Changes in serum cortisol, aldosterone and plasma renin activity during spontaneous attacks of paralysis in thyrotoxic patients (author's transl)

Abstract

In order to investigate the role of aldosterone in the pathogenesis of hypokalemic periodic paralysis, changes in serum cortisol (SC), aldosterone (SA) and plasma renin activity (PRA) were observed during 4 spontaneous attacks of paralysis in 3 thyrotoxic patients. The patient, H.I., a 26-year-old man, was admitted to Ito Hospital in April, 1977, for paralysis of the extremities. He had a subtotal thyroidectomy for Grave's disease in June, 1974. Physical examination revealed that he had a clear consciousness and no speech disturbance, but he was unable to lift his extremities against gravity. Laboratory findings on admission showed that serum thyroxine (T4) was 25.0-μg/ dl, triiodothyronine (T3) 720 ng/dl, K 2.4 mEq/L, SC 8.1 μg/dl, SA 2.0 ng/dl and PRA 5.3 ng/ml/hr. Immediately after recovery from the paralysis by the oral administration of aspara K 20 mEq, serum K was 3.4 mEq/L, SC 8.1 μg/dl, SA 2.0 ng/dl and PRA 3.9 ng/ml/hr. The next morning, serum K was 4.5 mEq/L, SC 8.7 mg/di, SA 5.0 ng/dl and PRA 1.0 ng/ml/hr. A similar attack of paralysis was observed after 6 months with serum K 2.0 mEq/L and SA 5.0 ng/dl. The patient, M.O., a 32-year-old man, was admitted to Ito Hospital in January, 1978, by ambulance for paralysis of the legs. Physical examination revealed a well-nourished man with a diffuse goiter. He had normal strength in the upper extremities but was unable to lift the lower extremities against gravity. Laboratory findings on admission showed that serum K was 1.8 mEq/L, SA 6.0 ng/dl, PRA 3.3 ng/ml/hr, T365 ng/dl and T4 25.0-μg/dl. Immediately after recovery from the paralysis by drip infusion of aspara K 6 mEq dissolved in 150 ml of 10% maltose, serum K was 3.7 mEq/L, SA 7.0 ng/dl and PRA 6.1 ng/dl. The next morning, serum K was 4.0 mEq/L, SA 6.0 ng/dl and PRA 3.6 ng/ml/hr. The patient, C.W., a 35-year-old man, was admitted to Ito Hospital in January, 1977, for palpitation and weight loss. Physical examination revealed that he was a man of average build with a diffuse goiter, and that he had normal muscle strength in the extremities. A thyroid function test showed a T3 of 745 ng/dl, T4 of 25.-μg/dl and 131 I-thyroidal uptake (24 hr) of 65%. On the 7th day after admission, he complained of an inability to stand up from a squatting position. At this time, serum K was 3.6 mEq/L, SC 12.8 μg/di, SA 8.0 ng/dl and PRA 2.3 ng/ml/hr. Without treatment, complete flaccid paralysis was observed at 2 hours after dinner with serum K 2.3 mEq/L and SA 1.0 ng/dl. After a spontaneous recovery from the paralysis, serum K was 4.1 mEq/L, SA 7.0 ng/dl and PRA 0.7 ng/ml/hr. Serum cortisol, aldosterone and plasma renin activity were measured by radioimmunoassay using commercial kits (Cortisol RIA kit, Eiken, Renin RIA kit, Dainabot, aldosterone 3H kit, Midori Juji, Japan). These findings suggested that aldosterone may not play a role in the pathogenesis of thyrotoxic periodic paralysis and may also not be an aggravating factor in paralysis induced by an unknown cause.