Clinical OpinionInduction of ovulation in infertile women with hyperandrogenism and insulin resistance☆,☆☆
Section snippets
Identification of unique phenotypes and genotypes in PCOS
It is likely that many unique reproductive disease processes cause both hyperandrogenism and anovulation (PCOS). A major goal of gynecologic endocrinology is to discover the many genes that influence the development of hyperandrogenism and anovulation in women and to understand the influence of environment in the development of PCOS. It is unlikely that substantial progress can be made in our understanding of the pathogenesis of PCOS if it is viewed as a single homogeneous disease with a single
How can clinicians detect insulin resistance and hyperinsulinemia
There is no clear consensus on how to detect insulin resistance and hyperinsulinemia. Laboratory tests that have been proposed to be useful in detecting insulin resistance include fasting insulin concentration, fasting glucose-to-insulin ratio, glucose or insulin response to an oral or intravenous glucose challenge, glucose response to an intravenous injection of insulin, and glucose-insulin clamp studies (eg, euglycemic hyperinsulinemic clamp). A major problem is that the least
Treatment of anovulation in infertile hyperandrogenic and insulin-resistant women
For the clinician a therapeutic imperative is to prescribe focused treatments that are based on the unique disease processes of each patient. It is probable, as the therapeutic armamentarium evolves, that each unique cause of hyperandrogenism and anovulation will be treated with focused and specific interventions. Although the concept has not been directly tested in clinical trials, women with PCOS who are lean, have a markedly elevated LH concentration, and have normal insulin and glucose
Use of metformin for ovulation induction
A hypothesis that is central to this Clinical Opinion article is that infertile anovulatory women with PCOS and no evidence of insulin resistance are not likely to ovulate when given an insulin sensitizer. It is likely that women with insulin resistance are more likely to respond to treatment with an insulin sensitizer. This hypothesis has not been directly tested in a clinical trial. Metformin may best be utilized as part of a stepwise approach to ovulation induction in infertile women with
References (25)
- et al.
Androgen and insulin response to an oral glucose challenge in hyperandrogenic women
Fertil Steril
(1987) - et al.
Hyperandrogenism, insulin resistance and acanthosis nigricans syndrome. A common endocrinopathy with distinct pathophysiologic features
Am J Obstet Gynecol
(1983) - et al.
Effect of body weight reduction on plasma androgens in obese infertile women
Fertil Steril
(1982) - et al.
Endocrine consequences of weight loss in obese, hyperandrogenic, anovulatory women
Fertil Steril
(1994) - et al.
The management of non-insulin dependent diabetes during pregnancy
Diabetes Res Clin Pract
(1986) - et al.
Metformin therapy improves the menstrual pattern with minimal endocrine and metabolic effects in women with polycystic ovary syndrome
Fertil Steril
(1998) - et al.
Effects of metformin on gonadotropin induced ovulation in women with polycystic ovary syndrome
Fertil Steril
(1999) - et al.
Effect of troglitazone on endocrine and ovulatory performance in women with insulin resistance–related polycystic ovary syndrome
Fertil Steril
(1999) - et al.
Pregnancy after treatment with the insulin-sensitizing agent troglitazone in an obese woman with the hyperandrogenic, insulin-resistant acanthosis nigricans syndrome
Fertil Steril
(1999) - et al.
The role of hyperinsulinemia in the pathogenesis of ovarian hyperandrogenism
Fertil Steril
(1988)
Hyperfunction of the hypothalamic-pituitary axis in women with polycystic ovary disease: indirect evidence for partial gonadotroph desensitization
J Clin Endocrinol Metab
Some genetic syndromes associated with hyperandrogenism
Contemp Ob Gyn
Cited by (0)
- ☆
Supported in part by grant HD-29164 from the National Institutes of Health.
- ☆☆
Reprint requests: Robert L. Barbieri, MD, Department of Obstetrics, Gynecology and Reproductive Biology, Brigham and Women’s Hospital, ASB1-3, 75 Francis St, Boston, MA 02115. E-mail: Rbarbieri@ partners.org.