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Research Article Free access | 10.1172/JCI106861

Evidence for a Specific Seminiferous Tubular Factor Affecting Follicle-Stimulating Hormone Secretion in Man

David H. Van Thiel, Richard J. Sherins, George H. Myers Jr., and Vincent T. De Vita Jr.

Reproduction Research Branch, National Institute of Child Health and Human Development, Surgery Branch, National Cancer Institute, Bethesda, Maryland 20014

Solid Tumor Service, National Cancer Institute, Bethesda, Maryland 20014

National Institutes of Health, Bethesda, Maryland 20014

Find articles by Van Thiel, D. in: JCI | PubMed | Google Scholar

Reproduction Research Branch, National Institute of Child Health and Human Development, Surgery Branch, National Cancer Institute, Bethesda, Maryland 20014

Solid Tumor Service, National Cancer Institute, Bethesda, Maryland 20014

National Institutes of Health, Bethesda, Maryland 20014

Find articles by Sherins, R. in: JCI | PubMed | Google Scholar

Reproduction Research Branch, National Institute of Child Health and Human Development, Surgery Branch, National Cancer Institute, Bethesda, Maryland 20014

Solid Tumor Service, National Cancer Institute, Bethesda, Maryland 20014

National Institutes of Health, Bethesda, Maryland 20014

Find articles by Myers, G. in: JCI | PubMed | Google Scholar

Reproduction Research Branch, National Institute of Child Health and Human Development, Surgery Branch, National Cancer Institute, Bethesda, Maryland 20014

Solid Tumor Service, National Cancer Institute, Bethesda, Maryland 20014

National Institutes of Health, Bethesda, Maryland 20014

Find articles by De Vita, V. in: JCI | PubMed | Google Scholar

Published April 1, 1972 - More info

Published in Volume 51, Issue 4 on April 1, 1972
J Clin Invest. 1972;51(4):1009–1019. https://doi.org/10.1172/JCI106861.
© 1972 The American Society for Clinical Investigation
Published April 1, 1972 - Version history
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Abstract

The interaction of the testis and gonadotropin secretion was studied in 15 men surviving chemotherapy for lymphoma. Azoospermia and complete destruction of all testicular germinal elements were present in 10 of the 15 men; however, Sertoli cells and Leydig cells were present. In these 10 men plasma follicle-stimulating hormone (FSH) levels were fourfold higher than in normal men of similar age whereas luteinizing hormone (LH) levels were normal. In contrast, both FSH and LH were normal in the remaining five men. Three had a full complement of spermatogenic tissue on biopsy and normal sperm concentrations. The other two men were azoospermic; one demonstrated full spermatogenesis in 30% of his tubules; the other had only a few spermatogonia in all tubules. In those patients with lower levels of gonadotropins pituitary insufficiency was excluded by the demonstration of appropriate responsiveness of FSH and LH to clomiphene administration. Similarly, Leydig cell function was normal since plasma testosterone was within the normal range in 13 of the 15 men and only slightly decreased in two. Thus, following chemotherapy, testicular damage was restricted to the germinal tissue, and this in turn was associated with a selective increase in FSH. The source of the FSH inhibitor is either the Sertoli cell or early germinal elements. However, since FSH levels are only half as high as those reported for castrate men, other testicular factors may modify FSH secretion.

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