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Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome.
It is concluded that women with PCOS should periodically have an OGTT and must be closely monitored for deterioration in glucose tolerance, particularly among those with IGT, the subgroup at highest risk for subsequent development of NIDDM.
Hirsutism: implications, etiology, and management.
The treatment of hirsutism resulting from functional ovarian hyperandrogenism is not as satisfactory; estrogen-progestin treatment is the most useful adjunct to cosmetic approaches to hirsUTism in this country.
Troglitazone improves defects in insulin action, insulin secretion, ovarian steroidogenesis, and fibrinolysis in women with polycystic ovary syndrome.
The ability of the beta-cell to appropriately detect and respond to an oscillatory glucose infusion improved significantly after troglitazone treatment; the normalized spectral power for the insulin secretion rate increased to 5.9 +/- 1.1 and the marked reduction in PAI-1 could be expected to improve the fibrinolytic response to thrombosis in these subjects.
The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited.
Polycystic ovary syndrome seems to arise as a complex trait that results from the interaction of diverse genetic and environmental factors, heritable factors include PCOM, hyperandrogenemia, insulin resistance, and insulin secretory defects.
Evaluation and treatment of hirsutism in premenopausal women: an endocrine society clinical practice guideline.
The Task Force suggests testing for elevated androgen levels in women with moderate or severe hirsutism or hirsUTism of any degree when it is sudden in onset, rapidly progressive, or associated with other abnormalities such as menstrual dysfunction, obesity, or clitoromegaly.
Polycystic ovary syndrome as a form of functional ovarian hyperandrogenism due to dysregulation of androgen secretion.
Patients with the severest cases may have hyperthecosis, a form in which there are no cysts, and those with milder ovarian dysfunction tend to have normal ovarian morphology.
Role of hormones in pilosebaceous unit development.
The biological and endocrinological basis of PSU development and the hormonal treatment of the PSU disorders hirsutism, acne vulgaris, and pattern alopecia are reviewed.
Insulin secretory defects in polycystic ovary syndrome. Relationship to insulin sensitivity and family history of non-insulin-dependent diabetes mellitus.
A history of NIDDM in a first-degree relative appears to define a subset of PCOS subjects with a greater prevalence of insulin secretory defects, which may enhance the risk of developing non-insulin-dependent diabetes mellitus among women with polycystic ovary syndrome.
Ovarian hyperandrogynism as a result of congenital adrenal virilizing disorders: evidence for perinatal masculinization of neuroendocrine function in women.
The hypothesis that congenital adrenal virilization programs the hypothalamic-pituitary axis for hypersecretion of LH at puberty is postulated to frequently cause ovarian hyperandrogenism even when adrenal androgen excess is subsequently controlled by glucocorticoid therapy.
Clinical review: Identifying children at risk for polycystic ovary syndrome.
  • R. Rosenfield
  • Medicine
    The Journal of clinical endocrinology and…
  • 1 March 2007
Identifying children at risk for PCOS offers the prospect of eventually preventing some of the long-term complications associated with this syndrome once the authors' understanding of the basis of the disorder improves.