17 ketosteroid reductase deficiency

Gynecomastia is a common adverse effect of bicalutamide (Casodex) therapy that may prompt some men to discontinue prostate cancer treatment. Tamoxifen has been recommended as a preventive agent for gynecomastia in these patients. A double-blind study of 282 men randomized to receive 20 mg of tamoxifen once per day with bicalutamide or bicalutamide alone found that after six months, gynecomastia and breast pain were significantly reduced in men who received tamoxifen ( versus percent in the control group). 41 An Italian randomized controlled trial of 80 participants also found that 20 mg of tamoxifen once per week is as effective as 20 mg once per day. 42

Dehydroepiandrosterone comes into subsequent oxidative transformation with production of 16Alpha-hydroxydehydroepiandrosterone . This oxidation is catalyzed by Cytochrome P450, family 3, subfamily A, polypeptide 7 ( CYP3A7) [10] , [11] , [12] and Cytochrome P450, family 3, subfamily A, polypeptide 4 ( CYP3A4) [13] , [10] , [11] . Oxidative metabolite of this reaction as well as Dehydroepiandrosterone can be further sulfated by steroid sulfatase (microsomal), isozyme S ( STS ) [14] , [15] , [16] , [15] , [14] . Dehydroepiandrosterone and Dehydroepiandrosterone sulfate can be transformed into other compounds with hormonal activity, Androstendiol and Androstendiol sulfate , respectively. These two reactions are catalyzed by Hydroxysteroid (17-beta) dehydrogenase 1 ( HSD17B1) [17] , [18] , [17] , [18] , Hydroxysteroid (17-beta) dehydrogenase 2 ( HSD17B2) [19] , [20] , [20] , [21] , and Hydroxysteroid (17-beta) dehydrogenase 7 ( HSD17B7 ) [22] , [23] , [23] , [24] .

17 ketosteroid reductase deficiency

17 ketosteroid reductase deficiency

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