GYNECOMASTIA in prepubertal children usually results from an increase in endogenous estrogen production. Estrogen biosynthesis involves the transformation of steroid precursors to androgens and then conversion of androgens to estrogens by the enzyme aromatase. Excessive production of estrogen may result from an increase in levels of endogenous substrate, aromatase activity, or both. A model for the isolated increase in aromatase activity is the Sebright Bantam rooster, in which the aromatase activity is increased 100-fold.1 A human counterpart of the Sebright Bantam rooster has also been described in which increased aromatase activity resulted in the overproduction of estradiol and gynecomastia.2 , 3 In. . .
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