Trends in Endocrinology & Metabolism
Insulin Resistance, Premature Adrenarche, and a Risk of the Polycystic Ovary Syndrome (PCOS)
Section snippets
Auxological outcome and pubertal milestones of girls with premature adrenarche
In the absence of enzymatic defects of adrenal steroidogenesis, and according to follow-up results in small groups of patients, the pubertal outcome of girls with premature adrenarche has been reported to be normal (Pang 1984). We undertook a study including 127 girls with isolated premature adrenarche from two European populations with similar ethnic characteristics, of whom 69 had entered puberty, 42 had reached menarche and 38 had attained final height (Ibáñez et al. 1992). Advanced bone age
Ovarian function in girls diagnosed with premature adrenarche
Although data on the auxological outcome appeared to be reassuring, an increased incidence of hirsutism and polycystic ovary syndrome (PCOS) in peripubertal and pubertal premature adrenarche girls, although not well documented, have been pointed out by some authors (Yen 1980Ibáñez et al. 1990).
Premature adrenarche and hyperinsulinemia
Hyperinsulinemia, insulin resistance and adrenal hyperandrogenism are common features both in obese and lean women and adolescents with PCOS and FOH (Lucky et al. 1986Jialal et al. 1987Dunaif et al. 1989Nestler et al. 1989O'Meara et al. 1993Rittmaster et al. 1993Apter et al. 1995Ibáñez et al. 1995bMorales et al. 1996). The defects producing insulin resistance in PCOS appear to be genetic, involving the early steps of insulin receptor-mediated signaling, and are associated with increased
Insulin and the peripubertal onset of PCOS/FOH
Puberty has been associated with increasing fasting and glucose- stimulated insulin concentrations and a decrease in insulin sensitivity (Caprio et al. 1989Amiel et al. 1991Potau et al. 1997). The insulin resistance during puberty is restricted to peripheral glucose metabolism, and is associated with concomitant increases in plasma growth hormone, IGF-I and IGFBP-3 levels and a decrease in IGFBP-1 and SHBG concentrations (Holly et al. 1989Amiel et al. 1991Potau et al. 1997). The transient
Dyslipemia and premature adrenarche
Prospective epidemiological studies suggest that hyperinsulinemia may be an independent risk factor for the development of cardiovascular disease, playing a major role in the genesis of dyslipemia in subjects with both normal and impaired glucose tolerance (Laakso et al. 1990Després et al. 1996). The cluster of highly atherogenic metabolic abnormalities of syndrome X [hyperinsulinemia, glucose intolerance, increased very low-density lipoproteins (VLDL) and triglycerides, decreased high-density
Conclusions
Premature adrenarche is not necessarily a benign condition. Long-term follow-up of these patients is highly recommended owing to the increased incidence of ovarian hyperandrogenism, hyperinsulinemia and dyslipemia. Prospective studies of premature adrenarche girls should be undertaken to clarify the pathogenetic link(s) between hyperandrogenism and hyperinsulinism.
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Central Precocious Puberty Secondary to Adrenocortical Adenoma in a Female Child: Case Report and Review of the Literature
2017, Journal of Pediatric and Adolescent GynecologyCitation Excerpt :Long-term estrogen and androgen exposure in our patient might also be the cause of multicystic ovaries. Multicystic ovaries develop in girls with premature adrenarche who have high androgen levels, and this finding can be clinical evidence of these experimental studies.8 Another issue for discussion is whether the treatment of antiestrogen or aromatase inhibitors should be given to prevent CPP.
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2015, Fertility and SterilityReproductive neuroendocrine dysfunction in polycystic ovary syndrome: Insight from animal models
2014, Frontiers in NeuroendocrinologyCitation Excerpt :A recent study found no effect of prenatal treatment with the insulin sensitizer rosiglitazone on PNA-induced disruptions in estradiol negative and positive feedback (Abi Salloum et al., 2012); however, GnRH/LH pulsatility in intact animals and other aspects of neuroendocrine function remain to be studied following this and similar prenatal interventions. Precocious puberty is a risk factor for PCOS (Ibáñez et al., 2001, 1998), although not all women with PCOS experience this condition. Interestingly, girls exhibiting the combination of low birth weight followed by precocious pubarche are at particular risk for the development of PCOS, and the progression to PCOS in these individuals can be ameliorated by chronic metformin treatment during puberty (Ibáñez et al., 2011, 2004).
Adolescent amenorrhea
2013, Journal de Pediatrie et de PuericultureOntogeny of polycystic ovary syndrome and insulin resistance in utero and early childhood
2013, Fertility and SterilityCitation Excerpt :Therefore, discerning care has to be given to reports involving PCOS adolescents. The origins of childhood insulin resistance and adolescent predisposition to PCOS have been linked to in utero adverse events (55, 56) and premature adrenarche in early childhood (57–60), together with major roles of family history and obesity (61) (Fig. 1). Animal studies, including rodents (62, 63), sheep (64), and monkeys (8, 19), repeatedly demonstrate how fetal T excess, possibly accompanying gestational hyperglycemia and hyperinsulinemia (65), determines a variety of PCOS-like phenotypes in adulthood, including the diversity encompassed by the “Rotterdam consensus” criteria (66).
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