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Sexual Precocity in Boys: Accelerated Versus Slowly Progressive Puberty Gonadotropin-Suppressive Therapy and Final Height

Institute for Endocrinology and Diabetes, Schneider Children’s Medical Center of Israel, Petah Tiqva 49202, Israel; and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel

Address all correspondence and requests for reprints to: M. Phillip, M.D., Institute for Endocrinology and Diabetes, Schneider Children’s Medical Center of Israel, 14 Kaplan Street, Petah Tiqva 49202, Israel.

Abstract

The indication for GnRH analog treatment in boys with central sexual precocity is based mainly on the age of onset of puberty. Our aim was to determine whether the rate of pubertal progression should also be taken into consideration.

Included in the study were 81 boys with central sexual precocity: 27 with true precocious puberty (onset at <9 yr) and 54 with early puberty (onset at 9–10.5 yr). At the time of analysis, all had completed puberty, and 66 (22 central precocious puberty, 44 early puberty) had achieved final height. Progression of puberty (Tanner stage 2 to 3) was accelerated (0.5–1.32 yr) in 42 boys (16 central precocious puberty, 26 early puberty) and slow (1.7–2.9 yr) in 39 (11 central precocious puberty, 28 early puberty). The boys with accelerated puberty had significantly elevated T levels (central precocious puberty and early puberty, P < 0.001), faster growth rate (change in height SD score/duration: central precocious puberty, P < 0.05; early puberty, P < 0.01), and faster bone maturation rate (change in bone age/duration: central precocious puberty, P < 0.05; early puberty, P < 0.001). All 42 boys with accelerated puberty were treated with GnRH analog for 2.3–4.2 yr; the duration to completion of puberty and the height gain after therapy was discontinued were similar for the boys with central precocious puberty and early puberty. The 39 boys with slow puberty received no treatment and had a prolonged course of puberty (central precocious puberty, 5.05 ± 0.3 yr; early puberty, 4.72 ± 0.77 yr; average normal, 3.5 yr). The final height achieved in the 35 (11 central precocious puberty, 24 early puberty) untreated boys was within the range of their respective target height. The 31 (11 central precocious puberty, 20 early puberty) treated boys also achieved their genetic target height. Predictions based on the Bayley-Pinneau method at Tanner stage 3 for all boys and at discontinuation of therapy for treated boys overestimated the achieved final height (P < 0.001).

In conclusion, boys with sexual precocity, whether central precocious puberty or early puberty, may have either accelerated or slow pubertal development. The decision to institute suppressive therapy should be based also on the rate of pubertal progression. Treatment should be offered only to those (either central precocious puberty or early puberty) with accelerated growth and bone maturation rates and rapid increase in T levels. Suppression therapy apparently converts accelerated puberty into nonsustained slow puberty and probably prevents compromised final height.

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