The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Original Article
PreviousPrevious
Volume 330:460-465 February 17, 1994 Number 7
NextNext

Hyperandrogenism in Polycystic Ovary Syndrome -- Evidence of Dysregulation of 11ß-Hydroxysteroid Dehydrogenase
Andrew Rodin, Hansa Thakkar, Norman Taylor, and Richard Clayton

 Sign up for free e-toc
 

This Article
-Full Text

Commentary
-Letters

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited

More Information
-PubMed Citation
ABSTRACT

Background Hyperandrogenemia is the hallmark of the polycystic ovary syndrome, yet the relative contributions of the adrenal cortex and ovary to the overproduction of androgen remain unclear. To identify possible causes of adrenocortical overactivity, we studied the metabolism of adrenal and ovarian steroid hormones in women with this disorder.

Methods We measured 24-hour urinary excretion of steroid hormone metabolites by high-resolution capillary gas chromatography in 65 women with the polycystic ovary syndrome and 45 normal women matched for body-mass index.

Results After adjustment for body-mass index, the urinary excretion of testosterone and androstenedione metabolites was 1.9 times higher in the women with the syndrome than in the normal women, and the excretion of dehydroepiandrosterone metabolites (C19 steroid sulfates) and cortisol metabolites was 1.5 and 1.3 times higher, respectively (P<0.01 for all comparisons). The affected women also had significantly higher ratios of 11-oxo (oxygenated) metabolites to 11-hydroxy metabolites of cortisol (1.4 times higher, P<0.001) and of 11-oxo to 11-hydroxy metabolites of corticosterone (1.8 times higher, P<0.001). In the group with the polycystic ovary syndrome, 55 percent of the nonobese women and 24 percent of the obese women had ratios above the upper limit of normal; the ratios in the obese women did not differ significantly from those in the nonobese women.

Conclusions Adrenal secretion of cortisol and androgens is increased in women with the polycystic ovary syndrome. The increases may be explained by dysregulation of 11{beta}-hydroxysteroid dehydrogenase causing increased oxidation of cortisol to cortisone, which cannot be accounted for by obesity.


Source Information

From the Division of Biochemical Medicine, St. George's Hospital Medical School (A.R.), the Department of Clinical Biochemistry, the Royal London Hospital (H.T.), and the Department of Clinical Biochemistry, King's College School of Medicine (N.T.), London; and the Department of Endocrinology, North Staffordshire Royal Infirmary, Stoke-on-Trent, United Kingdom (R.C.).

Address reprint requests to Professor Clayton at the Department of Endocrinology, North Staffordshire Royal Infirmary, Hartshill, Stoke-on-Trent ST4 7LN, United Kingdom.

Full Text of this Article


Related Letters:

Hyperandrogenism in Polycystic Ovary Syndrome
Stewart P. M., Edwards C. R.W., Rodin D. A., Clayton R. N.
Extract | Full Text  
N Engl J Med 1994; 331:131-132, Jul 14, 1994. Correspondence

This article has been cited by other articles:



HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  TERMS OF USE  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved.