Hyperandrogenism and Hyperinsulinism in Children of Women With Polycystic Ovary Syndrome: A Controlled Study.

Kent, Sarah C.; Gnatuk, Carol L.; Kunselman, Allen R.; Demers, Laurence M.; Lee, Peter A.; Legro, Richard S. Obstetrical & Gynecological Survey. 63(10):646-647, October 2008.


Both hyperandrogenism and insulin resistance are heritable family traits that may cluster in children whose mothers have polycystic ovary syndrome (PCOS). This case control study compared reproductive and metabolic abnormalities in 32 healthy “PCOS children,” 17 girls and 15 boys, and 38 children whose mothers did not have PCOS. The children ranged in age from 4 to 14 years. There were no differences between PCOS and control children in the length of gestation or birth weight.

Urinary levels of luteinizing hormone were significantly lower in Tanner IV-V PCOS girls than in control subjects. Urinary testosterone levels were significantly greater in Tanner II-III PCOS boys than in controls. No significant differences in levels of dehydroepiandrosterone (DHEA) or DHEA sulfate were observed. Fasting insulin levels did not differ significantly between PCOS and control children of either gender, whether saliva or blood samples were analyzed. Nevertheless, mean area-under-the-curve salivary insulin levels were significantly higher in Tanner IV-V PCOS girls in the later stages of puberty than in control children. Five of 15 PCOS children met the de Ferranti criteria for metabolic syndrome, compared to only one of 12 control children. No children in either group met criteria for abnormal fasting blood glucose. Although ovaries tended to be larger in PCOS girls, none of the children examined by transabdominal ultrasonography had evidence of polycystic ovaries based on morphological criteria.

This study suggests that hyperinsulinism may be a familial feature of PCOS children – at least girls – but it does not emerge until the later stages of puberty. It is possible that reproductive abnormalities characteristic of PCOS will develop later in life.

C) 2008 Lippincott Williams & Wilkins, Inc.


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