These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Hypogonadism in chronically lead-poisoned men.
    Author: Braunstein GD, Dahlgren J, Loriaux DL.
    Journal: Infertility; 1978; 1(1):33-51. PubMed ID: 12265605.
    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.
    [Abstract] [Full Text] [Related] [New Search]