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Less than 5% of all patients worldwide with CAH have 3-beta–hydroxysteroid dehydrogenase deficiency. In one study of 81 children with ambiguous genitalia, only 2 were found to have 3-beta–hydroxysteroid dehydrogenase deficiency. [10] The incidence is higher in some populations; 3-beta–hydroxysteroid dehydrogenase deficiency is relatively common in the Old Order Amish in North America associated with a HSD3B2 c.35G, a founder mutation. [11] Clinical perspectives in congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase type 2 deficiency. 21OHD and 11OHD impair steroidogenesis in the adrenal glands only [1,2,3, 6, 17]. In contrast, severe form of 3βHSD2D causes defects of steroidogenesis in both adrenal glands and gonads [2, 3, 15]. Figure 2 illustrates the pathophysiology of 3βHSD2D. In case of SW phenotype, 3βHSD2D is usually diagnosed within the first few weeks of life. In case of non-SW phenotype, patients may be diagnosed at any time before puberty [37]. However, the diagnosis has rarely been further delayed and patients can present with gender role related concerns during adulthood [38].
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