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3-Beta–hydroxysteroid dehydrogenase (3BHSD) deficiency is a rare genetic disorder of steroid biosynthesis that results in decreased production of all 3 groups of adrenal steroids, which include mineralocorticoids, glucocorticoids, and sex steroids. 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. Much heterogeneity is observed in the clinical presentation of this disorder. Although first described in male infants with ambiguous genitalia and severe salt wasting, 3-beta–hydroxysteroid dehydrogenase deficiency also occurs in 46,XX female infants (who may have mild clitoromegaly), as well as in older patients who present with a milder or so-called late-onset variant. [1] Anatomically, the adrenal gland can be divided into 3 zones, (1) the zona glomerulosa, which predominately produces mineralocorticoid, (2) the zona fasciculata, which predominately produces glucocorticoid, and (3) the zona reticularis, which predominantly produces androgens. Think of the zona glomerulosa and the zonae fasciculata and reticularis as 2 separate endocrine organs because they are under separate control. Aldosterone (mineralocorticoid) synthesis and secretion is regulated via the renin-angiotensin system, which is responsive to the state of electrolyte balance and the plasma volume. Aldosterone secretion is also directly stimulated by high serum potassium concentrations.
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