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"However, complexity arises from the presence of a second 3β-HSD isoform (HSD3B1) coded by a different gene, expressed in the liver and placenta, and unaffected in 3β-HSD-deficient CAH. The presence of this second enzyme has two clinical consequences. First, 3β-HSD II can convert enough of the excess 17α-hydroxypregnenolone to 17α-hydroxyprogesterone to produce 17α-hydroxyprogesterone levels suggestive of common 21-hydroxylase deficient CAH. Measurement of the other affected steroids distinguishes the two. Second, 3β-HSD I can convert enough DHEA to testosterone to moderately virilize a genetically female fetus.[citation needed]
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