Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome.
- D. Ehrmann, R. Barnes, R. Rosenfield, M. Cavaghan, J. Imperial
- MedicineDiabetes Care
- 1999
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.
The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited.
- R. Rosenfield, D. Ehrmann
- Biology, MedicineEndocrine reviews
- 26 July 2016
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.
Polycystic ovary syndrome as a form of functional ovarian hyperandrogenism due to dysregulation of androgen secretion.
- D. Ehrmann, R. Barnes, R. Rosenfield
- Medicine, BiologyEndocrine reviews
- 1 June 1995
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.
Hirsutism: implications, etiology, and management.
- R. Hatch, R. Rosenfield, M. Kim, D. Tredway
- Medicine, BiologyAmerican Journal of Obstetrics and Gynecology
- 1 August 1981
Troglitazone improves defects in insulin action, insulin secretion, ovarian steroidogenesis, and fibrinolysis in women with polycystic ovary syndrome.
- D. Ehrmann, D. Schneider, K. Polonsky
- Medicine, BiologyJournal of Clinical Endocrinology and Metabolism
- 1 July 1997
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.
Evaluation and treatment of hirsutism in premenopausal women: an endocrine society clinical practice guideline.
- K. Martin, R. J. Chang, B. A. Swiglo
- MedicineJournal of Clinical Endocrinology and Metabolism
- 1 April 2008
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.
The Diagnosis of Polycystic Ovary Syndrome during Adolescence
- S. Witchel, S. Oberfield, Peter A. Lee
- Medicine, BiologyHormone Research in Paediatrics
- 1 April 2015
While obesity, insulin resistance, and hyperinsulinemia are common findings in adolescents with hyperandrogenism, these features should not be used to diagnose PCOS among adolescent girls.
Role of hormones in pilosebaceous unit development.
- D. Deplewski, R. Rosenfield
- Medicine, BiologyEndocrine reviews
- 1 August 2000
The biological and endocrinological basis of PSU development and the hormonal treatment of the PSU disorders hirsutism, acne vulgaris, and pattern alopecia are reviewed.
Effects of metformin on insulin secretion, insulin action, and ovarian steroidogenesis in women with polycystic ovary syndrome.
- D. Ehrmann, M. Cavaghan, J. Imperial, J. Sturis, R. Rosenfield, K. Polonsky
- Medicine, BiologyJournal of Clinical Endocrinology and Metabolism
- 1 February 1997
It is concluded that hyperinsulinemia and androgen excess in obese nondiabetic women with PCOS are not improved by the administration of metformin.
Ovarian hyperandrogynism as a result of congenital adrenal virilizing disorders: evidence for perinatal masculinization of neuroendocrine function in women.
- R. Barnes, R. Rosenfield, I. Rosenthal
- Medicine, BiologyJournal of Clinical Endocrinology and Metabolism
- 1 November 1994
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.
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