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. 2005 Aug;90(8):4797-802.
doi: 10.1210/jc.2004-2217. Epub 2005 May 17.

Dyslipidemia and metabolic syndrome in the sisters of women with polycystic ovary syndrome

Affiliations

Dyslipidemia and metabolic syndrome in the sisters of women with polycystic ovary syndrome

Susan Sam et al. J Clin Endocrinol Metab. 2005 Aug.

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.

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Figures

Fig. 1
Fig. 1
Sisters with the PCOS and HA phenotypes had significantly higher (***, P ≤ 0.001) total cholesterol levels compared with unaffected sisters (UA) and control women (top left). Total triglyceride levels were significantly higher (*, P < 0.05) in sisters with the PCOS phenotype compared with sisters with the HA phenotype, unaffected sisters, and control women (top right). Sisters with the PCOS and HA phenotypes had significantly higher (**, P ≤ 0.01) LDL levels compared with unaffected sisters and control women (bottom left). HDL cholesterol levels did not differ significantly among the groups (bottom right). Black bars, Sisters with PCOS phenotype; gray bars, sisters with HA phenotype; white bars, unaffected sisters; and hatched bars, control women. To convert total, LDL, and HDL cholesterol to millimoles per liter, multiply by 0.02586; to convert total triglyceride to millimoles per liter, multiply by 0.01138.
Fig. 2
Fig. 2
Sisters with PCOS (n = 29) and HA (n = 17) phenotypes had significantly higher (***, P < 0.001 for PCOS vs. unaffected sisters; *, P < 0.05 HA vs. unaffected sisters) prevalence of metabolic syndrome compared with unaffected sisters (n = 85). There was a trend toward higher (P = 0.07) prevalence of metabolic syndrome in sisters with PCOS phenotype compared with sisters with HA phenotype. Black bars, Sisters with PCOS phenotype; gray bars, sisters with HA phenotype; white bars, unaffected sisters.
Fig. 3
Fig. 3
The prevalence of metabolic syndrome was significantly higher (*, P < 0.05) in overweight affected sisters (PCOS and HA phenotypes, n = 14) compared with unaffected sisters (n = 23). There was a trend toward higher (P = 0.07) prevalence of metabolic syndrome in obese affected sisters (n = 25) compared with unaffected sisters (n = 18). Black bars, Affected sisters; white bars, unaffected sisters.

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