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Premature adrenarche is the most common cause of the early appearance of pubic hair ("premature pubarche") in childhood. In a large proportion of children it seems to be a variation of normal development requiring no treatment. However, there are three clinical issues related to premature adrenarche.
In young females, premature pubarche is generally the first symptom to present. [21] The earliest known diagnosis was in a 6 month old female who developed pubic hair. [47] Additional symptoms include acne, menstrual irregularities and hirsutism in females as well as alopecia in males.
However, premature pubarche may also arise independently of adrenarche. Premature pubarche is a subset of precocious puberty which divide into 1) true precocious puberty that includes complete and central precocious puberty and 2) incomplete puberty which has 3 subsets: premature thelacrche, premature pubarche and isolated menarche. [13]
Individuals with precocious puberty, early adrenarche, and early normal puberty show less stress after treatment compared to individuals without preexisting developmental conditions. [ 46 ] Blockers are also used in the treatment of central precocious puberty resulting from conditions like hypothalamic hamartomas or congenital adrenal ...
Congenital adrenal hyperplasia (CAH) is a group of autosomal recessive disorders characterized by impaired cortisol synthesis. [ 1 ] [ 2 ] It results from the deficiency of one of the five enzymes required for the synthesis of cortisol in the adrenal cortex . [ 3 ]
Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency is an uncommon form of congenital adrenal hyperplasia (CAH) resulting from a mutation in the gene for one of the key enzymes in cortisol synthesis by the adrenal gland, 3β-hydroxysteroid dehydrogenase (3β-HSD) type II ().
Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency is an uncommon form of congenital adrenal hyperplasia (CAH) resulting from a mutation in the gene CYP17A1, which produces the enzyme 17α-hydroxylase. [1] [2] It causes decreased synthesis of cortisol and sex hormones, with resulting increase in mineralocorticoid production.
PWS is characterized by hypogonadism. This is manifested as undescended testes in males and benign premature adrenarche in females. Testes may descend with time or can be managed with surgery or testosterone replacement. Adrenarche may be treated with hormone replacement therapy. [citation needed]