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Forty-five uremic men, aged 20 to 68 years, undergoing periodic hemodialysis were investigated regarding their plasma testosterone (T) and human prolactin (hPRL); in 25 of those, plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), estrone (E1) and 17-β estradiol (E2) were also measured by radioimmunoassay (RIA). Means ± standard deviations were: T = 379 ± 157 ng/dl; hPRL = 24 ± 30 ng/ml; LH = 49 ± 48 mlU/ml; FSH = 10 ± 8 mlU/ ml; E1 = 108 ± 35 pg/ml; and E2 = 10 ± 6 pg/ml. Twenty percent had hyperprolactinemia, and 24% had hypotestosteronemia. LH was elevated in 95% of men, while FSH was higher than normal in only three cases (12%). E; was tentatively low in 60%, while E, was elevated in 76% of men. Hyperprolactinemia could be due to hemodilution, reduced renal excretion, stress, or hypothalamic-pituitary disregulation; it cannot be accounted for by E2 induction, since E2 was low in 60% of patients. Low T can be explained by a local toxic effect of uremia on the testis, and high LH would be the result of decreased negative feed-back. FSH is normal indicating that inhibin production by the testis was unaltered. Low E2 can be explained by testicular damage and/or reduced T. The increase in E1, mainly of adrenocortical origin, may be due to increased adrenocorticotropic hormone (ACTH) as a result of stress conditions imposed by chronic renal failure and periodic hemodialysis.
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Mastrogiacomo et al. (1982) studied this question.
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