Endocrinology and metabolism after premature pubarche in girls

The prevalence of functional ovarian hyperandrogenism, hyperinsulinism and dyslipidaemia is increased in adolescent girls with a history of premature pubarche, defined as the appearance of pubic hair before the age of 8 years. The ovarian hyperandrogenism is characterized by clinical signs of androg...

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Bibliographic Details
Published in:	Acta Paediatrica Vol. 88; no. s433; pp. 73 - 77
Main Authors:	Lbáñez, L, Potau, N, Zegher, F De
Format:	Journal Article
Language:	English
Published:	Oxford, UK Blackwell Publishing Ltd 01-12-1999
Subjects:	Birth Weight Child Female Functional ovarian hyperandrogenism Humans hyperinsulinism Insulin Resistance - physiology Insulin-Like Growth Factor I - physiology low birth weight Ovary - physiopathology Polycystic Ovary Syndrome - physiopathology premature pubarche Puberty, Precocious - metabolism Puberty, Precocious - physiopathology
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Summary:	The prevalence of functional ovarian hyperandrogenism, hyperinsulinism and dyslipidaemia is increased in adolescent girls with a history of premature pubarche, defined as the appearance of pubic hair before the age of 8 years. The ovarian hyperandrogenism is characterized by clinical signs of androgen excess and an exaggerated ovarian 17‐hydroxyprogesterone response to gonadotrophin‐releasing hormone aganist stimulation. The hyperinsulinism and dyslipidaemia are detectable before and during pubertal development, and they are commonly accompanied by low serum levels of insulin‐like growth factor binding protein‐1 (IGEBP‐1) and sex hormone binding globulin, and by an increased prevalence of anovulation from late adolescence onwards. In girls, premature pubarche, hyperinsulinism, low serum levels of IGFBP‐1 dyslipidaemia, anovulation and hyperandrogenism (or various combinations of these conditions) have been related to reduced fetal growth, indicating that these constellations or sequences may have a prenatal origin. These findings suggest that premature pubarche in girls should no longer be regarded as meaely a normal variant of development, but rather as a childhood marker pointing to an increased risk of a polyendocrine‐metabolic disorder of prenatal origin.
Bibliography:	istex:A5672CBD86237A649293BB3DFEC0E432FABF15ED ark:/67375/WNG-7D6K2RVL-T ArticleID:APA73
ISSN:	0803-5253 0803-5326 1651-2227
DOI:	10.1111/j.1651-2227.1999.tb14407.x