Susan Sam1, Richard S Legro, Rhonda Bentley-Lewis, Andrea Dunaif. 1. Division of Endocrinology, Metabolism, and Molecular Medicine, Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Tarry Building 15-709, Chicago, Illinois 60611-3008, USA.
Abstract
CONTEXT: Dyslipidemia is a feature of polycystic ovary syndrome (PCOS), but its pathogenesis remains controversial. OBJECTIVE: The objective of this study was to test the hypothesis that dyslipidemia is a heritable trait in sisters of women with PCOS. DESIGN: A case-control design was used. SETTING: The study took place at General Clinical Research Centers in four academic medical centers in the United States. PATIENTS: The subjects included 385 sisters of women with PCOS with the following reproductive phenotypes: sisters with PCOS (n = 51), sisters with hyperandrogenemia and regular menses (HA) (n = 38), unaffected sisters (n = 143), and unknown phenotypes (n = 153). One hundred twenty-five control women of comparable age, body mass index, and ethnicity to women with PCOS were included. INTERVENTIONS: Fasting blood was obtained for measurements of lipid profile, reproductive hormones, glucose, and insulin levels. MAIN OUTCOME MEASURES: The main outcome measures included lipid and lipoprotein levels and prevalence of metabolic syndrome. RESULTS: Sisters with PCOS and HA phenotypes had higher total (P < or = 0.001) and low-density lipoprotein cholesterol levels (P < or = 0.01) compared with unaffected sisters and control women. Triglyceride levels were elevated only in sisters with the PCOS phenotype (P < 0.05). The prevalence of metabolic syndrome was increased in sisters with the PCOS (n = 29) and HA (n = 17) phenotypes compared with unaffected sisters (n = 85) (P < 0.001 and P < 0.05, respectively). CONCLUSIONS: Low-density lipoprotein levels are increased in affected sisters of women with PCOS consistent with a heritable trait. The prevalence of metabolic syndrome is increased in affected sisters.
CONTEXT: Dyslipidemia is a feature of polycystic ovary syndrome (PCOS), but its pathogenesis remains controversial. OBJECTIVE: The objective of this study was to test the hypothesis that dyslipidemia is a heritable trait in sisters of women with PCOS. DESIGN: A case-control design was used. SETTING: The study took place at General Clinical Research Centers in four academic medical centers in the United States. PATIENTS: The subjects included 385 sisters of women with PCOS with the following reproductive phenotypes: sisters with PCOS (n = 51), sisters with hyperandrogenemia and regular menses (HA) (n = 38), unaffected sisters (n = 143), and unknown phenotypes (n = 153). One hundred twenty-five control women of comparable age, body mass index, and ethnicity to women with PCOS were included. INTERVENTIONS: Fasting blood was obtained for measurements of lipid profile, reproductive hormones, glucose, and insulin levels. MAIN OUTCOME MEASURES: The main outcome measures included lipid and lipoprotein levels and prevalence of metabolic syndrome. RESULTS: Sisters with PCOS and HA phenotypes had higher total (P < or = 0.001) and low-density lipoprotein cholesterol levels (P < or = 0.01) compared with unaffected sisters and control women. Triglyceride levels were elevated only in sisters with the PCOS phenotype (P < 0.05). The prevalence of metabolic syndrome was increased in sisters with the PCOS (n = 29) and HA (n = 17) phenotypes compared with unaffected sisters (n = 85) (P < 0.001 and P < 0.05, respectively). CONCLUSIONS: Low-density lipoprotein levels are increased in affected sisters of women with PCOS consistent with a heritable trait. The prevalence of metabolic syndrome is increased in affected sisters.
Authors: Erica T Wang; Piera M Cirillo; Chia-Ning Kao; Barbara A Cohn; Marcelle I Cedars Journal: Gynecol Endocrinol Date: 2013-06 Impact factor: 2.260
Authors: C M Ackerman; L P Lowe; H Lee; F Chen; E Hughes; P Cholod; A R Dyer; M G Hayes; B E Metzger; W L Lowe; M Urbanek Journal: J Clin Endocrinol Metab Date: 2010-05-05 Impact factor: 5.958
Authors: Sarah C Kent; Carol L Gnatuk; Allen R Kunselman; Laurence M Demers; Peter A Lee; Richard S Legro Journal: J Clin Endocrinol Metab Date: 2008-02-12 Impact factor: 5.958