Kinoshita K, Ishida H, Minowada S, Niijima T
Endocrinol Jpn. 1980 Dec;27(6):747-51. doi: 10.1507/endocrj1954.27.747.
We have studied plasma renin activity, the plasma aldosterone level and urinary metabolites of glucocorticoid precursors before and during a dexamethasone suppression test in three non-salt-losers with congenital adrenal hyperplasia due to 21-hydroxylase deficiency, who had never been treated with glucocorticoid. Plasma renin activity, the plasma aldosterone level and urinary pregnanetriol excretion were found to be abnormally elevated before dexamethasone administration. After 7 days' dexamethasone administration, plasma renin activity still remained high above the normal level, while the plasma aldosterone level as well as urinary 17KS and pregnanetriol excretion were lowered to the normal ranges. Several possible mechanisms for this discordant suppression of plasma renin activity and aldosterone level were discussed and the presence of mineralocorticoid resistance, which is not related to ACTH dependent aldosterone antagonists, was suggested in the case of these patients.
我们对三名因21-羟化酶缺乏导致先天性肾上腺皮质增生的非失盐型患者进行了研究,这些患者从未接受过糖皮质激素治疗,研究内容为地塞米松抑制试验前及试验期间的血浆肾素活性、血浆醛固酮水平和糖皮质激素前体的尿代谢产物。在地塞米松给药前,发现血浆肾素活性、血浆醛固酮水平和尿孕三醇排泄异常升高。给予地塞米松7天后,血浆肾素活性仍高于正常水平,而血浆醛固酮水平以及尿17KS和孕三醇排泄降至正常范围。讨论了血浆肾素活性和醛固酮水平这种不一致抑制的几种可能机制,并提示这些患者存在与促肾上腺皮质激素依赖性醛固酮拮抗剂无关的盐皮质激素抵抗。