Thyrotoxic hypokalaemic paralysis in a Black man.

Sir, A 32-year-old African-American male construction worker and martial arts student presented to the emergency room complaining of generalized weakness that was more pronounced in the lower extremities and confined him to bed. Weakness began about 12 h after vigorous physical exercise and ingestion of a high carbohydrate diet. He had no significant personal or family medical history. Initial blood pressure was 220/60 mmHg and resting pulse rate was regular at 98–104/min. His blood pressure normalized after 8 h without treatment (120/70 mmHg). Physical examination revealed a diffusely enlarged palpable thyroid gland and motor power of 3/5 in upper and 1–2/5 in the lower extremities. The rest of the examination was normal. In the emergency room the concentration of electrolytes were potassium 2.3 mEq/l (range 3.5–5.0 mEq/l), magnesium 2.2 mEq/l, calcium 9.5 mEq/l, phosphate 3.5 mEq/l. Serum creatinine phosphokinase (CPK) level was 474 U/L (24–195 U/L) and the blood pH was 7.45. Urine pH was 7.5 and specific gravity was 1.025. Concentrations of spot urine electrolytes were: potassium 13 mEq/l, sodium 177 mEq/l and chloride 132 mEq/l. Electrocardiogram showed mild sinus tachycardia (rate of 100/min) and U-waves in leads I, II, III, V1–V6. Treatment was started with intravenous administration of potassium chloride at 10 mEq/h and oral potassium chloride at 40 mEq every 8 h. Muscle weakness and hypokalaemia resolved within 24 h after the patient received a total of 360 mEq of potassium. Potassium supplementation was discontinued when serum potassium reached 4.6 mEq/l, but serum potassium continued to rise, peaking at 6.5 mEq/l on hospital day 3. Iatrogenic hyperkalaemia was treated with oral sodium polystyrene sulphonate 30 g every 4 h for three doses until serum potassium decreased to 4.6 mEq/l. On hospital day 3, repeat urine electrolyte concentrations (in a 24-h urine volume of 1.6 l) now were potassium 198 mEq/l (317 mEq/day), sodium 287 mEq/l (459.2 mEq/day) and chloride 380 mEq/l (608 mE/day). Plasma renin activity and aldosterone levels at admission and on hospital day 3 were within normal limits. Thyroid function tests 24 h after admission revealed hyperthyroidism. Thyroid-stimulating hormone (TSH) was -0.05 mU/l (0.4–5 mU/l), thyroxine (T-4) 18.26 mg/dl (5–12 mg/dl), free thyroxine (FT-4) 2.5 mg/dl (0.71–1.85 mg/dl), tri-iodothyronine resin uptake (T-3RU) 35.38% (25–35%), thyroidstimulating immunoglobulin was 84% (0–130, Quest Lab). TSH receptor antibody was 17.2% (-10%, Quest Lab), thyroglobulin antibodies 6.7% (-2%, Quest Lab). Tc thyroid uptake and scan revealed diffuse uptake. HLA type was A23 A74, B53B58, C4 and BW4q. Treatment for hyperthyroidism was started with propylthiouracil 150 mg twice daily, and the patient was discharged on hospital day 7. At further follow-up visits, the symptoms had not recurred after 2 years. He was clinically and biochemically euthyroid (Table 1) at the fourth month after initiation of propylthiouracil treatment, and has remained so thereafter. Our patient presented with Graves’ disease, inducing hypokalaemia and weakness. Given the low urinary potassium and absence of vomiting or diarrhoea at presentation, the cause of hypokalemia