yemenjmedYemen Journal of MedicinecoVolume 5 Issue 2MultidisciplinaryEnglishMay-August 2026NNY20260820ArticleUnusual Endocrine Causes of Acute Hypokalemic Paralysis: Two Case Reports and a Focused Review of the Diagnostic ApproachEnglishY451459Sumaira KanwalRafiqui1EnglishNAhmed FawzyAlnabulsi2EnglishY10.63475/yjm.v5i2.0452Acute hypokalemic paralysis is a neurological emergency characterized by sudden or progressive muscle weakness associated with marked hypokalemia. Although thyrotoxic periodic paralysis and familial hypokalemic periodic paralysis are well-recognized causes, endocrine disorders associated with renal potassium wasting may produce a similar clinical presentation and require a fundamentally different diagnostic and therapeutic approach. We report two men with acute hypokalemic paralysis caused by distinct endocrine disorders. A 39-year-old Egyptian man presented with progressive ascending weakness, severe hypokalemia (2.1 mEq/L), marked hypertension (210/120 mmHg), metabolic alkalosis, hyperglycemia, central obesity, purple abdominal striae, and hyperpigmentation. Endocrine evaluation demonstrated hypercortisolism with elevated adrenocorticotropic hormone (ACTH), establishing ACTH-dependent Cushing’s syndrome. Imaging did not identify a definitive source of ACTH secretion, and inferior petrosal sinus sampling was unavailable. Neurological symptoms improved after potassium replacement; however, hypokalemia and metabolic alkalosis persisted despite potassium supplementation and spironolactone. Bilateral adrenalectomy was considered because of severe and persistent hypercortisolism, but the patient declined surgery and was discharged against medical advice. The second patient, a 27-year-old Filipino man, developed profound generalized weakness after a large carbohydrate load. Serum potassium was 2.1 mEq/L, with no reported acid–base abnormality. Thyroid testing demonstrated suppressed thyroid-stimulating hormone and elevated total thyroxine, while technetium-99m thyroid scintigraphy showed low uptake, supporting thyrotoxicosis due to painless thyroiditis. His weakness rapidly resolved after intravenous potassium, and he was discharged on propranolol. These cases underscore the importance of considering mineralocorticoid excess and painless thyroiditis in the differential diagnosis of acute hypokalemic paralysis. A high index of suspicion for atypical endocrine pathologies is warranted when routine causes are excluded or when specific clinical features, such as hypertension or metabolic alkalosis, point toward alternative diagnoses.EnglishHypokalemic paralysis, Cushing syndrome, ACTH-dependent Cushing syndrome, thyrotoxic periodic paralysis, painless thyroiditis, hypokalemia, metabolic alkalosis, mineralocorticoid excesshttps://www.yemenjmed.com/admin/abstract?id=441References1619