Introduction Thyrotoxic periodic paralysis (TPP) is an uncommon endocrine emergency caused by rapid intracellular potassium redistribution during thyrotoxicosis. Carbohydrate exposure is a recognized precipitant, but direct observation of a first paralytic attack developing during supervised diagnostic glucose testing is unusual. Case Presentation A 29-year-old Indian man underwent a supervised oral glucose tolerance test (OGTT) for borderline fasting dysglycemia and episodic postprandial tremulousness. He had also experienced recent weight loss, heat intolerance, and palpitations but had no previous weakness. During the late phase of testing, progressive thigh heaviness evolved into symmetrical flaccid quadriparesis with lower-limb predominance, reduced reflexes, preserved sensation, and no respiratory involvement. Serial samples demonstrated a rapid transition from normal baseline potassium to severe hypokalemia, accompanied by hypophosphatemia and a marked insulin response. Normal acid-base status and suppressed urinary potassium excretion supported transcellular redistribution. Thyroid testing and antibody studies established previously undiagnosed Graves’ disease. Limited potassium replacement, magnesium supplementation, and propranolol produced complete neurological recovery without rebound hyperkalemia. Carbimazole therapy achieved progressive biochemical control, with no recurrent paralysis during 24 weeks of follow-up. Discussion Standardized glucose exposure and serial sampling documented the metabolic transition from normal potassium to paralytic hypokalemia. The episode supports an interaction between endogenous insulin stimulation and thyrotoxic skeletal-muscle susceptibility rather than hyperinsulinemia as an isolated cause. Conclusion Unrecognized thyrotoxicosis should be considered before carbohydrate provocation testing in patients with unexplained hyperadrenergic symptoms.
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