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Bars indicate SD. 3-Beta–hydroxysteroid dehydrogenase (3BHSD) deficiency is a rare form of congenital adrenal hyperplasia that results in decreased production of all 3 groups of adrenal steroids: mineralocorticoids, glucocorticoids, and sex steroids. In severely affected individuals, decreased mineralocorticoid secretion results in varying degrees of salt wasting in both males and females, and deficient androgen production results in ambiguous genitalia in 46,XY males. This condition is due to defects in type II 3-beta–hydroxysteroid dehydrogenase, an enzyme that occurs almost exclusively in the gonads and adrenal glands. A variety of mutations in the HSD3B2 gene affect the activity of this enzyme, resulting in the extremely variable, phenotypic presentations of 3-beta–hydroxysteroid dehydrogenase deficiency. Older patients with mild defects in 3-beta–hydroxysteroid dehydrogenase activity (late-onset or nonclassic variant) may present with premature pubic hair development, hirsutism, irregular menstrual cycles or primary amenorrhea. Patients with classic salt-losing 3-beta–hydroxysteroid dehydrogenase require initial replacement of glucocorticoids and mineralocorticoid, plus the addition of sex steroids at appropriate, pubertal age. Prognosis is usually good-to-excellent with adequate replacement (as needed) of glucocorticoids, mineralocorticoid, and sex steroid therapy, monitoring and follow-up. Palpites de jogos.
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