Myopericarditis and mitral insufficiency associated with ulcerative colitis treated with mesalazine.

To the Editors: Cardiac disease is an infrequent extraintestinal manifestation of inflammatory bowel disease (IBD). When it occurs, the most frequent presentation is acute pericarditis. This situation can arise as a true extraintestinal IBD event or as a secondary effect of the medication employed. We present a case of acute myopericarditis with severe mitral functional insufficiency (a complication not described in the literature) related to ulcerative colitis (UC) and its treatment. A 39-year-old man without prior history of clinical interest, was admitted to hospital with bloody diarrhea during the previous 2 months and abdominal pain. Cardiopulmonary auscultation was normal but with pain in the left lower quadrant abdomen. Among the laboratory data of interest were hemoglobin 13.8 g/dL, iron 15 mg/dL, albumin 2.9 g/L, erythrocyte sedimentation rate 22 mm, fibrinogen 535 g/L, C-reactive protein 113 mg/dL, and a1-acid-glycoprotein 201 mg/dL. Chest and abdomen x-ray was normal as was the electrocardiogram. A colonoscopy was performed, which showed severe ulcerative pancolitis (confirmed subsequently by histology). Treatment was commenced with methylprednisolone (intravenous 1 mg/kg/day), mesalazine (oral, 4 g/day; topical, enema 1 g/12 hours), low-molecular-weight heparin, calcium, vitamin D, and enteral nutrition. Two days later, while previous symptoms continued, the patient developed fever and retrosternal chest pressure worsened on inspiration accompanied by tachycardia. Auscultation suggested a mitral systolic murmur that had not been previously encountered. The C-reactive protein and a1-acid-glycoprotein increased progressively up to 258 and 275 mg/dL, respectively. The measured cardiac enzymes were troponin T 0.12 ng/mL (normal G0.03); creatinine kinase (CK) and CK-MB mass were normal. Chest x-ray showed cardiomegaly and the electrocardiogram showed signs of acute pericarditis. With a probable diagnosis of acute myopericarditis, an echocardiogram was performed that identified a dilation of the left cardiac cavities, with left ventricular function at the lower limit of normality (ejection fraction of 56%), which, with a severe mitral insufficiency of an anatomically normal valve, was interpreted as functional variation resulting from ventricular dilatation. There was no pericardial effusion. A chestYabdomen CT scan was performed and showed a slight enlargement of the sigmoid wall. Other determinations such as blood, urine, and stool cultures, rheumatoid factor, antinuclear and anti-DNA antibodies, complement, and serology for Chlamydia, Mycoplasma pneumoniae, Epstein-Barr virus, and Cytomegalovirus were negative. The suspicion was that the myopericarditis and the acute mitral insufficiency were caused by the treatment, and thus the use of mesalazine was suspended. Treatment with oral corticoids was maintained and enalapril was added. Within 36 hours, a clear improvement in the intestinal symptoms was observed and the chest pain resolved. In the following days the blood analysis, radiographs, and the electrocardiograph alterations returned to normal and the echographic parameters improved significantly. The prednisone dose was reduced progressively and azathioprine treatment was initiated. Two months later the patient was asymptomatic and his last echocardiogram showed a normalization of the cardiac morphology. Cardiac involvement can be associated with IBD, principally with UC, as an extraintestinal occurrence. Cardiac findings include pericarditis (70%), myocarditis (10%), myopericarditis, pericardial and pleural effusion, conduction defects, and cardiac tamponade. The myopericarditis described in some patients with IBD has been attributed to the toxicity of the treatment, for example, in the use of mesalazine, sulfasalazine, and azathioprine. The association between myopericarditis and mesalazine can be produced by immediate hypersensitivity, generally during the first weeks of treatment, but on occasion, following treatment extending over years. To distinguish myopericarditis as a true extraintestinal manifestation of IBD from that of a secondary effect of the treatment is not always easy. In all of the cases identified as being the result of treatment toxicity, there had been, as in the present case, a clear improvement following the suspension of the medication. This suggests an etiopathogenic implication that is little known. The cardiac valve alterations have not been described in the literature (MEDLINE search) nor has their resolution following the discontinuation of the treatment. Although infrequent, the possibility of cardiac involvement needs to be considered in patients with IBD who are being treated with salicylates and who present with chest symptoms. In those cases in which the symptoms can be attributed to the treatment, a favorable clinical evolution is obtained when the drugs are withdrawn; these drugs become contraindicated for future use.