Yonemura K, Furuya R, Oki Y, Matsushima H, Ohishi K, Hishida A
First Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Miner Electrolyte Metab. 1998;24(5):341-7. doi: 10.1159/000057394.
We evaluated the causal role of glucocorticoid deficiency in the hyponatremia that developed in a 57-year-old Japanese man with hypothyroidism following the performance of a total thyroidectomy for laryngeal cancer. The plasma concentration of vasopressin (1.78 pg/ml) was not suppressed in the presence of hyponatremia (125 mEq/l). The urinary excretion 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 concentration of vasopressin. An oral water load (20 ml/kg of body weight) did not suppress the plasma vasopressin level or induce diuresis. Pretreatment with hydrocortisone normalized the response of plasma vasopressin to the water load was well as the diuretic response during the hypothyroid state. The urinary excretion of 17-hydroxycorticosteroids was below normal in the hypothyroid state in the face of normal serum cortisol concentration. The correction of the hypothyroidism returned these abnormalities to normal. A disturbed metabolism of glucocorticoid may have been responsible for the hyponatremia and disturbance in plasma vasopressin regulation observed in this hypothyroid patient.
我们评估了糖皮质激素缺乏在一名57岁日本男性喉癌患者行全甲状腺切除术后发生甲状腺功能减退伴低钠血症中的因果作用。在低钠血症（125 mEq/l）情况下，血管加压素血浆浓度（1.78 pg/ml）未被抑制。尿钠排泄增加，血浆肾素活性和血浆醛固酮浓度被抑制。输注高渗盐水可增加血浆渗透压，但不增加血管加压素血浆浓度。口服水负荷（20 ml/kg体重）未抑制血浆血管加压素水平或诱导利尿。氢化可的松预处理使血浆血管加压素对水负荷的反应以及甲状腺功能减退状态下的利尿反应恢复正常。在血清皮质醇浓度正常的情况下，甲状腺功能减退状态下17-羟皮质类固醇的尿排泄低于正常水平。甲状腺功能减退的纠正使这些异常恢复正常。糖皮质激素代谢紊乱可能是该甲状腺功能减退患者低钠血症及血浆血管加压素调节紊乱的原因。
