• Polycystic Ovary Disorder
• Lipid Disorders

Dyslipidemia occurs in up to 70% of women with polycystic ovary syndrome (PCOS) in the United States. Tracy Lynn Setji, MD, Duke University Medical Center, Durham, North Carolina, USA, discussed the latest findings on the etiology, screening, and treatments for PCOS. Roughly 60% of women with PCOS are obese and insulin-resistant. At menopause, a woman with PCOS is likely to have had multiple cardiac risk factors for several decades [McGowan MP. Curr Treat Cardiovasc Med 2011].

PCOS is the most common endocrinopathy among women of reproductive age, impacting 5% to 10% of premenopausal American women. Up to 40% of women with the syndrome will develop diabetes by the age of 50 years, and many are dyslipidemic [McGowan MP. Curr Treat Options Cardiovasc Med 2011]. Beyond known alterations in triglycerides and high-density lipoprotein-cholesterol (HDL-C), women with PCOS have higher low-density lipoprotein-cholesterol (LDL-C) and non-HDL-C, regardless of their body mass index (BMI).

A recent systematic review and meta-analysis found that triglyceride levels were 26 mg/dL higher (95% CI, 17 to 35) and HDL-C concentrations 6 mg/dL lower (95% CI, 4 to 9) in women with PCOS than in controls. LDL-C and non-HDL-C concentrations were also higher in PCOS subjects by 12 mg/dL (95% CI, 10 to 16) and 19 mg/dL (95% CI, 16 to 22), respectively [Wild RA et al. Fertil Steril 2011].

Dr. Setji reported that the atherogenic lipoprotein profile is likely related to insulin resistance. The elevation in LDL-C also appears to be due in part to hyperandrogenemia. Free androgen index (FAI), which is associated with increased LDL-C, is improved with administration of flutamide [Gambineri A et al. Clin Endocrinol (Oxf) 2004].

Androgens are involved in the regulation of lipoprotein lipase and hepatic lipase activity (Table 1). While estrogens increase the rate of LDL-C clearance by inducing upregulation of LDL-C receptors, androgens attenuate this process, decreasing catabolic removal of LDL-C [Diamanti-Kandarakis E et al. Trends Endocrinol Metab 2007]. Testosterone administration has significant effects on lipid profiles but not on insulin resistance [Cupisti S et al. Fertil Steril 2010].

Geographic, genetic, and lifestyle factors also affect the severity of dyslipidemia. Studies that compare women with PCOS from the Mediterranean region and the United States highlight these differences. Additionally, within the US, African-American women with PCOS have better lipid profiles than Caucasian women with the syndrome.

According to Wild et al. [Wild RA et al. Fertil Steril 2011], women with PCOS should have a complete lipid profile, with reassessment every 2 years if normal and sooner if significant weight gain occurs (Table 2).

Besides modest increases in LDL-C, with a higher concentration of small, dense LDL-C, dyslipidemia in PCOS is also associated with a reduction in subclass HDL₂. This category contains more cholesterol molecules per unit of alipoprotein than HDL₃ and may put women with the syndrome at higher risk for coronary artery disease [Demacker PN et al. Atherosclerosis 1986]. Some studies also show decreases in apoA-1.

Lifestyle modification is first-line therapy, with low-fat diet and regular moderate-intensity exercise. Even without weight loss, moderate-intensity exercise (at least 30 minutes) a day can improve dyslipidemia in PCOS [Brown AJ et al. Med Sci Sports Exerc 2009].

• © 2011 MD Conference Express