Cardiometabolic abnormalities in the polycystic ovary syndrome: Pharmacotherapeutic insights

Department of Internal Medicine, University Medical Center Utrecht, The Netherlands.
Pharmacology [?] Therapeutics (Impact Factor: 9.72). 07/2008; 119(3):223-41. DOI: 10.1016/j.pharmthera.2008.04.009
Source: PubMed


The polycystic ovary syndrome (PCOS) affects 5-10% of all premenopausal women. It is diagnosed by a combination of oligo-amenorrhea and hyperandrogenism (NIH criteria) or by the presence of two out of three of: oligo-amenorrhea, hyperandrogenism, polycystic ovaries on ultrasound (Rotterdam criteria). PCOS is associated with obesity, insulin resistance and dyslipidemia. Different patterns of dyslipidemia can be present, both in lean and obese PCOS. Low HDL-cholesterol, with or without elevated TG, is the most prominent lipid abnormality. In addition, smaller HDL and LDL particles and elevated postprandial TG responses are reported. Hyperandrogenism, anovulation and insulin resistance affect multiple steps in lipid metabolism in PCOS, as will be discussed. Surrogate markers for atherosclerosis are consistently abnormal in PCOS, while studies on clinical CVD endpoints are limited and non-conclusive. The (pharmaco-) therapy of dyslipidemia in PCOS will be discussed. In addition, the effects of other PCOS related (pharmaco-) therapies, primarily aimed at hyperandrogenism, anovulation or insulin resistance, on lipid metabolism will be addressed.

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    ABSTRACT: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women, characterized by anovulation, hyperandrogenism and polycystic ovaries at ultrasonography. In addition to its reproductive consequences, PCOS is associated with metabolic abnormalities of which altered sensitivity to insulin appears to play a pivotal role in the development of the disorder. Currently, PCOS is considered to be a developmental disorder with varying clinical presentations depending on age. This review provides an overview of the manifestations associated with PCOS from preconception until the post-reproductive years.
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    ABSTRACT: Background: Evidence regarding endothelial function in both obese and nonobese women with PCOS is contradictory. It is unknown whether obese women with PCOS carry an increased risk related to body mass index (BMI).Aim: To identify endothelial function and investigate its relationship to body mass index and insulin resistance in young women with PCOS.Subjects and methods: Twenty-two obese women with PCOS (BMI 35.2 ± 3.2) as well as fourteen lean women (BMI 22.8 ± 2.1)with PCOS were included in the study. Fasting serum insulin, blood glucose were estimated and HOMA and Quicki index were calculated. All patients were subjected to ultrasound recording of brachial artery diameter at rest and after reactive hyperemia (FMD) for assessment of endothelial function. Ten age matched healthy females with normal BMI were chosen as a control group.Results: There were higher basal insulin levels with lower Quicki index and higher HOMA index in women with PCOS than normal group, but the differences were significant only between obese PCOS subgroup and control. On the other hand, FMD was significantly and equally decreased in both groups of women with PCOS, compared with control subjects (3.7 ± 3.2% in the nonobese subgroup and 3.5 ± 2.8% in the obese one vs. 10.6 ± 4.1% in control subjects, P, 0.001). FMD was not correlated with BMI nor insulin resistance indices.Conclusions: Endothelial dysfunction is already present in young women with PCOS. In this patient group, it cannot be attributed to insulin resistance or obesity.
    Obesity Research & Clinical Practice 01/2010; 4(1):e1-e82. DOI:10.1016/j.orcp.2009.08.001 · 1.18 Impact Factor
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