Clozapine-induced myocarditis: Two case reports and review of clinical presentation and recognition.

Myocarditis is a potentially fatal cardiac disease marked by inflammation of the heart muscle. With a noted black-box warning, rates of clozapine-induced myocarditis are reportedly as high as 3%. Since the first case of clozapine-induced myocarditis was documented in 1994, more than 250 cases have been described in literature with an approximate 33% case-fatality rate. We report 2 cases of patients with primary psychotic disorders treated with clozapine, who developed signs and symptoms of myocarditis. The first was a 35-year-old white male patient with a primary diagnosis of schizoaffective disorder (bipolar type) who was initiated on clozapine after nonresponse to several therapies. On day 26, the patient was admitted to the emergency department for chest pain presenting with eosinophilia and notable elevations in several biomarkers, including troponin and C-reactive protein. The second patient was a 45-year-old black male who was initiated on clozapine for treatment-resistant schizophrenia. On day 13, the patient reported cardiac-related concerns (tachycardia) and flu-like symptoms resulting in hospitalization. Similarly, this patient demonstrated elevated biomarkers (troponin and creatine kinase). Both patients experienced resolution of symptoms after discontinuation of clozapine. Clozapine was not rechallenged for either patient. Review of literature further elucidates the relationship between clozapine and myocarditis, including potential risk factors, pathophysiology, and symptom presentation. Due to the potentially fatal nature of this condition, clinical vigilance and awareness is warranted upon initiation of clozapine through monitoring of symptoms along with cardiac and inflammatory biomarkers as indicated.

Levocarnitine for valproate-induced hyperammonemia in the psychiatric setting: A case series and literature review.

INTRODUCTION: Hyperammonemia is a potential adverse effect of valproic acid (VPA) therapy, which is often asymptomatic but can lead to severe, life-threatening encephalopathy. Carnitine deficiency due to VPA is the proposed mechanism for hyperammonemia and the development of VPA-induced hyperammonemic encephalopathy (VHE). Levocarnitine, the active form of carnitine, has been suggested for treatment and prevention of VHE. METHODS: Data was collected by chart review of 3 patients who received oral levocarnitine supplementation in the psychiatric setting for VPA-induced hyperammonemia. Review of the literature was performed through June 2017 using the following PubMed search terms: valproate, valproic acid, hyperammonemia, altered mental status, encephalopathy, and levocarnitine. Articles were included if they described use of levocarnitine in VPA-treated patients with psychiatric disorders. RESULTS: One patient developed encephalopathy with resolution of symptoms after VPA discontinuation. Valproic acid was restarted with the addition of levocarnitine to prevent VHE reoccurrence. In the other 2 cases, levocarnitine was started prophylactically in patients who developed hyperammonemia without emergence of any clinical symptoms. Ammonia levels were reduced to normal in all cases, and no symptoms consistent with encephalopathy were reported. The literature search identified 6 additional cases with 5 of 6 reports supporting use of levocarnitine for decreased ammonia levels as well as an observational trial. DISCUSSION: This literature review and case series illustrates successful use of levocarnitine supplementation for reduction of ammonia levels in the setting of VPA-induced hyperammonemia among patients with psychiatric disorders. However, clinical significance of ammonia reduction in asymptomatic patients is difficult to determine.

A Pharmacist-Led Transitional Care Program to Reduce Hospital Readmissions in Older Adults.

Medication reconciliation and patient education during admission and after discharge helped older patients remain independent at home.