negative virology, and imaging findings, mesalazine–related cardiotoxicity was considered highly likely. Mesalazine was permanently discontinued and class avoidance recommended; steroids were continued with a revised taper and an alternative non–5–ASA maintenance strategy planned (immunomodulator/biologic according to phenotype). Symptoms resolved and troponin normalized. Follow–up At 1 month, off mesalazine, the patient was asymptomatic with normal labs; repeat CMR showed regression of myocardial edema and complete resolution of pericarditis signs. Conclusion 5–ASA myopericarditis may present with normal ECG and negative inflammatory markers; troponin and CMR are key for diagnosis and follow–up. In recently treated IBD patients, pericarditic chest pain with troponin rise should promptly raise suspicion of drug–induced cardiotoxicity and trigger early multidisciplinary management.
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Rossi et al. (2026) conducted a case report in Ulcerative colitis and acute myopericarditis (n=1). Mesalazine was evaluated on Myopericarditis. Mesalazine therapy in a 28-year-old man with ulcerative colitis caused acute myopericarditis, which completely resolved one month after drug discontinuation.
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