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Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2004-2217
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The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 8 4797-4802
Copyright © 2005 by The Endocrine Society

Dyslipidemia and Metabolic Syndrome in the Sisters of Women with Polycystic Ovary Syndrome

Susan Sam1, Richard S. Legro1, Rhonda Bentley-Lewis and Andrea Dunaif

Division of Endocrinology, Metabolism, and Molecular Medicine (S.S., A.D.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Obstetrics and Gynecology (R.S.L.), Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033; and Division of Endocrinology, Diabetes, and Hypertension (R.B.-L.), Brigham and Women’s Hospital, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Andrea Dunaif, M.D., 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. E-mail: a-dunaif{at}northwestern.edu.

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 ≤ 0.001) and low-density lipoprotein cholesterol levels (P ≤ 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.




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