clozapine and Rhabdomyolysis

Topics: Antipsychotic Agents; Benzodiazepines; Cardiomyopathies; Catatonia; Clozapine; Heart Failure; Humans; Olanzapine; Rhabdomyolysis

We present the case of a middle-aged man with a chronic history of schizoaffective disorder, depressed type, stable on a second-generation antipsychotic. Psychotic symptoms recurred contingent to medication noncompliance necessitating hospitalization. Treatment was complicated by the development of neuroleptic malignant syndrome (NMS). In addition, subsequent medication rechallenges failed because of recurrent rhabdomyolysis and atypical NMS. Electroconvulsive therapy (ECT) treatment was initiated, affording remission of psychotic symptoms and nonrecurrence of NMS and rhabdomyolysis. Our experience confirmed the efficacy of ECT treatment in providing symptom relief of psychosis complicated by recurrent episodes of NMS and atypical NMS. Likewise, it illustrated the efficacy of ECT treatment for rhabdomyolysis.

Topics: Adult; Antipsychotic Agents; Benzodiazepines; Clozapine; Electroconvulsive Therapy; Humans; Male; Neuroleptic Malignant Syndrome; Olanzapine; Patient Compliance; Rhabdomyolysis; Schizophrenia; Treatment Outcome

Topics: Adult; Antimanic Agents; Antipsychotic Agents; Clozapine; Dose-Response Relationship, Drug; Drug Monitoring; Drug Therapy, Combination; Fluid Therapy; Humans; Lithium Compounds; Male; Psychiatric Status Rating Scales; Psychotic Disorders; Rhabdomyolysis; Time Factors

The neuroleptic malignant syndrome (NMS) is a rare, but potentially lethal side effect of conventional and atypical antipsychotic drugs. We present a 62 years old male patient who was admitted to our institution because of sudden onset of mild hyperthermia, muscle rigidity, stupor, leucocytosis and massive rhabdomyolysis after 30 years uneventful treatment with clozapine. The medication with clozapine was suspended because of the suspicion of NMS. When the acute symptoms were abated, the treatment with clozapine was resumed again after 14 days. The very next day, the patient suffered again from raised body core temperature, leucocytosis, elevated serum creatine kinase and new catatonia. The therapy with clozapine was stopped definitively and benzodiazepines were administered assuming a relapse of an alleviated, probably reconvening NMS. Under the treatment with benzodiazepines the patient was free of symptoms even after 1 month. To our knowledge, the latency of 30 years between the beginning of the treatment with clozapine and the onset of NMS is the longest period in the literature. According to our case, the differential diagnosis of NMS is not always trivial and is therefore discussed.

Topics: Antipsychotic Agents; Body Temperature; Clozapine; Diagnosis, Differential; Humans; Male; Middle Aged; Neuroleptic Malignant Syndrome; Rhabdomyolysis; Schizophrenia

We report on a case of rhabdomyolysis induced by the correction of hyponatremia after psychogenic polydipsia and clozapine use, where the switch to a high dose of olanzapine resulted in the non-recurrence of rhabdomyolysis. The 46-year-old patient with the diagnosis of schizophrenia paranoid type, who had been on clozapine treatment for the previous 4 years, was admitted with the symptoms of generalized seizure and vomiting, and as severe hyponatremia was proved, its correction with the parallel use of clozapine treatment was done. CK concentrations increased to 48 120 U/L without any symptom of neuroleptic malignant syndrome. To prevent acute renal insufficiency, high-volume alkaline diuresis was initiated and clozapine was tapered and stopped. On the day 12 of treatment, olanzapine was started and was elevated to 30 mg/day. CK concentration began to fall returning to the normal concentration on day 20. Six months after the switch to olanzapine no recurrence of rhabdomyolysis was detected; clinical and laboratory findings were normal. We suggest that after a benzodiazepine-type antipychotic-induced rhabdomyolysis, a switch to another atypical antipsychotic can be a cautious clinical strategy.

Topics: Antipsychotic Agents; Benzodiazepines; Clozapine; Creatine Kinase; Humans; Male; Middle Aged; Olanzapine; Rhabdomyolysis; Schizophrenia; Water Intoxication

Mild myopathy is a common manifestation of the X-linked McLeod neuroacanthocytosis syndrome. We present a patient with McLeod syndrome and a primarily subclinical myopathy, who developed severe rhabdomyolysis with renal insufficiency after a prolonged period of excessive motor restlessness due to an agitated psychotic state and a single dose of clozapine. Other possible causes for rhabdomyolysis such as prolonged immobility, trauma, hyperthermia, generalized seizures, toxin exposure, or metabolic changes were excluded. Clinical course was favorable, with persistent slight elevation of serum creatine kinase levels caused by the underlying myopathy. Our findings suggest that McLeod myopathy is a predisposing factor for severe rhabdomyolysis. This possibly life-threatening condition should be added to the clinical spectrum of McLeod syndrome, and serum creatine kinase levels should be carefully monitored in patients with this syndrome, particularly if a hyperkinetic movement disorder is present or neuroleptic medication is used.

Topics: Acanthocytes; Clozapine; GABA Antagonists; Humans; Hyperkinesis; Male; Middle Aged; Motor Activity; Neuromuscular Diseases; Rhabdomyolysis; X Chromosome

To report a case of rhabdomyolysis related to rapid correction of hyponatremia attributable to compulsive drinking of water, possible complicated by clozapine use.. A 42-year-old white man treated with clozapine for schizophrenia was admitted for a generalized seizure. Marked hyponatremia due to psychogenic polydipsia was present. He developed a marked elevation of creatine kinase concentrations after correction of hyponatremia with hyperosmolar sodium solution, without clinical signs of rhabdomyolysis.. Rhabdomyolysis associated with hyponatremia due to water intoxication has been reported in 17 patients to date. A possible explanation may lie within the framework of the calcium-sodium exchange across the skeletal muscle cell membrane. By increasing muscle cell permeability, clozapine treatment may possibly enhance the destruction of muscle cells.. Hyponatremia due to water intoxication and concurrent use of clozapine should be considered in the differential diagnosis of rhabdomyolysis, especially in the severely psychiatrically disabled population.

Topics: Adult; Antipsychotic Agents; Clozapine; Drinking Behavior; Humans; Hyponatremia; Male; Rhabdomyolysis; Schizophrenia, Paranoid; Schizophrenic Psychology; Sodium Chloride

In case I, a 31-year-old man who had undergone unusual high-performance training, painful swellings occurred in the left arm and creatine kinase activity was raised (28,644 U/l), as well as that of the transaminases. A rapid urine test for blood was positive, but the sediment was free of red blood cells. There were no other pathological findings. Fluid intake was increased to 31 daily and on the third day he was symptom-free and creatine kinase activity had fallen to 6475 U/l, reaching normal values on the 15th day. Case 2 concerned a 28-year-old woman with paranoid schizophrenia who had taken several tablets of clozapine and then remained in bed for 3 days. She complained of pain in the region of the gluteus maximus muscles, exacerbated on pressure but otherwise unremarkable. Creatine kinase was raised to 21,492 U/l, creatine to 186 mumol/l, and the transaminases were likewise increased. The urine strip-test for blood was twice positive. She was treated with frusemide (80 mg daily) and infusions of electrolyte solution (21 daily). She became pain-free on the second day and the various enzyme activities rapidly fell to normal.

Topics: Adult; Clozapine; Combined Modality Therapy; Creatine Kinase; Drug Overdose; Exercise; Female; Fluid Therapy; Furosemide; Hematuria; Humans; Male; Physical Education and Training; Rhabdomyolysis; Schizophrenia, Paranoid