Abstract

Mesalamine (5-aminosalycilic acid) is a first line anti-inflammatory agent used for treatment of inflammatory bowel disease. Mesalamine is thought to reduce colonic inflammation by inhibiting the cyclooxygenase pathway and the γ-form of peroxisomal proliferator-activated receptors (PPAR-γ) signaling pathway. A 30-year-old male with a medical history significant for ulcerative colitis diagnosed 1 year prior, presented with chest pain, fever, chills, and generalized weakness. His symptoms began spontaneously six hours prior to coming to the Emergency room. The patient described a localized chest pain to his mid-sternum, that was sharp, non-radiating, and unalleviated by over-the-counter analgesics. He denied pleurisy, shortness of breath, diaphoresis, palpitations. His chest pain resolved after aspirin 325 mg and 0.5 inch topical nitroglycerin at the emergency department. The patient gave a history of starting budesonide 9 mg QD and an increase in his mesalamine dose from 800 mg to 1600 mg TID, 6 weeks prior. These medication regimen change occurred after an ulcerative colitis flair which developed after the patient had stopped taking his mesalamine for 2 weeks. His initial electrocardiogram showed normal variant study. Chest xray was negative. The case was discussed with his primary gastroenterologist and on-call cardiologist. Considering the strong association of the patients' recent symptoms with increase in his mesalamine dose, only budesonide was continued at admission. Subsequently, TEE showed grade II left ventricular dysfunction and left ventricular ejection fraction of 61 %. After thorough clinical evaluation, the patient was diagnosed with mesalamine-induced-myocarditis, and cardiac catherization was deferred, with recommendations for supportive care. Mesalamine induced-myocarditis is rare. The exact mechanism of which is unclear, but is thought to be secondary to a hypersensitivity reaction rather than direct myocardiotoxicity. This ideology of hypersensitivity myocarditis is supported by cases of acute recurrence of pleuropericarditis with re-exposure to mesalamine. Mesalamine-induced myocarditis has been associated with chronic use, often more than not with a recent increase in dosage in patients who are also concomitantly taking steroids as exemplified in our case. We hope that this report will further increase the awareness of prescribers to myocarditis caused by an increased dosage of mesalamine and with its chronic use.

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