The syndrome of male pseudohermaphroditism secondary to 5α-reductase deficiency is reviewed, as are hormonal evaluation and tissue studies documenting the enzyme deficiency. These studies reveal that the 5α-metabolite dihydrotestosterone is essential for differentiation of the external genitalia and prostate. Studies of male rat fetuses treated with 5α-reductase inhibitors during the critical period of sexual differentiation in utero reveal incomplete masculinization of the external genitalia and impaired prostate growth and development. Thus, conclusive evidence is provided for the hypothesis that 5α-reductase activity and dihydrotestosterone formation are essential for normal differentiation of the male external genitalia and the prostate.

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