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KEY POINTS
■ The etiology of polycystic ovarian syndrome (PCOS) is not understood; however, it is believed to be an intrinsic hypothalamic-pituitary axis abnormality in the ovary that leads to an increased release of gonadotropin releasing hormone (GnRH). This, in turn, stimulates the synthesis and release of a higher level of luteinizing hormone (LH) than follicle-stimulating hormone (FSH). The higher LH:FSH ratio triggers an ovarian production of testosterone, thus increasing free testosterone and contributing to the hyperandrogenism seen in patients with the syndrome.
■ Metabolic syndrome manifests in 43.6% of women with PCOS and is characterized by the presence of three of the following five symptoms: lower HDL levels, higher triglyceride levels, hypertension, hyperglycemia, and increased waist circumference.
■ No single medication treats PCOS as a whole disease; treatment focuses on management of the presenting complications to improve quality of life, increase fertility, and reduce cardiovascular disease risk factors.
■ When developing a treatment plan, consider whether the patient wants a pregnancy. Treatment options are complicated and should be individualized according to patient presentation and desired outcome.
Polycystic ovarian syndrome (PCOS) encompasses much more than ovarian morphology. It also involves hyperandrogenism, oligo-ovulation or anovulation, and multiple metabolic and cardiovascular manifestations. Polycystic ovarian syndrome affects 5% to 10% of women of reproductive age.1 The condition is not only the most common cause of anovulatory infertility in the United States, it can increase the risk of cardiovascular disease (CVD) in those affected.1 PCOS affects 5 to 6 million females in the United States, and an estimated 50% to 75% of cases remain undiagnosed.2 Physician assistants should be aware of the clinical presentation of and the complications associated with PCOS. Treatment can ease many of its manifestations, improve quality of life, and lower the risks for cardiovascular disease.
PATHOPHYSIOLOGY
The etiology of polycystic ovarian syndrome is not understood; however, it is believed to be an intrinsic hypothalamic-
pituitary axis abnormality in the ovary that leads to an increased release of gonadotropin-releasing hormone (GnRH).
This, in turn, stimulates the synthesis and release of a higher level of luteinizing hormone (LH) than follicle-stimulating hormone (FSH).2,3 The higher LH:FSH ratio triggers an ovarian production of testosterone, thus increasing free testosterone and contributing to the hyperandrogenism seen in patients with polycystic ovarian syndrome.2
PCOS-related insulin resistance stimulates androgen excess.3 Research suggests that skeletal muscle is insulin resistant, whereas the ovaries remain sensitive to insulin. The characteristic hyperinsulinemia stimulates an excess of testosterone biosynthesis in the ovaries;4 therefore, the inherent insulin resistance seen with PCOS leads to an increase in circulating androgens via tissue-specific insulin sensitivity.4,5 Finally, insulin inhibits hepatic synthesis of sex-hormone-binding globulin (SHBG), which typically binds free testosterone.2 This inhibition also increases free testosterone levels, and it can exacerbate hirsutism.2
CLINICAL PRESENTATION
Women with PCOS experience a variety of clinical signs and symptoms. Clinical presentation may include chronic menstrual irregularities, infertility, hypertension, obesity, male-pattern alopecia, and slowly progressive hirsutism.3 Hyperandrogenism manifests as treatment-resistant acne and central adiposity; hirsutism as terminal hair growth in a male-pattern distribution; and insulin resistance as acanthosis nigricans and skin tags, although these occur more rarely.2 Patients often do not present with all these clinical signs apparent; some are discovered after further evaluation. Typically, patients seek treatment for a singular complaint of menstrual irregularity, infertility, or hirsutism;6 however, clinical suspicion of PCOS should be high in patients with both menstrual irregularity and signs of hirsutism.
Often, PCOS-related complications have already manifested at presentation because many of them are inherent to the disease pathology.7 Therefore, the patient cannot be fully assessed without considering the role of associated complications in the manifestation of PCOS. Insulin resistance and compensatory hyperinsulinemia are characteristic of the syndrome and appear to be common factors in associated long-term complications, such as a higher risk of developing type 2 diabetes, metabolic syndrome, atherosclerosis, dyslipidemia, and cardiovascular disease.6,7