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CLINICAL REVIEW 14 Pathophysiology and Treatment of Sexual Precocity

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

Address requests for reprints to: Selna L. Kaplan, M.D., Ph.D., Department of Pediatrics, University of California, San Francisco, San Francisco, California 94143-0434.

The complex maturational changes in both organization and activation of the hypothalamic GnRH-pituitary gonadotropin-gonadal system can be viewed as a continuum extending from its ontogeny in the fetus, through puberty, to the attainment of full sexual maturation and fertility. Restraint of the onset of puberty resides in the central nervous system (1, 2). All of the other components which include the hypothalamic GnRH pulse generator, pituitary gland, gonads, and sex steroid target organs can be activated by the appropriate stimulus at any stage between infancy and the normal age of puberty. Reactivation of the GnRH pulse generator induces increased GnRH secretion, stimulation of the pituitary gonadotropes, and subsequently increased secretion of gonadal steroids. Increased nighttime pulsatile release of LH both in frequency and amplitude and increased LH response to administration of GnRH occur with the onset of puberty. An independent process regulated by a different mechanism results in the increase in adrenal androgen secretion 2 yr before reactivation of the hypothalamic GnRH pulse generator (1).

^* This work was supported in part by a grant from NICHHD, NIH (R01-HD-02335), and the Pediatric Clinical Research Center (NIH RR-01271).

Received April 10, 1990.

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