Abstract

Precocious puberty is the development of secondary sexual characteristics before the age of 8 years in girls (onset of thelarche) and 9 years in boys (increase in testicular volume). 1 Clinical and biochemical assessment is directed at determining whether the underlying process is gonadotrophin-dependent (central precocious puberty (CPP)), associated with activation of the hypothalamic-pituitary-gonadal (HPG) axis, or gonadotrophin-independent (peripheral precocious puberty (PPP)) which is characterised by elevated sex steroids but low gonadotrophin levels. Although less common, the clinical consequences of PPP are no less severe, and the diagnosis is crucial to ensure appropriate management. 2 The inherited forms of PPP include non-salt wasting forms of Congenital Adrenal Hyperplasia, McCune-Albright Syndrome (MAS) and familial male-limited precocious puberty. Acquired PPP occurs secondary to exposure to endogenous (eg. adrenal, gonadal or other malignancies) or exogenous sex steroids. 3 We present cases of siblings with virilisation from transdermal exposure to 'bioidentical' testosterone (bioT).

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