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Key Features

  • Puberty is considered precocious in boys if secondary sexual characteristics appear before age 9 years

  • While the frequency of central precocious puberty is much lower in boys than girls, boys are more likely to have an associated CNS abnormality

  • In addition, several types of gonadotropin-independent (peripheral) precocious puberty occur in boys

Clinical Findings

  • Increased linear growth rate and growth of pubic hair are the most common presenting signs

  • Testicular size differentiates central precocity, in which the testes enlarge, from gonadotropin-independent causes, in which the testes usually remain small (< 2 cm in the longitudinal axis)

  • In familial male precocious puberty and HCG-mediated precocious puberty, there may be some testicular enlargement

  • Tumors of the testis are associated with either asymmetric or unilateral testicular enlargement


  • Elevated testosterone levels verify early pubertal status but do not differentiate the source

  • Basal high-sensitivity serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) concentrations will be in the pubertal range in boys with central precocious puberty and the LH response to gonadotrophin-releasing hormone (GnRH) stimulation testing is pubertal

  • Sexual precocity caused by congenital adrenal hyperplasia is usually associated with abnormal plasma adrenal androgens

  • Serum β-HCG concentrations signify the presence of an HCG-producing tumor (eg, CNS dysgerminoma or hepatoma) in boys with precocious puberty and testicular enlargement but suppressed gonadotropins following GnRH testing

  • In all boys with central precocious puberty, cranial MRI should be obtained to evaluate for a CNS abnormality

  • If testing suggests peripheral precocious puberty and laboratory studies are not consistent with congenital adrenal hyperplasia, imaging may be useful in detecting hepatic, adrenal, and testicular tumors


  • Underlying cause should be treated

  • GnRH analogs may be used

  • Boys with McCune-Albright syndrome or familial testotoxicosis can be treated with

    • Agents that block steroid synthesis (ketoconazole)

    • A combination of antiandrogens (spironolactone) and aromatase inhibitors (anastrozole or letrozole) that block the conversion of testosterone to estrogen

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