Recurrent hypokalemic paralysis: An atypical presentation of hypothyroidism
A 30-year-old female presented with recurrent attacks of acute flaccid paralysis of all four limbs since last 1 year. Each episode lasted for 2 to 5 days followed by spontaneous complete recovery without potassium supplement in any form. Frequency of attack gradually increased up to three episodes per month. It usually started with early morning weakness without any diurnal variation. There was no history suggestive of altered sensorium, convulsion, visual, respiratory, or bulbar weakness. She had no symptom suggestive of hypothyroidism.\nThe patient had quadriparesis with hypotonia, diminished deep tendon reflexes except delayed relaxation of ankle jerks, flexor plantar response, and prominent neck muscle weakness. She had normal higher mental function without any cranial nerve, sensory, or sphincter involvement. She was thin built without pallor or edema. Her thyroid gland was not palpable. Other system examination including chest and abdomen was within normal limit.\nLaboratory investigations showed normal hemoglobin with high ESR, low potassium, and normal sodium and serum creatine phosphokinase (CPK) level was very high (1067 mg/dl). Her electromyography and nerve conduction study were normal. Thyroid function test revealed very low level of thyroxine (both T3 and T4) with very high thyroid-stimulating hormone (TSH > 100). Serum anti-TPO antibody titer was also very high (386.4 IU/ml). Hypokalemia persisted during attack ranging from 1.6 to 3.2 meq/L. Hypokalemic paralysis was diagnosed based on clinical and biochemical parameters. No cause of secondary hypokalemia could be detected. Her 24-h urinary potassium excretion was 11.14 meq/L which was much below normal (normal range 25-120 meq/L). Normal serum magnesium and urinary calcium excretion ruled out the possibility of Gitelman's syndrome. Urine pH was within normal limit. The computed tomography (CT) scan of the abdomen demonstrated normal adrenal gland. Her plasma rennin activity (PRA) was measured normal (2.6 ng/ml/h).\nDuring the acute period in hospital, the patient was treated with intravenous potassium (IV potassium chloride, 40 meq/L of normal saline through peripheral vein at a rate of 20 meq/h) for a week that lead to clinical recovery and also biochemical improvement to some extent. After starting oral levothyroxine replacement, the patient continued with oral potassium replacement (oral potassium chloride solution 40 meq twice daily) for another 2 weeks after which she could be safely maintained with levothyroxine only. Hypokalemic state persisted up to 4 weeks of levothyroxine replacement though the patient was clinically well. Subsequently, serum TSH became normal with normal serum potassium level. With adequate control of hypothyroidism, the patient did not have the need to take potassium supplement and no further attack of acute flaccid weakness has been reported so far (for a period of 1 year during follow up).