Extract

The relative quiescence of the hypothalamic-pituitary-gonadal (HPG) axis before puberty poses a challenge to clinical evaluation of the reproductive system in prepubertal children. During childhood, barring early infancy and puberty, the pituitary gonadotropes are exceptionally sensitive to negative feedback from low doses of sex steroids, and the HPG axis is under tonic central inhibition (1–3). Parturition appears to trigger a brief surge of LH in male neonates that stimulates a transitory rise in testosterone concentrations for about 12 h (4). The secretion of testosterone then rapidly declines, and serum values are indistinguishable from those in females by 24 h of age. The decline in placental and gonadal steroids after birth eliminates sex steroid-mediated inhibition of gonadotropin secretion, leading to activation of the HPG axis at 1–2 wk of age (5–8). With the loss of negative feedback, the increased secretion of FSH and LH stimulates the production of gonadal steroids in a sex-specific profile for several months. Subsequently, the reproductive axis is again tonically suppressed until puberty, with males and females exhibiting differential sensitivity to sex steroid inhibition (1–3). The postnatal surge of reproductive hormones, termed the “minipuberty” of infancy, confirms that the various components of the reproductive system are functional in the newborn, although the HPG axis undergoes further subtle maturational changes before the onset of pubertal maturation.

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