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Women with polycystic ovary syndrome seek health care for 3 major reasons: infertility, menstrual irregularity, and androgen excess. The infertility is associated with anovulation. The menstrual irregularity is typically chronic, beginning with menarche. Although amenorrhea may sometimes occur, the more common presentation is irregular bleeding characteristic of anovulation. Androgen excess may be manifested by varying degrees of hirsutism. Patients may also report acne. The rapid development of virilizing signs, such as deepening of the voice, increased muscle mass, and temporal balding, should prompt a search for a tumor and lead one away from a diagnosis of polycystic ovary syndrome. Typically treatment is directed at alleviating the symptoms: ovulation induction for infertility, oral contraceptives or a progestin for menstrual irregularity, and oral contraceptives or spironolactone for hirsutism. On the basis of recent epidemiologic data suggestive of increased cardiovascular risk among women with polycystic ovary syndrome, such treatment might be complemented by a long-term approach that addresses the underlying pathophysiology of insulin resistance. (Am J Obstet Gynecol 1998;179:S89-93.)
Polycystic ovary syndrome is characterized clinically by a history of chronic anovulatory bleeding in combination with some evidence of androgen excess, such as hirsutism, acne, elevated serum androgen concentrations, or a combination of these. This clinical definition is reflective of a 1990 National Institutes of Health–National Institute of Child Health and Development consensus conference
in which “definite or probable” criteria for polycystic ovary syndrome included menstrual dysfunction and androgen excess and excluded congenital adrenal hyperplasia and other causes. It is interesting to note that the 58 experts at the National Institutes of Health conference who completed a questionnaire on diagnostic criteria showed poor agreement; no single criterion was endorsed as “definite or probable” by more than 64% of respondents.
Factors such as insulin resistance, elevated ratio of luteinizing hormone (LH) to follicle-stimulating hormone (FSH) and ovaries appearing polycystic on ultrasonography were considered to be “possible” criteria.
In clinical practice, women with polycystic ovary syndrome are seen for 3 major reasons: infertility (mean incidence 74%), menstrual irregularity (mean incidence of dysfunctional bleeding 29%, mean incidence of amenorrhea 51%), and androgen excess (mean incidence of hirsutism 69%, mean incidence of virilization, 21%).
Because polycystic ovary syndrome is typically characterized by oligo-ovulation rather than amenorrhea, women with polycystic ovary syndrome sometimes conceive on their own without ovulation induction. In the absence of other male or female infertility factors, however, a clinically useful working hypothesis for an infertile woman with polycystic ovary syndrome is that the infertility is due to anovulation. Indeed, in 40% of women with polycystic ovary syndrome, infertility is a presenting problem.
Moreover, if ovulation is successfully induced in women with polycystic ovary syndrome, the infertility can be successfully treated: a cumulative pregnancy rate of 80% has been reported after 9 ovulatory cycles.
Although amenorrhea may occur, the more typical presentation is irregular bleeding characteristic of anovulation.
Because progesterone is produced by the ovary only after ovulation, women with polycystic ovary syndrome often have chronic estrogen exposure unopposed by progesterone. Women who have had long-standing chronic anovulation without periodic progestin exposure thus may have endometrial hyperplasia or endometrial cancer. Such women should be evaluated by means of endometrial sampling, uterine ultrasonography, or both.
The androgen excess of polycystic ovary syndrome is usually manifested by varying degrees of hirsutism. Patients may also report acne. Such symptoms are usually associated with serum total testosterone concentrations >60 ng/dL and androstenedione concentrations >200 ng/dL. More advanced signs of androgen excess, such as clitorimegaly and loss of female body contour, can be associated with hyperthecosis. The rapid development of virilizing signs, such as deepening of the voice, increased muscle mass, and temporal balding, should prompt a search for a tumor and lead one away from a diagnosis of polycystic ovary syndrome.
Typically treatment is directed at alleviating the presenting symptoms: ovulation induction for infertility, oral contraceptives or a progestin for menstrual irregularity, and oral contraceptives or spironolactone for hirsutism. On the basis of accumulating epidemiologic data, however, such treatment might ultimately be complemented by a long-term approach that addresses the underlying pathophysiology of insulin resistance by means of insulin-lowering drugs.
The fundamental pathophysiologic defect of polycystic ovary syndrome remains unknown and is a source of controversy and ongoing study. There is a growing consensus, however, that the key features include insulin resistance, androgen excess, and abnormal gonadotropin dynamics.
There is a linear correlation between serum androgen levels and measures of hyperinsulinemia, such as fasting insulin level.
What is the direction of causation in polycystic ovary syndrome? On balance, the weight of the evidence indicates that the direction of causation is from insulin to androgen, rather than the reverse. For example, when androgens are suppressed with a gonadotropin-releasing hormone analog in patients with polycystic ovary syndrome, insulin resistance does not decline.
The prevalence of polycystic ovary syndrome cannot be determined with precision because it depends on the definition. A strict, research-based definition that relies on endocrine characteristics is associated with a 3% prevalence of polycystic ovary syndrome,
Table ILipid profiles in women with polycystic ovary sydrome
Lipid profile (mg/dL)
PCOS (N = 206)
Control (N = 206)
195.4 ± 33.5
185.6 ± 37.8
P = .01
51.1 ± 14.5
57.8 ± 14.5
P < .0001
7.8 ± 6.22
11.7 ± 7.34
P < .0001
118.4 ± 31.5
110.7 ± 34.6
P = .32
129 ± 88.8
85.9 ± 63.4
P < .001
Results are expressed as mean ± SD. Modified with permission from Talbott E, Guzick D, Clerici A, Berga S, Detre K, Weimer K, et al. Coronary heart disease risk factors in women with polycystic ovary syndrome. Arterioscler Thromb Vasc Biol 1995;15:821-6. PCOS, Polycystic ovary syndrome; TC , total cholesterol; HDLT, total high-density lipoprotein; HDL , high-density lipoprotein; LDL , low-density lipoprotein.
An ongoing study of cardiovascular risk in patients with polycystic ovary syndrome, involving >200 patients with polycystic ovary syndrome and control subjects, offers further support to the hypothesis that women with polycystic ovary syndrome are at increased risk for cardiovascular disease.
Patients with polycystic ovary syndrome were found to have an adverse lipid profile after controlling for body-mass index and other potentially confounding variables. Moreover, preliminary data suggest increased intima-media thickness of the carotid artery among patients with polycystic ovary syndrome
; these data have been confirmed in a larger sample, controlling for body mass index and other variables (Talbott E, et al, unpublished data, 1998). Confirmation of cardiovascular risk must be accomplished through prospective cohort studies, with cardiovascular events as end points.
In view of the role of insulin resistance as a fundamental element in the pathophysiology of polycystic ovary syndrome and also of the possible long-term consequences of polycystic ovary syndrome with respect to cardiovascular disease, the use of insulin-lowering drugs in the treatment of polycystic ovary syndrome has begun to be studied. These promising investigations are reviewed elsewhere in this supplement.
Women with polycystic ovary syndrome are typically seen with symptoms of infertility, menstrual irregularity, and androgen excess. The fundamental pathophysiologic defect is not known, but important features include insulin resistance, androgen excess, and altered gonadotropin dynamics. Accumulating evidence suggests the possibility that women with polycystic ovary syndrome may be at increased risk for cardiovascular disease. It will be important to test this hypothesis by means of long-term follow-up of patients with polycystic ovary syndrome with respect to actual cardiovascular events.
Diagnostic criteria for polycystic ovary syndrome: towards a rational approach.