To ascertain if androgen insensitivity causes severe oligospermia or azoospermia we studied three unrelated, phenotypically normal men with long histories of infertility. The mean plasma concentrations and production rates of testosterone were 14.3 ng per milliliter and 10.1 mg per day, respectively, values approximately twice the average found in normal men. Serum luteinizing hormone concentrations were elevated in two of the three subjects. The specific high-affinity dihydrotestosterone binding capacity of cultured genital-skin fibroblasts was 8, 0 and 10 fmol per milligram of cellular protein, values half (or less) of those from normal men and women but similar to values in subjects with partial androgen insensitivity manifested by incomplete testicular feminization or Reifenstein syndrome. The low amount of androgen receptor and the combination of high serum gonadotropins and plasma testosterone production rates suggest that the defective spermatogenesis in these infertile men was the consequence of androgen insensitivity.

A B S T R A C T 17f3-estradiol

A B S T R A C T Previous studies have suggested that dihydrotestosterone accumulation in the prostate may be involved in the pathogenesis of prostatic hyperplasia in man and dog. However, the fact that the administration of 10 mg dihydrotestosterone/d to castrated, mongrel dogs (0.5 mg/kg body wt) causes little growth in the prostate, whereas identical doses of 3a-androstanediol regularly induce prostatic hyperplasia (>14 g weight) has raised the possibility that the dihydrotestosterone accumulation may be the result rather than the cause of the pathology. To investigate the mechanism of this phenomenon, we measured the levels of dihydrotestosterone and 3a-androstanediol in prostates from 75 dogs. In both naturally occurring and 3a-androstanediol-induced prostatic hyperplasia, the levels of dihydrotestosterone were high (>5 ng/g), whereas in immature glands and glands from dihydrotestosterone-treated animals, levels were similar (2.1 and 2.6 ng/g, respectively). 3a-Androstanediol levels were no different in animals treated with dihydrotestosterone or 3a-androstanediol.Therefore, because exogenous 3a-androstanediol is a better precursor of prostatic dihydrotestosterone than exogenous dihydrotestosterone itself, the effects of treatment with larger doses (2.5 mg/kg per d) of dihydrotestosterone and 3a-androstanediol for 12 wk were examined. In these amounts, dihydrotestosterone was as effective as 3a-androstanediol in inducing the development of prostatic hyperplasia and in elevating prostatic dihydrotestosterone concentration.Because dihydrotestosterone accumulates in spontaneous prostatic hyperplasia, because the administration of sufficient amounts of dihydrotestosterone to the

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