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Serum 11 β-Hydroxyandrostenedione as an Indicator of the Source of Excess Androgen Production in Women with Polycystic Ovaries^*

Departments of Obstetrics and Gynaecology and Chemical Pathology (M.J.R., M.J.S., V.H.T.J.), St. Mary’s Hospital Medical School London, W2 1PG United Kingdom

Address all correspondence and requests for reprints to: Dr. M. J. Reed, Department of Chemical Pathology, St. Mary’s Hospital Medical School, London, W2 1PG United Kingdom.

Serum 11β-hydroxyandrostenedione levels (11-OHA) were measured in normal women and women with polycystic ovaries (PCO) to assess their value in localizing the source of excessive androgen production in women with PCO. Serum 11-OHA was undetectable (<1.5 nmol/L) in an adrenalectomized woman, a woman with 11-hydroxylase deficiency, and a woman receiving chronic dexamethasone therapy, confirming the specificity of the antiserum used in this study. Serum 11-OHA concentrations were similar in normal women [mean, 5.0 ± 2.3 (±SD) nmol/L] and women with PCO (5.0 ± 2.1 nmol/L); serum androstenedione concentrations were increased in women with PCO. Thus, the ratio of androstenedione to 11-OHA was significantly higher (P < 0.001) in women with PCO (2.0 ± 0.7) than in normal women (1.1 ± 0.5). Serum 11-OHA levels after adrenal suppression or stimulation were similar in women with PCO who had an ovulatory response and those who failed to ovulate after clomiphene administration.

Administration of dexamethasone (1 mg) and injection of ACTH (250 µg) were associated with marked suppression and subsequent stimulation of serum 11-OHA levels in both normal women and women with PCO, and the responses were similar in the two groups. Also, the hour to hour and diurnal variations in serum 11-OHA were similar to those of androstenedione and cortisol during a 24-h period, indicating the adrenal origin of 11-OHA.

Our finding of similar serum 11-OHA levels in the presence of increased serum androstenedione levels in women with PCO supports the concept that the ovary is the major source of excess androgen production in women with PCO.

^* This work was supported by a grant from Sandoz (Basel, Switzerland).

Received May 28, 1987.

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