The Response of Pituitary Gonadotropes to Synthetic LRF in Children with Glucocorticoid-Treated Congenital Adrenal Hyperplasia: Lack of Effect of Intrauterine and Neonatal Androgen Excess

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Abstract
Previous studies have demonstrated that the secretory reserve of the pituitary gland during childhood and adolescence is characterized by an age-related increase in LH secretion and a sex dichotomy of FSH secretion evoked by LRF. To determine if prenatal and neonatal androgen excess alters hypothalamic-pituitary-gonadal function, as in the neonatally androgenized rodent, we assessed pituitary sensitivity to 100 μg synthetic LRF in 9 girls and 2 boys with glucocorticoid-treated congenital virilizing adrenal hyperplasia (CAH). In the 7 prepubertal girls with CAH, plasma LH following LRF rose to 2.0 ± 0.4 (se) ng/ml (LER 960) and did not differ from normal prepubertal children (1.7 ± 0.1) and was lower (P < 0.002) than in normal pubertal children (4.9 < 0.3). The 2 pubertal girls had LH rises in the pubertal range. In the 2 boys with CAH, the one with the more advanced boneage, 11-6/12 yr, developed true precocious puberty following initiation of cortisone treatment and had a pubertal LRF-evoked LH release on 3 occasions; the more immature boy, bone age 10, had a prepubertal LH rise. In the 7 prepubertal girls with CAH, plasma FSH rose to 8.1 < 1.6 (se) ng/ml (LER 869), which did not differ from normal prepubertal girls (5.3 < 1.9), but was significantly (P < 0.001) greater than in normal prepubertal boys (2.9 ± 0.4). In these girls with CAH, basal plasma T (27.4 ± 4.0 (se) ng/dl) and 17-OHP (2703 ± 1143 (se) ng/dl) were greater than in prepubertal children, but plasma E1 and E2 were in the normal range. The pubertal boy had plasma T, E1; and E2 levels appropriate for his degree of sexual maturation. The results suggest: (1) age-related LH secretione voked by LRF in glucocorticoid-treated CAH is appropriate for skeletal maturation; (2) the sex dichotomy of FSH secretion following LRF is preserved in CAH despite intrauterine and variable postnatal exposure to excess androgen and continuing slightly elevated plasma T during childhood; and (3) precocious puberty may follow initiation of cortisone treatment in a child with CAH whose bone age and secretory reserve of pituitary gonadotropins are in the pubertal range.

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