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The Pubertal Growth Spurt in Eight Patients with True Precocious Puberty and Growth Hormone Deficiency: Evidence for a Direct Role of Sex Steroids^*

KENNETH M. ATTIE, NELSON R. RAMIREZ, FELIX A. CONTE, SELNA L. KAPLAN and MELVIN M. GRUMBACH

Department of Pediatrics, University of California San Francisco, California 94143-0106

The relative contributions of GH, insulin-like growth factor-I (IGF-I), estradiol, and testosterone to the pubertal growth spurt are incompletely understood. We studied 8 patients (5 girls and 3 boys) with true precocious puberty and GH deficiency due to CNS lesions to assess the role of sex steroids in pubertal growth independent of an increase in circulating GH. Included is 1 patient with an unusual hypothalamic lesion due to head trauma. A control group of 17 GH-sufficient patients with true precocious puberty (13 girls and 4 boys) was matched for chronological age.

The GH-deficient girls grew at a mean velocity of 9.2 cm/yr (range, 7.2–14.4), and the boys' mean height velocity was 7.9 cm/yr (6.1–9.9). Mean bone age was advanced in the GHdeficient group (girls, +2.7 SD; boys, +2.6 SD), but not as much as the GH-sufficient controls (girls, +5.4 SD; boys, +4.3 SD). The mean concentration of plasma IGF-I was lower in the GHdeficient group than in the control group, but was greater than the mean concentration in age-matched prepubertal GH-deficient patients.

Four GH-deficient patients were treated with a potent agonist of LRF. This caused suppression of gonadal sex steroid concentrations and a fall in mean height velocity from 9.1 to 4.3 cm/yr after 1 yr of therapy; however, circulating GH and IGF-I values were not uniformly altered.

We conclude that a substantial pubertal growth spurt can occur in patients with true precocious puberty and GH deficiency that is dependent on gonadal sex steroids yet unaccompanied by normal pubertal levels of circulating GH or IGF-I. Reversal of this growth acceleration is possible with sex steroid suppression. The results, in light of previous in vivo and in vitro studies, suggest that the normal pubertal growth spurt is mediated in part by direct effects of sex steroids at the growth plate.

^* This work was supported in part by a grant from the NICHHD, NIH (R01-HD-02335) and the Pediatric Clinical Research Center (NIH RR-01271). This work was presented in part at the Annual Meeting of the American Pediatric Society and the Society for Pediatric Research, Washington, D.C., May 1988 (Pediatr Res 23:272A, 1988).

Trainee in Pediatric Endocrinology under a program sponsored by the NIDDK, NIH (T32-DK-07161).

To whom all correspondence and requests for reprints should be addressed.

Received October 16, 1986.

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