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+An 18-year-old male was diagnosed with attention-deficit hyperactivity disorder (ADHD) in 2005.
+He was overweight with a body mass index (BMI) of 40.
+He was started on quetiapine fumarate (Seroquel®) 900 mg daily in April 2005 and methylphenidate (Concerta®) 54 mg daily in September 2005.
+In the beginning of August 2006 he was admitted to his local hospital with severe dyspnoea, tachypnea, tachycardia, and cyanosis.
+On admission the blood pressure was 120/80 mmHg, and the arterial blood gas revealed a pH of 7.45, pCO2 of 3.55 kPa, paO2 of 7.76 kPa, and BE of −5.1 mmol/l.
+C-reactive protein was not elevated.
+The chest X-ray showed an enlarged heart.
+He developed hemoptysis and was treated with unfractionated heparin in suspicion of pulmonary embolism.
+He subsequently developed cardiogenic shock and was treated with vasoactive drugs.
+In spite of the treatment he became oliguric and his liver enzymes were rising.
+He was referred to our hospital for further treatment.
+On admission the blood pressure was 90/60 mmHg, despite infusion with noradrenaline.
+His heart rate was 130/minute and his temperature was 38.4 °C.
+A thoracic computed tomography scan did not show pulmonary embolism.
+Echocardiography revealed biventricular failure and left ventricular end diastolic diameter was 7 cm.
+The left ventricle was severely hypokinetic with an ejection fraction (EF) of 20%–25%.
+The left ventricular end diastolic pressure was markedly elevated, and there was a moderate mitral regurgitation.
+Intermittent hemodialysis was initiated.
+His liver function improved slightly, but despite dialysis the renal function deteriorated with increasing creatinine values.
+After three days there was a further worsening of the left ventricular systolic function with an ejection fraction of 10%–12% and marked pulmonary hypertension with systolic pulmonary pressure estimated to 30 mmHg.
+The clinical picture resembled dilated cardiomyopathy with low output failure causing renal and liver failure.
+We suspected drug-induced cardiomyopathy and methylphenidate and quetiapine fumarate were discontinued.
+Screening for infectious pathogens, immunological markers, and iron or amyloid deposition were all negative.
+After three days he was transferred to the National Hospital (Rikshospitalet, Oslo) with ongoing noradrenaline and dobutamine infusions.
+Shortly after admission an intraaortic balloon pump (IABP) was inserted and noradrenaline was replaced by nitroprusside.
+Coronary angiography was normal.
+Endomyocardial biopsy from the right ventricle did not reveal any distinct myocardial pathology.
+On treatment with IABP, nitroprusside, and dialysis, the clinical situation gradually improved and the liver function returned to normal.
+His renal function also improved with increasing diuresis and creatinine fell from 798 to 98 μmol/l.
+His EF was still markedly reduced (15%).
+Because of behavioral problems and adipose stature, he was denied a heart transplant.
+He was treated with IABP for 26 days, and after 28 days he was transferred back to our hospital.
+At that time his liver and renal functions were normal.
+He was treated with an angiotensin-converting enzyme (ACE)-inhibitor, a beta-blocker, and diuretics.
+During the following two weeks his clinical status improved and he was subsequently discharged to his home.
+The echocardiography still showed markedly dilated left ventricle with EF of 20%.
+In March 2007, his clinical status was improved and he was in function class II (New York Heart Association) with an EF estimated by echocardiography to 30%–35%.