Koide Y, Oda K, Shimizu K, Shimizu A, Nabeshima I, Kimura S, Maruyama M, Yamashita K
Endocrinol Jpn. 1982 Jun;29(3):363-8. doi: 10.1507/endocrj1954.29.363.
A 45-year-old woman with myxedema coma due to primary hypothyroidism manifested hyponatremia, impaired water excretion, and elevated urine osmolarity as well as natriuresis suggestive of a syndrome of inappropriate antidiuretic hormone secretion. However, plasma vasopressin was undetectable or very low and plasma aldosterone levels were suppressed in the presence of hyponatremia. Subsequent replacement therapy with levothyroxine caused a rapid decline in sodium clearance which was independent of the change in glomerular filtration rate, and corrected the impaired water excretion and hyponatremia. Plasma vasopressin levels returned to the normal range after the correction of hyponatremia. Thus, the results indicate that neither vasopressin nor aldosterone plays a dominant role in the pathogenesis of the hyponatremia in this patient. It appears that thyroid hormone deficiency itself caused the derangement of tubular cell function, which resulted in the development of the impaired water excretion and hyponatremia.
一名因原发性甲状腺功能减退症导致黏液性水肿昏迷的45岁女性,表现为低钠血症、排水功能受损、尿渗透压升高以及钠利尿,提示抗利尿激素分泌不当综合征。然而,血浆血管加压素检测不到或非常低,且在低钠血症情况下血浆醛固酮水平受到抑制。随后用左甲状腺素进行替代治疗导致钠清除率迅速下降,这与肾小球滤过率的变化无关,并纠正了排水功能受损和低钠血症。低钠血症纠正后,血浆血管加压素水平恢复到正常范围。因此,结果表明血管加压素和醛固酮在该患者低钠血症的发病机制中均不发挥主导作用。甲状腺激素缺乏本身似乎导致了肾小管细胞功能紊乱,进而导致排水功能受损和低钠血症的发生。