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The reference standard for diagnosis is the myocardial biopsy, rarely performed. Usually the diagnosis is based on symptomatology, physical examination, laboratory tests, electrocardiogram and imaging techniques, particularly cardiac magnetic resonance (CMR). Symptoms can range from chest pain to frank heart failure. Most cases of myocarditis are resolved without sequelae. Although the etiology is often unknown, a variety of infectious agents, toxic agents, systemic diseases, and drugs can cause this clinical entity.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">1</span></a> Mesalazine, first-line drug in the treatment of different forms of inflammatory bowel disease, has been linked to causing myocarditis by a hypersensitivity mechanism, although this finding has been rarely published in the medical literature.</p><p id="par0010" class="elsevierStylePara elsevierViewall">We report the case of a 22-year-old patient with no history of drug allergies, cardiovascular risk factors or toxic habits. Two weeks before admission to our hospital, the patient was diagnosed with Crohn's disease (CD) and began treatment with mesalazine 1<span class="elsevierStyleHsp" style=""></span>g every 12<span class="elsevierStyleHsp" style=""></span>h and budesonide 3<span class="elsevierStyleHsp" style=""></span>mg daily. The patient reports a 4-day symptomatology of left chest pain unrelated to exercise, predominantly at night and it increases with coughing, in supine position and with inhaling. No remarkable signs were found on physical examination. The ECG showed a decreased and prolonged PR interval (240<span class="elsevierStyleHsp" style=""></span>ms) and an incomplete right bundle branch block. The chest X-ray was normal. Laboratory tests revealed increased cardiac enzymes (peak troponin 1 was 11.3<span class="elsevierStyleHsp" style=""></span>ng/ml, with normal value below 0.04<span class="elsevierStyleHsp" style=""></span>ng/ml). The transthoracic echocardiogram showed a left ventricle with normal dimensions and function, with 70% ejection fraction. No valvular abnormalities or pericardial effusion. The patient was admitted to the Cardiology Unit with the presumptive diagnosis of acute myocarditis. Serology was performed for hepatitis viruses A, B and C, HIV, <span class="elsevierStyleItalic">Borrelia burgdorferi</span>, Epstein–Barr virus, cytomegalovirus, <span class="elsevierStyleItalic">Brucella</span>, parvovirus B19, adenovirus, Coxsackie B and herpes 1 and 2, with an autoimmune panel and Mantoux test. All the results were negative. CMR was performed two weeks after the onset of symptoms, which showed several sources of epicardial late gadolinium enhancement (LGE) on the side wall of the left ventricle. Given the possibility of mesalazine-induced toxicity as a cause of myocarditis in this patient, the drug was discontinued. The symptoms disappeared within 48<span class="elsevierStyleHsp" style=""></span>h with symptomatic treatment with NSAIDs. Mesalazine discontinuation did not lead to an outbreak of CD. Therefore it was discontinued permanently due to the risk of relapse. The patient is asymptomatic and without recurrence one year after discharge.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Mesalazine is considered a first-line drug in the treatment of inflammatory bowel disease and therefore is widely used in this patient population. Like all drugs, mesalazine has side effects, myocarditis being very rare. Regarding the etiological possibility of such a reaction and applying the Naranjo causality scale,<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">2</span></a> we obtained a score that qualifies myocarditis as probably mesalazine-induced in this patient. We have analyzed 7 cases published in the medical literature of mesalazine-induced myocarditis.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">3–9</span></a> Five of them were male. Age, mesalazine dosage and duration of treatment varied. In cases with available information, systolic dysfunction was frequent. Troponin elevation is always present, although with different amount in each case. The CMR was performed in 4 of the 7 cases, and in 3 of them LGE was reported. The mechanism of this finding remains unknown, but appears to be a hypersensitivity response. Careful study of all other causes of myocarditis is essential. Removal and replacement of mesalazine is required since cases have been reported in which the reintroduction of the drug may lead to a recurrence of myocarditis.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Thus, any patient treated with mesalazine developing chest pain <span class="elsevierStyleItalic">de novo</span> is recommended to undergo a thorough study to rule out a toxic myocarditis. Treatment should be discontinued and other therapeutic alternatives should be used.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Querol-Fernández JC, Isasti G. Miocarditis inducida por mesalazina. 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Vol. 146. Issue 2.
Pages e7-e8 (January 2016)
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Vol. 146. Issue 2.
Pages e7-e8 (January 2016)
Letter to the Editor
Mesalamine-induced myocarditis
Miocarditis inducida por mesalazina
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Juan Carlos Querol-Fernández, Guillermo Isasti
Corresponding author
Unidad de Cardiología, Hospital Universitario de Ceuta, Ceuta, Spain
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