Thirty-five male patients with hypogonadism (excluding those suffering from complete hypopituitarism) have been studied. A system of classification is outlined based on the following features: (1) the clinical picture; in particular, evidence for androgen deficiency, (2) the histology of the Leydig cells, (3) the function of the seminiferous tubules as assessed by histology and sperm counts in semen, and (4) the excretion of gonadotrophins. The patients have been classified into those with primary testicular failure and those with failure of pituitary gonadotrophin secretion; the former group includes the patients with Klinefelter's syndrome. Difficulties arose in deciding when gonadotrophin excretion was definitely subnormal because the values in the lower part of the normal range overlap some of those from patients who were obviously deficient in pituitary gonadotrophin.
Some patients showed evidence of hypothyroidism, probably related to testosterone deficiency.
The excretion of 17-oxosteroids is shown to be a poor guide to the assessment of androgen deficiency. This is partly due to the secretion of adrenal androgen, which may be greater than normal in some patients with Leydig-cell deficiency. Patients with primary Leydig-cell failure responded to stimulation by corticotrophin (ACTH) with a relatively greater increase in 17-oxosteroids than normal. Patients with deficiency of pituitary gonadotrophin responded to ACTH stimulation with a much smaller increase in 17-oxosteroid excretion than normal individuals. The evidence presented suggests that a mechanism exists for the integration of androgen production by both gonad and adrenal.
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