Indirect evidence of chronic Leydig cell desensitization in Klinefelter's syndrome

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Abstract
The basal plasma 17.alpha.-hydroxyprogesterone (17-OHP) and testosterone (T) levels were proportionally decreased in 10 hypergonadotropic patients with Klinefelter''s syndrome. The ratio 17-OHP to T was about twice as high as in 10 eugonadal male controls; this implies the presence of a block in the conversion of 17-hydroxylated steroids to androgens in the Klinefelter patients under basal circumstances. Administration of human chorionic gonadotropin (hCG, 1500 IU i.m. daily for 3 days) to the Klinefelter patients disclosed a response pattern quite different from that observed in controls. In the control subjects 17-OHP and the ratio 17-OHP/T sharply rose to maximum values at 24 h after the 1st injection. Thereafter both progressively fell to lowest values at 72 h, when T levels reached their maximum. In the Klinefelter patients the T response to hCG administration was greatly diminished, but the 17-OHP response was similar to that in the controls. Maximum 17-OHP and 17-OHP/T values were not achieved until 72 h after the 1st injection when T levels also reached their maximum. Unlike the controls in the Klinefelter patients, maximum 17-OHP and T increments and the 17-OHP and T levels 48 and 72 h after the injection were positively correlated. A decreased T synthesis and reserve in the presence of relative 17-OHP accumulation (further increasing after acute hCG administration in a pattern quite different from that in normal men) suggest that in Klinefelter''s syndrome the Leydig cells may be chronically desensitized by the persistent endogenous hypergonadotropism.

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