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. 2022 May 31;13:906381. doi: 10.3389/fendo.2022.906381

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Copyright © 2022 Edelsztein, Valeri, Lovaisa, Schteingart and Rey

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Serum AMH as a biomarker of intratesticular androgen concentration in boys with central precocious puberty (A) or with gonadotropin-independent precocious puberty (B, C). Serum AMH is low at diagnosis, indicating the inhibitory effect of high androgen concentration reflected in high serum testosterone levels in all cases. When testosterone production is effectively curtailed by the adequate treatment, such as a GnRH analogue in the patient with central precocious puberty (A) or ketoconazole in the patient with gonadotropin-independent precocious puberty (B), Sertoli cells recover their immature status and increase AMH production until treatment is discontinued. Conversely, when adherence to treatment is erratic (C), intratesticular and serum testosterone concentration does not remain at prepubertal levels and Sertoli cells do not revert their pubertal status, which is reflected in low serum AMH. Modified with permission from Rey et al. (48) ^© 1993 The Endocrine Society.