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Impairment of AVP regulation in 17alpha-hydroxylase deficiency, a unique form of adrenal insufficiency.

Abstract：

:17alpha-hydroxylase deficiency (17alpha-OHDS) results in decreased production of cortisol and sex steroids and hypokalemia secondary to excess mineralocorticoids. It has long been known that glucocorticoid deficiency is associated with impaired urinary dilution and increased secretion of vasopressin (AVP). On the other hand, chronic hypokalemia is a well-established cause of nephrogenic diabetes insipidus. We evaluated the status of AVP secretion in a patient with 17alpha-OHDS and in 8 normokalaemic control subjects during hypertonic saline infusion (5% NaCl 0.06 ml.kg.min.120 min). The patient was evaluated on 3 separate occasions: pre-treatment (PT), and daily treatment with 0.375 mg (T1) and 0.5 mg (T2) dexamethasone. Blood was collected for AVP, corticosterone (B), plasma osmolality (pOsm) and electrolyte determination. In the control group plasma AVP levels increased from 0.8 +/- 0.1 to 4.1 +/- 0.6 pmol/l and pOsm increased from 282 +/- 2 to 302 +/- 11.5 mosmol/kg. In the patient, plasma AVP levels increased from 9.3 to 12.3; 4.5 to 6.2; and 2.5 to 6.2 pmol/l, and pOsm increased from 282 to 302, from 290 to 307, and from 291 to 311 mosmol/kg during the PT, T1 and T2 conditions, respectively. Serum potassium levels were low (2.6 mmol/l) during PT and reached normal values after treatment. There was a significant negative correlation between plasma AVP and serum potassium levels (r=-0.71; p<0.001). The results originally indicate that high plasma AVP levels may be found in 17alpha-OHDS, suggesting an effect of F deficiency per se. In addition, a concealed partial nephrogenic diabetes insipidus secondary to chronic hypokalemia cannot be excluded.

journal_name

J Endocrinol Invest

journal_title

Journal of endocrinological investigation

authors

Leal AM,Elias PC,Moreira AC

doi

10.1007/BF03345089

keywords:

subject

Has Abstract

pub_date

2002-07-01 00:00:00

pages

635-8

issue

7

eissn

0391-4097

issn

1720-8386

pii

5916

journal_volume

25

pub_type

杂志文章

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