17β‐Oestradiol, androstenedione and inhibin levels in fluid from individual follicles of normal and polycystic ovaries, and in ovaries from androgen treated female to male transsexuals*
- 1 June 1992
- journal article
- Published by Wiley in Clinical Endocrinology
- Vol. 36 (6) , 565-571
- https://doi.org/10.1111/j.1365-2265.1992.tb02266.x
Abstract
OBJECTIVE The aim was to monitor carefully follicular growth arrest in polycystic ovarles by assay of hormones in individual follicies.DESIGN AND PATIENTS Fluid from follicles < 10 mm was obtained from ovarles of 16 regularly cycling women between days 1 and 12 of the follicular phase (controls, n = 120 follicles), polycystic ovarles of five women with polycystic ovary syndrome (n= 43), and polycystic ovaries from 14 long‐term testosterone treated female to male transsexuals (n= 120).MEASUREMENTS Fluid was assayed for oestradiol, androstenedione, and immunoactive inhibin. Lutelnizing hormone, follicle‐stimulating hormone, and testosterone levels were estimated in serum.RESULTS Median serum LH was lower in transsexuals than in controls (P P P 10 mm could be detected. In the three groups, between‐patient differences in mean oestradiol, androstenedione, Inhibin, and androstenedlone/oestradiol ratio were significantly larger than expected in view of the variation between follicles within individuals. Taking into account this between‐patient difference, no significant differences could be established between the three groups for all endocrine parameters. The percentage of presumed healthy follicles (androstenedlone/oestradiol ratio In vivo in small antral follicles, and the proportion of presumed healthy follicles is not different from that encountered in normal ovaries; (3) oestradlol levels are not different between non‐dominant follicles of normal and polycystic ovaries, suggesting that only enhancement of aromatase activity by FSH may be disrupted In polycystic ovaries, (4) because androstenedione levels are not different comparing follicles of normal and polycystic ovaries, hyperandrogenaemia in the syndrome seems to originate from the abnormally high number of cystic atretlc follicles generally observed in polycystic ovaries; (5) marked variation in the endocrine folllcular microenvironment within and between‐women precludes pooling fluid from several follicles. The authors gratefully acknowledge the technical assistance of Monica Verwoort, Cobie Steenbergen, and their colleagues from the laboratory. They also express their gratitude to Cees Bax for his assistance in data processing. They are grateful to the NICHHD for the gift of the reagents for the INH radioimmunoassay.Keywords
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