A rare case report of acute severe hypokalemia induced by monosialotetrahexosylganglioside therapy.

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RationaleMonosialotetrahexosylganglioside (GM1), an exogenous ganglioside, is widely used as an adjuvant in treating cerebrovascular diseases and Parkinson disease. While its association with Guillain-Barré syndrome is well-established, GM1-induced hypokalemia presenting-with overlapping clinical features such as muscle weakness-has not been previously reported. Severe hypokalemia can cause neurological deficits and electrocardiographic abnormalities, emphasizing the need to recognize this potential adverse effect.Patient concernsA 68-year-old male with parkinsonism developed severe lower extremity weakness (inability to walk unassisted) and absent tendon reflexes 6 days after initiating GM1 therapy.DiagnosesLaboratory testing confirmed severe hypokalemia (serum potassium: 2.05 mmol/L). The Naranjo Adverse Drug Reaction Probability Scale scored 6 for GM1, indicating GM1 as the more probable cause.InterventionsImmediate potassium supplementation was administered, and GM1 was discontinued.OutcomesFollowing interventions, the patient's muscle strength and tendon reflexes improved significantly (serum potassium: 3.99 mmol/L), with resolution of hypokalemia.LessonsOlder adults with comorbidities are vulnerable to GM1-associated hypokalemia. Clinicians should monitor potassium levels during GM1 therapy, and further research into underlying mechanisms is warranted.

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