PubMed · 3516182
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H Sugita. 1986. [Progressive muscular dystrophy].. https://pubmed.ncbi.nlm.nih.gov/3516182/
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BACKGROUND: Hyponatremia associated with neuroleptic malignant syndrome has thus far been described as a syndrome of inappropriate secretion of antidiuretic hormone. OBJECTIVES: To ascertain and describe the role of cerebral salt-wasting syndrome as the cause of hyponatremia in a patient with neuroleptic malignant syndrome. PATIENT: A psychotic patient being treated with olanzapine presenting with sopor, muscle rigidity, polyuria, tachycardia, pyrexia, and severe hyponatremia. METHODS: Serial serological examinations of plasma tonicity (sodium level and osmolality), brain natriuretic peptide, and antidiuretic hormone were performed, and sodium excretion and urine osmolality were determined from 24-hour urine collection. In addition, markers for rhabdomyolysis were monitored. RESULTS: The patient shows clear symptoms of cerebral salt-wasting syndrome in association with neuroleptic malignant syndrome, characterized by severe hyponatremia, volume depletion, and elevated brain natriuretic peptide but normal antidiuretic hormone levels. Cerebral salt-wasting syndrome improved under dantrolene sodium treatment and concomitant fluid and sodium replacement. CONCLUSION: Hyponatremia in patients with neuroleptic malignant syndrome might more likely reflect cerebral salt-wasting syndrome than a syndrome of inappropriate secretion of antidiuretic hormone as an additional aspect of autonomic dysregulation caused by antidopaminergic drugs.
PURPOSE OF REVIEW: Lipid-lowering drugs are associated with myotoxicity, which ranges in severity from myalgias to rhabdomyolysis resulting in renal failure and death. Although rhabdomyolysis is rare, muscle symptoms and serum creatine kinase elevations are sufficiently frequent during the course of lipid-lowering drug therapy to pose diagnostic challenges for the clinician. Progress in our understanding of this form of myotoxicity is reviewed. RECENT FINDINGS: Muscle pain and weakness are the cardinal symptoms and often interfere with vigorous exercise. These symptoms may occur with or without serum creatine kinase elevations. The risk of myotoxicity is increased by combination statin-fibrate therapy as well as by factors that elevate tissue levels of the lipid-lowering drug, including the dose, drug-drug interactions, and host factors. Underlying neuromuscular diseases may become clinically apparent during statin therapy and may predispose to myotoxicity. The pathophysiology of myotoxicity most probably involves metabolic effects of the statins on the isoprenoid pool and on mitochondrial function. SUMMARY: Management of myotoxicity requires an evaluation of risk factors prior to prescribing lipid-lowering drugs, attention to muscle symptoms, and withdrawal of drug in the event of significant abnormalities.
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