Evidence of a treatable endocrinopathy in infertile men

Christian Pavlovich, Peggyann King, Marc Goldstein, Peter N. Schlegel

Research output: Contribution to journalArticle

Abstract

Purpose: We establish whether a subset of infertile men have decreased serum testosteroneto-estradiol ratios and whether this condition can be corrected with an oral aromatase inhibitor. Materials and Methods: The serum testosterone-to-estradiol ratios of 63 men with severe male factor infertility or hypergonadotropic hypogonadism (mean follicle-stimulating hormone 21.2 ± 1.8) were compared with those of an age matched, fertile, control reference group. Of the 63 men 43 were azoospermic with biopsy proved severe male infertility and 20 were oligospermic. The men with the lowest ratios (less than 20th percentile) were treated with 50 to 100 mg. of the aromatase inhibitor testolactone orally twice daily. Testosterone-to-estradiol ratios and semen analyses were evaluated during testolactone therapy. Results: Men with severe male infertility had significantly lower testosterone (328 versus 543 ng./dl., p <0.01) and higher estradiol (58.4 versus 43.5 ng./1., p = 0.01) than fertile control reference subjects, resulting in a decreased testosterone-to-estradiol ratio (x10-1 = 6.9 ± 0.6 versus 14.5 ± 1.2, respectively, p <0.01). Of the 45 men treated with testolactone a correction of these abnormalities was seen and ratios (× 10-1) increased into the normal range (5.0 ± 0.3 to 12.7 ± 1.2, p <0.01). Semen analyses were considered evaluable only in men with sperm in the ejaculate before aromatase inhibitor treatment. Semen analyses before and during testolactone treatment revealed significant increases in sperm concentration (16.1 to 28.9 million sperm per ml., p = 0.03) and motility (27.1% to 45.3%, p <0.01) in 12 oligospermic men. Conclusions: We identified an endocrinopathy in men with severe male factor infertility that is characterized by a decreased serum testosterone-to-estradiol ratio. This ratio can be corrected by aromatase inhibition, resulting in a significant improvement in semen parameters in oligospermic patients.

Original languageEnglish (US)
Pages (from-to)837-841
Number of pages5
JournalJournal of Urology
Volume165
Issue number3
StatePublished - 2001
Externally publishedYes

Fingerprint

Testolactone
Estradiol
Male Infertility
Testosterone
Aromatase Inhibitors
Semen Analysis
Spermatozoa
Serum
Aromatase
Hypogonadism
Follicle Stimulating Hormone
Semen
Reference Values
Therapeutics
Biopsy
Control Groups

Keywords

  • Endocrine diseases
  • Estradiol
  • Infertility
  • Testosterone

ASJC Scopus subject areas

  • Urology

Cite this

Pavlovich, C., King, P., Goldstein, M., & Schlegel, P. N. (2001). Evidence of a treatable endocrinopathy in infertile men. Journal of Urology, 165(3), 837-841.

Evidence of a treatable endocrinopathy in infertile men. / Pavlovich, Christian; King, Peggyann; Goldstein, Marc; Schlegel, Peter N.

In: Journal of Urology, Vol. 165, No. 3, 2001, p. 837-841.

Research output: Contribution to journalArticle

Pavlovich, C, King, P, Goldstein, M & Schlegel, PN 2001, 'Evidence of a treatable endocrinopathy in infertile men', Journal of Urology, vol. 165, no. 3, pp. 837-841.
Pavlovich C, King P, Goldstein M, Schlegel PN. Evidence of a treatable endocrinopathy in infertile men. Journal of Urology. 2001;165(3):837-841.
Pavlovich, Christian ; King, Peggyann ; Goldstein, Marc ; Schlegel, Peter N. / Evidence of a treatable endocrinopathy in infertile men. In: Journal of Urology. 2001 ; Vol. 165, No. 3. pp. 837-841.
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N2 - Purpose: We establish whether a subset of infertile men have decreased serum testosteroneto-estradiol ratios and whether this condition can be corrected with an oral aromatase inhibitor. Materials and Methods: The serum testosterone-to-estradiol ratios of 63 men with severe male factor infertility or hypergonadotropic hypogonadism (mean follicle-stimulating hormone 21.2 ± 1.8) were compared with those of an age matched, fertile, control reference group. Of the 63 men 43 were azoospermic with biopsy proved severe male infertility and 20 were oligospermic. The men with the lowest ratios (less than 20th percentile) were treated with 50 to 100 mg. of the aromatase inhibitor testolactone orally twice daily. Testosterone-to-estradiol ratios and semen analyses were evaluated during testolactone therapy. Results: Men with severe male infertility had significantly lower testosterone (328 versus 543 ng./dl., p <0.01) and higher estradiol (58.4 versus 43.5 ng./1., p = 0.01) than fertile control reference subjects, resulting in a decreased testosterone-to-estradiol ratio (x10-1 = 6.9 ± 0.6 versus 14.5 ± 1.2, respectively, p <0.01). Of the 45 men treated with testolactone a correction of these abnormalities was seen and ratios (× 10-1) increased into the normal range (5.0 ± 0.3 to 12.7 ± 1.2, p <0.01). Semen analyses were considered evaluable only in men with sperm in the ejaculate before aromatase inhibitor treatment. Semen analyses before and during testolactone treatment revealed significant increases in sperm concentration (16.1 to 28.9 million sperm per ml., p = 0.03) and motility (27.1% to 45.3%, p <0.01) in 12 oligospermic men. Conclusions: We identified an endocrinopathy in men with severe male factor infertility that is characterized by a decreased serum testosterone-to-estradiol ratio. This ratio can be corrected by aromatase inhibition, resulting in a significant improvement in semen parameters in oligospermic patients.

AB - Purpose: We establish whether a subset of infertile men have decreased serum testosteroneto-estradiol ratios and whether this condition can be corrected with an oral aromatase inhibitor. Materials and Methods: The serum testosterone-to-estradiol ratios of 63 men with severe male factor infertility or hypergonadotropic hypogonadism (mean follicle-stimulating hormone 21.2 ± 1.8) were compared with those of an age matched, fertile, control reference group. Of the 63 men 43 were azoospermic with biopsy proved severe male infertility and 20 were oligospermic. The men with the lowest ratios (less than 20th percentile) were treated with 50 to 100 mg. of the aromatase inhibitor testolactone orally twice daily. Testosterone-to-estradiol ratios and semen analyses were evaluated during testolactone therapy. Results: Men with severe male infertility had significantly lower testosterone (328 versus 543 ng./dl., p <0.01) and higher estradiol (58.4 versus 43.5 ng./1., p = 0.01) than fertile control reference subjects, resulting in a decreased testosterone-to-estradiol ratio (x10-1 = 6.9 ± 0.6 versus 14.5 ± 1.2, respectively, p <0.01). Of the 45 men treated with testolactone a correction of these abnormalities was seen and ratios (× 10-1) increased into the normal range (5.0 ± 0.3 to 12.7 ± 1.2, p <0.01). Semen analyses were considered evaluable only in men with sperm in the ejaculate before aromatase inhibitor treatment. Semen analyses before and during testolactone treatment revealed significant increases in sperm concentration (16.1 to 28.9 million sperm per ml., p = 0.03) and motility (27.1% to 45.3%, p <0.01) in 12 oligospermic men. Conclusions: We identified an endocrinopathy in men with severe male factor infertility that is characterized by a decreased serum testosterone-to-estradiol ratio. This ratio can be corrected by aromatase inhibition, resulting in a significant improvement in semen parameters in oligospermic patients.

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