Yura T, Takamitsu Y, Yuasa S, Miki S, Takahashi N, Bandai H, Sumikura T, Uchida K, Kiyomoto H, Matsuo H
Second Department of Internal Medicine, Kagawa Medical School, Japan.
Nihon Jinzo Gakkai Shi. 1990 Jul;32(7):829-33.
We report a case of 47-year-old woman with an isolated deficiency of adrenocorticotropic hormone. She was admitted complaining of fatigue and frequent loss of consciousness. The patient developed severe hyponatremia (100 mEq/l) after five days of the admission. Her plasma renin activity and plasma aldosterone concentration were low though she was dehydrated. After the treatment of dehydration, plasma osmolality was low but high plasma antidiuretic hormone (ADH) level sustained. Both high urinary sodium excretion and low urinary aldosterone excretion still remained after one month of replacement therapy with prednisolone. But, glomerular filtration rate and a response of urinary volume to acute water loading were normalized. These results suggested that severe hyponatremia of the patient was caused by an inappropriate secretion of ADH and suppression of renin-aldosterone system. We consider the suppression of renin-aldosterone system was partially independent of an inappropriate secretion of ADH.
我们报告一例47岁女性孤立性促肾上腺皮质激素缺乏症。她因疲劳和频繁意识丧失入院。入院五天后患者出现严重低钠血症(100 mEq/l)。尽管她处于脱水状态,但其血浆肾素活性和血浆醛固酮浓度较低。脱水治疗后,血浆渗透压较低,但血浆抗利尿激素(ADH)水平持续升高。泼尼松龙替代治疗一个月后,尿钠排泄仍高而尿醛固酮排泄仍低。但是,肾小球滤过率以及尿量对急性水负荷的反应恢复正常。这些结果提示患者严重低钠血症是由ADH分泌不当和肾素-醛固酮系统受抑制所致。我们认为肾素-醛固酮系统受抑制部分独立于ADH分泌不当。