SAT-316 - Graves’ disease with thyrotoxic hypokalemic periodic paralysis, A rare reported association

Thyrotoxic periodic paralysis (TPP) is an uncommon yet potentially life threatening complication of thyrotoxicosis, characterized by episodic flaccid weakness with hypokalemia primarily from transcellular potassium shift (often with accompanying hypophosphatasemia and mild hypomagnesaemia), rather than true potassium depletion. TPP is reported to occur in ~0.1–0.2% of hyperthyroid patients in North America and is strikingly male predominant (reported male: female 17:1–76:1), despite Graves’ disease being far more common in women; this epidemiologic discordance can delay recognition in female patients. Episodes are frequently nocturnal and may be precipitated by adrenergic/insulin surges after high carbohydrate intake, rest after exercise, or medications including corticosteroids.

A 27 year old woman with no personal or family history of thyroid disease presented after routine labs revealed profound thyrotoxicosis (TSH 0.01 mIU/L; free T4 >7.77 ng/dL; free T3 >32.55 pg/mL; total T3 >651 ng/dL). TRAb/TSI were positive, confirming Graves’ disease. She was tachycardic (HR 126–133 bpm) with a palpable diffuse goiter and mild bilateral proptosis; neurologic examination showed preserved strength at the time of initial discharge. Thyroid ultrasound demonstrated an enlarged, diffusely inhomogeneous, hypervascular gland (right lobe 6.5×3.0×3.2 cm; left 6.5×2.8×3.1 cm; isthmus 9.7 mm) without dominant nodules. She was treated with methimazole 20 mg twice daily, propranolol LA 60 mg daily, and one dose of hydrocortisone. On the night of discharge, she developed abrupt bilateral lower extremity weakness and fell at home. At an outside facility, potassium was 2.6 mmol/L with concomitant hypomagnesaemia (Mg 1.78 mg/dL); weakness improved with monitored electrolyte repletion. Potassium subsequently stabilized (3.7 mmol/L) while biochemical hyperthyroidism persisted.

This case underscores the importance of considering TPP in any acute hypokalemic paralysis regardless of sex and highlights the management pitfall of over aggressive potassium replacement: rebound hyperkalemia has been reported in a substantial minority of treated episodes. Rapid control of thyrotoxicosis with non selective beta blockade and antithyroid therapy is central to abort attacks and prevent recurrence.

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