monensin and Rhabdomyolysis

Monensin is a commonly used veterinary antibiotic with a narrow safety range. Overdose of monensin can cause animal poisoning or even death. Monensin poisoning is rare in humans, and there is no effective detoxification protocol in clinical treatment.. We report here two cases of monensin-induced rhabdomyolysis and hepatotoxicity by oral ingestion. The two patients were a couple and both were admitted to the hospital due to oral ingestion of monensin 5 days prior. Patient 1, with a past history of chronic bronchitis and hypertension, presented with severe rhabdomyolysis, hepatotoxicity, and hypoxemia. After treatment with fluid replacement and alkalinization of urine, his condition deteriorated the next day and irreversible cardiopulmonary arrest occurred. Patient 2 was diabetic and using oral hypoglycemic drugs and had obvious rhabdomyolysis from the fifth day of admission. After treatment with fluid replacement, urine alkalization, and continuous renal replacement therapy (CRRT), the patient recovered and was discharged 1 month later.. The ingestion of monensin can lead to life-threatening toxicity, with rhabdomyolysis and hepatotoxicity as the main manifestations. Comprehensive treatment including CRRT in the early stage of rhabdomyolysis may improve the condition and prognosis.

Topics: Aged; Chemical and Drug Induced Liver Injury; Female; Fluid Therapy; Humans; Male; Monensin; Rhabdomyolysis

Monensin is a veterinary antibiotic with a narrow therapeutic window that has led to lethal intoxication in many animal species. Only two prior cases of human toxicity have been reported, both fatal. We present the first case of survival from severe toxicity following monensin ingestion.. A 58-year-old man presented with 8 days of vomiting and abdominal pain. Due to delusions of central nervous system toxoplasmosis, he ingested 300 mg of monensin. His laboratory studies revealed severe rhabdomyolysis without renal dysfunction. Total creatine kinase (CK) peaked above 100,000 U/L. His CK decreased to 5192 U/L after 15 days of aggressive hydration and sodium bicarbonate therapy. His ejection fraction on echocardiogram decreased from 69 to 56%.. Reports on acute clinical effects after human exposure to monensin are limited. Ingestion is known to cause skeletal and cardiac muscle rhabdomyolysis and necrosis. Animal studies demonstrate that monensin's toxicity is due to increases in intracellular sodium concentrations and Ca. Monensin is a veterinary medication not approved for human use by the US Food and Drug Administration. Though poorly studied in humans, this case demonstrates the severe harm that may occur following ingestion.

Topics: Anti-Bacterial Agents; Fatal Outcome; Humans; Male; Middle Aged; Monensin; Rhabdomyolysis; Severity of Illness Index; Veterinary Drugs

Myoglobinuria or rhabdomyolysis occurs when myoglobin escapes into the blood and then into the urine after acute muscle necrosis. It can be a serious medical condition leading to renal failure and death. There are many causes including exertion, crush syndromes, ischaemia, metabolic disorders, exogenous toxins and drugs, heat stroke and hereditary disorders such as malignant hyperthermia. We report the case of a 17 year-old boy who developed myoglobinuria, renal failure and death 11 days after ingesting sodium monensin, possibly with the intention of developing muscles. Sodium monensin, the active principle of Rumensin(R), is a dietary additive used as a growth promoter for confined cattle. There are no previous reports of human intoxication. Accidental or experimental sodium monensin intoxication in animals produces similar findings to those seen in this case.

Topics: Acute Disease; Acute Kidney Injury; Adolescent; Fatal Outcome; Food Additives; Humans; Male; Monensin; Muscle Development; Rhabdomyolysis

We report a case of human monensin intoxication; to our knowledge, this is the first reported case in the medical literature. The patient took a dose of monensin three times higher than a dose considered lethal for cattle and developed a clinical picture similar to that reported in veterinary medicine. There was an early and extremely severe rhabdomyolysis followed by acute renal failure, heart failure, and death. The main changes observed at autopsy were extensive skeletal muscle necrosis, complement deposition at the myocardial level, pulmonary edema, and acute tubular damage.

Topics: Acute Kidney Injury; Adolescent; Complement C9; Fatal Outcome; Humans; Immunohistochemistry; Ionophores; Kidney; Male; Monensin; Muscle, Skeletal; Myocardium; Myoglobin; Rhabdomyolysis