Hypogonadism in chronically lead-poisoned men.

Braunstein Gd, James Dahlgren, Loriaux Dl

PubMed · 1978 · 87 citations · 0 references

Concepts

Abstract

The hypothalamic-pituitary-testicular axis was evaluated in 10 men with occupational lead exposure, 9 of whom had noted a decrease in libido and frequency of intercourse following this exposure. 6 of these men had clinically apparent lead poisoning while 4 were classified as being only lead-exposed. Results of the endocrine evaluation of these patients were compared to those obtained on 9 age and socioeconomically matched control patients. Both lead poisoned and lead-exposed patients had reduced basal serum testosterone levels and normal basal serum testosterone-estradiol-binding globulin capacity, estradiol, LH, FSH, and prolactin levels. Both groups demonstrated an appropriate rise in serum testosterone following hCG stimulation and a normal increment in serum FSH in response to clomiphene citrate and gonadotropin-releasing hormone in comparison to the control group. The lead poisoned patients demonstrated a significantly reduced increment in serum LH after clomiphene citrate and gonadotropin-releasing hormone administration while the lead-exposed patients had normal LH dynamics. Testicular biopsies carried out on the 2 most severely lead-poisoned men showed peritubular fibrosis, oligospermia, and vacuolization of the Sertoli cells. These results suggest that lead poisoning may lead to a pituitary-hypothalamic defect in LH secretion and may also result in direct testicular seminiferous tubular injury.