Talk:Polycystic ovary syndrome

Article Checklist for "Polycystic ovary syndrome"

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References: with notes

Ehrmann DA. Polycystic ovary syndrome.[Review] [144 refs] New England Journal of Medicine. 352(12):1223-36, 2005 Mar 24. UI: 15788499 Several factors contribute to difficulties in the diagnosis of the polycystic ovary syndrome. Presenting signs and symptoms are heterogeneous and vary over time; in addition, a precise and uniform definition of the syndrome has been lacking. An international consensus group [3] recently proposed that the syndrome can be diagnosed after the exclusion of other medical conditions that cause irregular menstrual cycles and androgen excess (Figure 1 and Table 1) and the determination that at least two of the following are present: oligoovulation or anovulation (usually manifested as oligomenorrhea or amenorrhea), elevated levels of circulating androgens (hyperandrogenemia) or clinical manifestations of androgen excess (hyperandrogenism), and polycystic ovaries as defined by ultrasonography. [4] Women with the polycystic ovary syndrome almost always have some aberration in gonadotropin secretion as compared with women who have normal menstrual cycles. [8] However, since gonadotropin concentrations vary over the menstrual cycle and are released in a pulsatile fashion into the circulation, a single measurement of luteinizing hormone and follicle-stimulating hormone provides little diagnostic sensitivity. Thus, in routine clinical practice, abnormal gonadotropin levels (an elevated level of luteinizing hormone or an elevated ratio of luteinizing hormone to follicle-stimulating hormone) need not be documented to diagnose the polycystic ovary syndrome.

Chronic anovulation most often manifests as oligomenorrhea (fewer than nine menses per year) or amenorrhea. Anovulatory cycles may lead to dysfunctional uterine bleeding and decreased fertility. Cutaneous manifestations of hyperandrogenemia in the polycystic ovary syndrome include hirsutism, acne, and male-pattern hair loss (androgenic alopecia), whereas acanthosis nigricans is a cutaneous marker of hyperinsulinemia. No single etiologic factor fully accounts for the spectrum of abnormalities in the polycystic ovary syndrome. In response to stimulation by luteinizing hormone, the ovarian theca cell synthesizes androgens (Figure 2). Androgen biosynthesis is mediated by cytochrome P-450c17, an enzyme with 17(alpha)-hydroxylase and 17,20-lyase activities, both of which are required to form androstenedione. The androgenic steroid is then converted by 17(beta)-hydroxysteroid dehydrogenase (17(beta)-HSD) to form testosterone or is aromatized by the aromatase enzyme (cytochrome P-450arom) to form estrone. Studies performed both in vivo and in vitro (in cultured theca cells) consistently suggest that ovarian theca cells in affected women are more efficient at converting androgenic precursors to testosterone than are normal theca cells. [16,17]

The polycystic ovary syndrome remains one of the most common hormonal disorders in women, with a prevalence estimated between 5 and 10 percent. [20-22] Variance in prevalence among populations may reflect the effect of ethnic origin, race, and other environmental factors on the phenotype. [23,24]

Several lines of evidence suggest that the polycystic ovary syndrome is heritable, [25-29] and various approaches have been initiated to attempt to define a specific genetic cause. [30,31] In rare instances, single-gene mutations can give rise to the phenotype of the syndrome. [32] Current understanding of the pathogenesis of the syndrome suggests, however, that it is a complex multigenic disorder. Candidate genes that may regulate the hypothalamic-pituitary-ovarian axis, as well as those responsible for insulin resistance and its sequelae, have been the principal focus of linkage and case-control studies. Microarray analyses of target tissues in the polycystic ovary syndrome [31] have been used to identify novel candidate genes involved in the condition, and a number of them appear to contribute modestly to the phenotype (Table 2). [30,57,58]

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Lorenz LB. Wild RA. Polycystic ovarian syndrome: an evidence-based approach to evaluation and management of diabetes and cardiovascular risks for today's clinician. [Review] [60 refs] Clinical Obstetrics & Gynecology. 50(1):226-43, 2007 Mar. UI: 17304038

"This review systematically addresses the evidence confirming polycystic ovary syndrome (PCOS) as a cardiovascular health threat. Literature in this area is void of long-term prospective studies to adequately evaluate outcome, but there is important evidence using surrogate markers for future development of and presence of cardiovascular disease and diabetes in women with PCOS. In addition, this article reviews the evidence regarding evaluation and management of cardiovascular risk factors in the population of women with PCOS." "Although previously identified as a cause of abnormal uterine bleeding, the term polycystic ovary syndrome (PCOS) was coined in 1935 after Stein and Leventhal reported 7 women who had amenorrhea, hirsutism, obesity, and multicystic appearing ovaries. Since then, a great deal of investigation has gone into why these women have problems of irregular menses, infertility, and hirsutism."

• "Women with PCOS develop diabetes at higher rates and at younger ages than usual. The metabolic syndrome is very prevalent in women with PCOS" "Diabetes does develop earlier and more frequently in women with PCOS."despite this, unlike diabetics-"Some researchers have noted no higher morbidity or mortality rates from circulatory diseases in women with PCOS." "Because of both the high prevalence of type 2 diabetes and impaired glucose tolerance in women with PCOS, we recommend screening all PCOS women using a fasting and 2-hour oral (75 g) glucose tolerance level."
• "Central obesity associated with PCOS is possibly the single most important risk factor for the development of diabetes and cardiovascular disease."
• "Exercise is of obvious benefit in weight reduction and cardiovascular health. In a small (n=21) longitudinal study comparing homocysteine levels in exercising versus nonexercising women with PCOS, Randeva et al found a significant decline in homocysteine levels at 6 months. Patients who complied with a brisk walking regimen showed declines in homocysteine (10.06±3.22 to 7.36±1.96, P<0.001). Homocysteine levels still remained above normal compared to reference range, however. There was also a significant decrease in waist-to-hip ratio, but no decrease in BMI."
• "The use of oral contraceptives in women with PCOS is widespread, and remains a mainstay in the treatment for hirsutism and to protect the endometrium in patients who are oligoovulatory. Given studies in non-PCOS patients which have shown that oral-contraceptive use can confer a higher risk of myocardial infarction, some have questioned the possible deleterious effects of oral contraceptives on the cardiovascular health of patients with PCOS. Several small studies of oral contraceptive use in women with PCOS show worsening of insulin sensitivity, worsening of glucose tolerance in obese patients (but not in nonobese patients)"
• "The goal is to keep the blood pressure <120/80 through lifestyle approaches. Pharmacotherapy is indicated when blood pressure is >140/90. Pharmacotherapy should be initiated at even lower blood pressure cutoff levels in the setting of target organ damage or diabetes. Thiazide diuretics should be part of the regimen for most patients, unless contraindicated. Angiotensin converting enzyme inhibitors or angiotensin receptor blocker are the drugs of choice for those with the metabolic syndrome and hypertension. These should not be used if pregnancy is contemplated."

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Essah PA. Wickham EP. Nestler JE. The metabolic syndrome in polycystic ovary syndrome. [Review] [109 refs] Clinical Obstetrics & Gynecology. 50(1):205-25, 2007 Mar. UI: 17304037

• "Approximately one-third to one-half of all women and adolescent girls with polycystic ovary syndrome (PCOS) has the metabolic syndrome, associated with increased risk for cardiovascular disease and type 2 diabetes. Evidence suggests that insulin resistance is the likely link between PCOS and the metabolic syndrome."

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Himelein MJ. Thatcher SS. Polycystic ovary syndrome and mental health: A review. [Review] [81 refs] [Journal Article. Review] Obstetrical & Gynecological Survey. 61(11):723-32, 2006 Nov. UI: 17044949

"More recently, researchers compared stress responses among women with PCOS with those of women in 2 other groups: women with functional hypothalamic secondary amenorrhea (FHSA), or psychogenic amenorrhea, and a control group of normally menstruating women (40). The investigators introduced a cognitive stressor, the Stroop Color Word test, and judged its impact by assessing both cognitive performance and physiological indices in participants. Although women with PCOS did not differ from control group women in cognitive response, the stressor did cause a rise in cortisol levels among women with PCOS that was not observed in control group women. However, the FHSA group was most affected by the stressor, significantly differing from the PCOS and control groups on both types of measures. Consequently, evidence for heightened susceptibility to stress among women with PCOS is at best slight."

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Rosenfield RL. Clinical practice. Hirsutism.[see comment]. [Review] [55 refs] [Journal Article. Research Support, N.I.H., Extramural. Review] New England Journal of Medicine. 353(24):2578-88, 2005 Dec 15. UI: 16354894

"Physicians' impressions about hirsutism range from considering it simply a cosmetic problem to assuming it is de facto evidence of excess androgen. The truth lies somewhere in between. Although unwanted hair is often due to an ethnic or familial trait, about half the cases of hirsutism are due to hyperandrogenism."

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