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Hum. Reprod. Advance Access published online on September 9, 2005
Human Reproduction, doi:10.1093/humrep/dei289
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© The Author 2005. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved.
Received April 30, 2005
Revised July 29, 2005
Accepted August 5, 2005

Article

Nicholas A. Cataldo 1*, Fahim Abbasi 2, Tracey L. McLaughlin 3, Marina Basina 3, Patricia Y. Fechner 4, Linda C. Giudice 1, and Gerald M. Reaven 2

1 Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Stanford, CA 94305, USA
2 Division of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
3 Division of Endocrinology, Gerontology and Metabolism, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
4 Division of Endocrinology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA

* To whom correspondence should be addressed.
Nicholas A. Cataldo, E-mail: nixie54{at}yahoo.com


  Abstract

BACKGROUND: Insulin sensitizers have favourable metabolic and ovarian effects in polycystic ovary syndrome (PCOS). This study examined rosiglitazone, a thiazolidinedione, in PCOS. METHODS: In a prospective, open-label study, the effects of rosiglitazone on metabolism and ovarian function were examined in 42 non-diabetic women with PCOS classified according to the National Institute of Child Health and Human Development criteria and insulin resistance (IR) by steady-state plasma glucose (SSPG) 310 mmol/l on octreotide-modified insulin suppression testing. Participants were randomized to rosiglitazone 2, 4 or 8 mg daily for 12 weeks. Endpoints included ovulation and menstrual pattern; serum testosterone, sex hormone-binding globulin (SHBG), and LH; and changes in IR and glucose-insulin responses on 8 h mixed-meal profile. RESULTS: After rosiglitazone 8 mg daily for 12 weeks, SSPG declined and insulinaemia fell by 46%; lower doses gave lesser effects. Serum LH, total and free testosterone were unchanged; SHBG increased. With rosiglitazone, ovulation occurred in 23/42 women (55%), without significant dose dependence. Both before and during treatment, ovulators on rosiglitazone had lower circulating insulin and free testosterone and higher SHBG than non-ovulators. Testosterone declined only in a subgroup of ovulators with early vaginal bleeding after starting rosiglitazone. CONCLUSIONS: Rosiglitazone in insulin-resistant PCOS promoted ovulation and dose-dependently decreased IR and insulinaemia; ovulators had lower circulating insulin and testosterone.

Keywords: hyperandrogenism/insulin resistance/ovulation/polycystic ovary syndrome/rosiglitazone.


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