Clozapine-Induced Myocarditis in a Young Man with Refractory Schizophrenia: Case Report of a Rare Adverse Event and Review of the Literature.

BACKGROUND Myocarditis is cardiac muscle inflammation caused by infectious or noninfectious agents. Rarely, clozapine, an atypical antipsychotic drug used to treat resistant schizophrenia, has been reported to cause myocarditis, as we report in this case. CASE REPORT A 29-year-old man, who was known to have schizophrenia and was on olanzapine therapy, presented in our Emergency Department with active psychosis, and was subsequently admitted to the psychiatric ward for refractory schizophrenia. He was started on clozapine, which was cross-titrated with olanzapine. On day 20 of being treated with clozapine, he developed a high-grade fever and chest pain. EKG demonstrated new-onset prolonged QT corrected for heart rate (QTc), premature ventricular contractions, ST-T wave changes with an increased ventricular rate, and ventricular bigeminy with elevated troponin and inflammatory markers. Echocardiography showed a reduced left ventricular ejection fraction. Coronary angiography showed normal coronary arteries, low cardiac output, and cardiac index consistent with cardiogenic shock was also observed. Other pertinent laboratory results included negative respiratory viral panel, including COVID-19 PCR, negative blood cultures, and negative stool screen for ova and parasite. Clozapine was discontinued and the patient received management for heart failure with reduced ejection fraction. He improved clinically with return of EKG to normal sinus rhythm and improved left ventricular ejection fraction on repeat echocardiogram. CONCLUSIONS Acute myocarditis can occur due to a myriad of causes, both infectious and noninfectious; thus, determining the lesser-known causes, such as drug-related etiology, is essential to provide appropriate treatment for patients.

A Rare Case of Esophageal Leukoplakia in Achalasia.

Esophageal leukoplakia refers to a clinical finding of a white patch on the mucous membrane surface that cannot be scraped off. It has been associated with alcohol and tobacco use and chronic acid reflux. An association with squamous cell dysplasia and carcinoma has been reported with potential for malignant transformation warranting endoscopic intervention or surveillance, but no guidelines exist. We present a case of a 77-year-old female with a history of longstanding achalasia requiring multiple Botox injections. After presenting with weight loss, esophageal dysphagia, and acid reflux the patient underwent an esophagogastroduodenoscopy (EGD) showing a 20 mm white plaque in the middle third of the esophagus and histopathology consistent with esophageal leukoplakia. After repeated Botox injection and treatment with PPI and H2 blocker, no findings of esophageal leukoplakia were noted on repeat EGD. With this case, we aim to increase awareness of this rare disease pathology, especially in the setting of underlying achalasia. This case also raises the question if maximum anti-reflux therapy could have a potential benefit in avoiding the recurrence of esophageal leukoplakia.

Recent Advances and Therapeutic Options in Lambert-Eaton Myasthenic Syndrome.

Lambert-Eaton Myasthenic Syndrome (LEMS) is an autoimmune-mediated neurological disorder that manifests as muscle fatigue, diminished tendon reflexes, with symptoms of cholinergic overactivity. It can be associated with certain neoplastic conditions, the most common being small cell lung carcinoma (SCLC). The basic pathophysiology involved is antibody-mediated targeting of voltage-gated calcium channels (VGCC), which decreases the release of acetylcholine in the synaptic junction. Multiple treatment options have been introduced in the past and, recently, a new drug, amifampridine, has been approved by the Food and Drug Administration (FDA) for the treatment of weakness associated with these patients. We summarize this newly introduced drug with a brief description of other treatment options available.

Juvenile Parkinson Disease.

Juvenile Parkinson's disease (JPD) is a rare movement disorder that presents before the age of 21 years. Kufor-Rekab syndrome (KRS) is one of the distinct types of JPD caused by the ATP13A2 mutation and inherited as an autosomal recessive. The pathogenesis of KRS is related to an interrelated metabolism of ATP13A2 with Mn+2 and Zn+2, bioenergetics of mitochondria, autophagy lysosomal dysfunction, and synuclein metabolism. Clinically, KRS has a variable phenotype and may present with pyramidal or extrapyramidal symptoms and cognitive impairment. Early diagnosis of KRS is important as most of these patients are levodopa-responsive and genetic counseling and screening is important for the whole family. We present a case of a 16-year-old boy who presented with tremors and walking difficulty. His physical examination showed an expressionless face, decrease in eye blink frequency, and slow vertical saccadic eye movements. His movements were slow. All laboratory investigations were normal, except the genetic study, which led to the diagnosis of KRS.