IMPAIRED WATER-EXCRETION IN A HYPONATREMIC PATIENT FOLLOWING THYROIDECTOMY - CAUSAL ROLE OF GLUCOCORTICOID DEFICIENCY

We evaluated the causal role of glucocorticoid deficiency in the hypon atremia that developed in a 57-year-old Japanese man with hypothyroidi sm following the performance of a total thyroidectomy for laryngeal ca ncer. The plasma concentration of vasopressin (1.78 pg/ml) was not sup pressed in the presence of hyponatremia (125 mEq/l). The urinary excre tion of sodium was increased, and the plasma renin activity and plasma aldosterone concentration were suppressed. The infusion of hypertonic saline increased the plasma osmolality, but not the plasma concentrat ion of vasopressin. An oral water load (20 ml/kg of body weight) did n ot suppress the plasma vasopressin level or induce diuresis. Pretreatm ent with hydrocortisone normalized the response of plasma vasopressin to the water load was well as the diuretic response during the hypothy roid state. The urinary exretion of 17-hydroxycorticosteroids was belo w normal in the hypothyroid state in the face of normal serum cortisol concentration. The correction of the hypothyroidism returned these ab normalities to normal. A disturbed metabolism of glucocorticoid may ha ve been responsible for the hyponatremia and disturbance in plasma vas opressin regulation observed in this hypothyroid patient.