Antipsychotics
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Myocarditis and lack of efficacy: case report. A 22-year-old man developed myocarditis during treatment with clozapine for treatment-resistant schizophrenia (TRS). Additionally, he exhibited lack of efficacy to olanzapine, quetiapine and risperidone for schizophrenia [not all routes and dosages stated]. The man had a history of polysubstance use disorder and schizophrenia. He was hospitalised due to tactile, auditory and visual hallucination, violence and agitation. He reported constant use of marijuana, methamphetamine and alcohol. During admission, urine toxicology was positive for methamphetamines. He was started on olanzapine, which was switched to risperidone due to lack of improvement. He required several administrations of diphenhydramine and haloperidol due to persistent symptoms. A diagnosis of TRS was confirmed. On day 22 of admission, he was initiated on clozapine. He had been receiving clozapine 100mg in morning and 200mg in the evening. Subsequently, agitation and psychosis resolved with improved symptoms. On day 16 of clozapine initiation, he developed weakness, loose stools, flu-like symptoms, sudden-onset chest pain and fever. Initial ECG revealed sinus tachycardia with a heart rate of 112 beats/min, a prolonged QTc of 482, nonspecific T abnormalities in lateral leads and no acute ischemic changes. A diagnosis of myocarditis was considered. The man’s clozapine therapy was discontinued and he was initiated on unspecified supportive care along with risperidone. However, his symptoms deteriorated further and he was transferred to a medical unit. He was noted to have transaminitis secondary to positive hepatitis A serology. His B-type natriuretic peptide was elevated to 999 ng/mL, CRP 20.8 mg/dL, troponin 0.72 µg/L, erythrocyte sedimentation rate >100 mm/h, leukocyte count 11.4 x 109/L, eosinophil count 1.1 x 109/L, creatine Kinase 272 U/L, haemoglobin 10.8 g/dL, RBC 3.57 x 1012/L, D-dimer 2018 ng/mL and reactive hepatitis A IgM antibody. Transesophageal echocardiography (TEE) revealed heart failure, dilated right-sided heart chambers with reduced ejection fraction of 25%, and a pulmonary artery pressure of 36mm Hg. He was treated with lisinopril and metoprolol succinate in addition to the supportive care. He was kept on contact isolation precautions due to hepatitis A. Over the next 3 weeks, his clinical symptoms resolved. Repeat blood test were normal. Repeat lab examinations revealed resolution of transaminitis and ECG showed improved fraction of 45–50%. Clozapine was considered as a most likely cause for cardiac function impairment. Despite high doses of quetiapine, his hallucinations returned with worsening psychosis. Under close supervision his clozapine was restarted slowly at an initial dose of 12.5mg, which was further increased to 25mg every 48 hours. Approximately after 3 weeks, a repeat ECG revealed sinus tachycardia of 102 beats/min, a normal QTc of 442 and borderline ST elevation. His close monitoring was continued and clozapine dose was titrated to 100mg in the morning and 200mg in t
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