Sperm motion parameters after suppression of spermatogenesis with a gonadotropin-releasing hormone antagonist plus testosterone supplementation.
OBJECTIVE
To evaluate whether the chronic administration of a GnRH antagonist supplemented with T enanthate affects sperm motion parameters.


METHODS
Prospective study.


METHODS
Academic medical research environment.


METHODS
Six normospermic men of reproductive age.


METHODS
A 20-week treatment included the administration of 10 mg of GnRH antagonist every day and 25 mg of T enanthate once a week.


METHODS
Computerized sperm motion analysis on each participant every 2 weeks for a period of 11 months.


RESULTS
Sperm concentration decreased after 4 weeks of the GnRH antagonist administration, accompanied by a reduction of sperm motility from an initial mean value of 56% to 34% on treatment week 4 and 21% on treatment week 6. In contrast, sperm velocity, linearity, amplitude of the lateral head displacement, and beat cross-frequency values did not significantly change in spite of reduced overall sperm concentration and motility. Azoospermia was reached within 6 to 12 weeks of the GnRH administration, and it was sustained during the treatment period. During recovery of spermatogenesis, sperm movement parameters returned to initial values earlier than sperm concentration and normal morphology. All participants recovered initial semen parameters 20 weeks after the end of treatment.


CONCLUSIONS
The administration of a GnRH antagonist supplemented with T enanthate successfully induced reversible suppression of spermatogenesis. The sperm motion characteristics appeared to be the last parameters to decline and the first to return to initial values after the treatment.
Bastias
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Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2515.
Kamijo
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Pavlou
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D000328:Adult; D005640:Follicle Stimulating Hormone / Q000096:biosynthesis; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors / Q000494:pharmacology; D006801:Humans; D007986:Luteinizing Hormone / Q000096:biosynthesis; D008297:Male; D013076:Sperm Count / Q000187:drug effects; D013081:Sperm Motility / Q000187:drug effects*; D013091:Spermatogenesis / Q000187:drug effects*; D013094:Spermatozoa / Q000187:drug effects / Q000648:ultrastructure; D013739:Testosterone / Q000494:pharmacology*; D013997:Time Factors; D017329:Triptorelin Pamoate / Q000031:analogs & derivatives*
C057805:LHRH, N-Ac-2-Nal(1)-4-Cl-Phe(2)-3-Pal(3)-Arg(5)-Glu(6)-AlaNH2(10)-; D017329:Triptorelin Pamoate; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; C019176:Tryptal; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone