Spoudeas H A, Slater J D, Rumsby G, Honour J W, Brook C G
Endocrine Unit, Middlesex Hospital, London, UK.
Clin Endocrinol (Oxf). 1993 Aug;39(2):245-51. doi: 10.1111/j.1365-2265.1993.tb01782.x.
We report a child in whom DOC excess secondary to congenital adrenal hyperplasia (CAH, 11 beta-hydroxylase deficiency) caused malignant hypertension. Clinical and metabolic control could be achieved only by replacement of both glucocorticoid and mineralocorticoid, thus confirming in clinical practice the hypothesis that DOC is produced from both the zonae fasciculata and glomerulosa of the adrenal cortex under the independent control of the ACTH and renin-angiotensin systems respectively.
我们报告了一名儿童，其因先天性肾上腺皮质增生症（CAH，11β-羟化酶缺乏）导致脱氧皮质酮（DOC）过量，进而引发恶性高血压。只有通过同时补充糖皮质激素和盐皮质激素才能实现临床和代谢控制，这在临床实践中证实了以下假说：DOC分别在促肾上腺皮质激素（ACTH）和肾素-血管紧张素系统的独立控制下，由肾上腺皮质束状带和球状带产生。
