Endocrine Abstracts

Case: A fit strong 26-year-old Caucasian male presented with recurrent falls. He attended the accident and emergency department with a three-month history of episodic weakness of the lower limbs. There was no previous history of medical problems and he was not on medication. On admission a full neurological examination was normal except for reduced power in the lower limbs. He had a raised creatinine kinase 472 U/l (0–170). Potassium was 3.8 mmol/l (3.5–5.3). He was reviewed by a neurologist and a muscle biopsy was ordered. However, he recovered quickly and was discharged. He was readmitted three weeks later with similar symptoms and examination findings although he had sinus tachycardia of 110 beats per minute. His potassium however was 1.5 mmol/l. Thyroid function tests indicated Free T₄ 65 pmol/l (11–24), TSH<0.01 mU/l (0.3–5.5), Free T₃ 22.7 pmol/l (3.5–6.7). A diagnosis of thyrotoxic hypokalaemic periodic paralysis was made. He made a quick recovery following cautious replacement with a potassium infusion and treatment with Propanolol and Carbimazole as well as a low carbohydrate diet.

Discussion: Thyrotoxic hypokalaemic periodic paralysis is a known complication of hyperthyroidism that is not common in western populations. It predominately affects the extremities, particularly the lower limbs. Many patients present with few symptoms of thyrotoxicosis. This frequently leads to a delayed diagnosis. Measurement of thyroid function is important in distinguishing the condition from hypokalaemic periodic paralysis (HPP), a commoner cause of paralysis in western populations. Early recognition is important to prevent complications of initial hypokalaemia. The pathophysiology is related to increased activity of Na⁺/K⁺ ATPase channels in muscle and liver causing an intracellular shift of potassium with no change in total body potassium levels. Definitive management remains the control of hyperthyroidism, which abolishes attacks.