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Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. I: Plasma luteinizing hormone, follicle stimulating hormone, testosterone, estradiol, and inhibin concentrations.
J Clin Endocrinol Metab. 1993 Jul; 77(1):290-3.JC

Abstract

Sex-steroid based male contraceptive regimes induce azoospermia in only 40-70% of Caucasian men. The reason(s) why the remainder maintains a low level of spermatogenesis (oligozoospermia) despite gonadotrophin suppression is unclear. In order to improve our understanding of this phenomenon, we examined the changes in sperm density and plasma LH, FSH, testosterone (T), oestradiol (E2), and inhibin (IN) in 28 normal men who received 200 mg testosterone enanthate (TE) im weekly during a male contraceptive efficacy trial. Gonadotrophins were measured by an ultrasensitive time-resolved immunofluorometric assay (DELFIA) with a sensitivity of 0.04 U/L, to determine the adequacy of suppression. Seventeen of the 28 men achieved azoospermia; the other 11 remained oligozoospermic (sperm density 3.3-4.7 x 10(6)/mL) after 6 months of TE exposure. Azoospermic subjects displayed a more rapid decline in sperm density, a significant difference being apparent by 5 weeks after starting TE. During TE treatment, both LH and FSH were consistently suppressed to below the limits of detection, whereas there was a 2.5-fold rise in T and E2 with a similar decrease in IN. There were no consistent differences in any of these hormone concentrations between the azoospermic and oligozoospermic groups. Recovery of sperm density to baseline levels or above 20 x 10(6)/mL was significantly slower in the azoospermic group. During the recovery phase, the azoospermic men exhibited significantly higher LH and FSH levels compared to baseline and to the oligozoospermic subjects even though no differences in circulating T, E2, or IN were observed. We conclude that incomplete gonadotrophin suppression or differences in sex steroid or inhibin levels are unlikely to be responsible for the maintenance of minor degrees of spermatogenesis in some men during TE administration. The rebound rise in gonadotrophins in azoospermic but not oligozoospermic responders during recovery may reflect a more profound degree of spermatogenic suppression in the former group.

Authors+Show Affiliations

Department of Clinical Biochemistry, Royal Infirmary Edinburgh, Scotland.No affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8325955

Citation

Wallace, E M., et al. "Comparison Between Testosterone Enanthate-induced Azoospermia and Oligozoospermia in a Male Contraceptive Study. I: Plasma Luteinizing Hormone, Follicle Stimulating Hormone, Testosterone, Estradiol, and Inhibin Concentrations." The Journal of Clinical Endocrinology and Metabolism, vol. 77, no. 1, 1993, pp. 290-3.
Wallace EM, Gow SM, Wu FC. Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. I: Plasma luteinizing hormone, follicle stimulating hormone, testosterone, estradiol, and inhibin concentrations. J Clin Endocrinol Metab. 1993;77(1):290-3.
Wallace, E. M., Gow, S. M., & Wu, F. C. (1993). Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. I: Plasma luteinizing hormone, follicle stimulating hormone, testosterone, estradiol, and inhibin concentrations. The Journal of Clinical Endocrinology and Metabolism, 77(1), 290-3.
Wallace EM, Gow SM, Wu FC. Comparison Between Testosterone Enanthate-induced Azoospermia and Oligozoospermia in a Male Contraceptive Study. I: Plasma Luteinizing Hormone, Follicle Stimulating Hormone, Testosterone, Estradiol, and Inhibin Concentrations. J Clin Endocrinol Metab. 1993;77(1):290-3. PubMed PMID: 8325955.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. I: Plasma luteinizing hormone, follicle stimulating hormone, testosterone, estradiol, and inhibin concentrations. AU - Wallace,E M, AU - Gow,S M, AU - Wu,F C, PY - 1993/7/1/pubmed PY - 1993/7/1/medline PY - 1993/7/1/entrez KW - Androgens KW - Biology KW - Clinical Research KW - Clinical Trials KW - Comparative Studies KW - Contraception KW - Contraceptive Agents KW - Contraceptive Agents, Male KW - Developed Countries KW - Endocrine System KW - Estradiol KW - Estrogens KW - Europe KW - Family Planning KW - Follicle Stimulating Hormone KW - Gonadotropins KW - Gonadotropins, Pituitary--changes KW - Hormones KW - Luteinizing Hormone KW - Male Contraception KW - Northern Europe KW - Physiology KW - Research Report KW - Reversibility KW - Spermatogenesis Blocking Agents KW - Studies KW - Testosterone KW - United Kingdom SP - 290 EP - 3 JF - The Journal of clinical endocrinology and metabolism JO - J Clin Endocrinol Metab VL - 77 IS - 1 N2 - Sex-steroid based male contraceptive regimes induce azoospermia in only 40-70% of Caucasian men. The reason(s) why the remainder maintains a low level of spermatogenesis (oligozoospermia) despite gonadotrophin suppression is unclear. In order to improve our understanding of this phenomenon, we examined the changes in sperm density and plasma LH, FSH, testosterone (T), oestradiol (E2), and inhibin (IN) in 28 normal men who received 200 mg testosterone enanthate (TE) im weekly during a male contraceptive efficacy trial. Gonadotrophins were measured by an ultrasensitive time-resolved immunofluorometric assay (DELFIA) with a sensitivity of 0.04 U/L, to determine the adequacy of suppression. Seventeen of the 28 men achieved azoospermia; the other 11 remained oligozoospermic (sperm density 3.3-4.7 x 10(6)/mL) after 6 months of TE exposure. Azoospermic subjects displayed a more rapid decline in sperm density, a significant difference being apparent by 5 weeks after starting TE. During TE treatment, both LH and FSH were consistently suppressed to below the limits of detection, whereas there was a 2.5-fold rise in T and E2 with a similar decrease in IN. There were no consistent differences in any of these hormone concentrations between the azoospermic and oligozoospermic groups. Recovery of sperm density to baseline levels or above 20 x 10(6)/mL was significantly slower in the azoospermic group. During the recovery phase, the azoospermic men exhibited significantly higher LH and FSH levels compared to baseline and to the oligozoospermic subjects even though no differences in circulating T, E2, or IN were observed. We conclude that incomplete gonadotrophin suppression or differences in sex steroid or inhibin levels are unlikely to be responsible for the maintenance of minor degrees of spermatogenesis in some men during TE administration. The rebound rise in gonadotrophins in azoospermic but not oligozoospermic responders during recovery may reflect a more profound degree of spermatogenic suppression in the former group. SN - 0021-972X UR - https://www.unboundmedicine.com/medline/citation/8325955/Comparison_between_testosterone_enanthate_induced_azoospermia_and_oligozoospermia_in_a_male_contraceptive_study__I:_Plasma_luteinizing_hormone_follicle_stimulating_hormone_testosterone_estradiol_and_inhibin_concentrations_ DB - PRIME DP - Unbound Medicine ER -