Abstract
The peripheral serum levels of FSH, LH, testosterone and low polar oestrogens and the urinary excretion of LH, low polar oestrogens, dehydroepiandrosterone, androsterone and aetiocholanolone and 17‐oxogenic steroids were determined in five groups of infertile men. Together with the hormone determinations, the in vitro metabolism of [7‐3H, 21‐14C]progesterone by testicular biopsy specimens was studied. The five groups were defined by their testicular histology: Normal spermatogenesis, hypospermatogenesis with thickening of the lamina propria, spermatogenetic arrest and Sertoli cell only syndrome. Cases with azoospermia and normal testicular histology constitute our reference material.The group of hypospermatogenesis with normal lamina propria was characterized by increased urinary excretion of 17‐oxogenic steroids (P < 0.05), of androsterone (P < 0.02) and in some cases also of dehydroepiandrosterone.The group of hypospermatogenesis with thickening of the lamina propria showed also elevation of the urinary excretion of androsterone (P < 0.01) but also of aetiocholanolone (P < 0.05). Elevated serum values of FSH (P < 0.05) and testosterone (P < 0.05) were also seen. The results of in vitro conversion of progesterone were not normally distributed, revealing one subgroup with normal bioconversion pattern and one with an immature pattern.In the group of spermatogenetic arrest significantly elevated values of FSH (P < 0.05) and of prolactin (P < 0.05) were found. In this group some cases with elevated urinary excretion of dehydroepiandrosterone were also found. Bioconversion pattern was normal in all cases except one in which the most immature pattern in the cntire matcrial was found. The Scrtoli cell only group showed significant elcvations of serum FSH (P < 0.01) and LH (P < 0.01). Also in this group were cases with immature bioconversion pattern found.The findings indicate that the pituitary‐testicular interrelationship is disturbed in cases of hypospcrmatogcnesis and spermatogenic arrest, either via a general adrenal interaction (cases with normal lamina propria) or specifically by increased dehydroepiandrosterone, which in the cases of spermatogenetic arrest may be induced by prolactin. The significance of altered ratios of FSH/LH is discussed. It is suggested that an abnormal bioconversion pattern may be due either to adrcnal overactivity or to an altered FSH/LH‐ratio, or to both.
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