madman
Super Moderator
Context: Recombinant human FSH (r-hFSH), given to prepubertal boys with hypogonadotropic hypogonadism (HH), may induce Sertoli cell proliferation and thereby increase sperm-producing capacity later in life.
Objective: To evaluate the effects of r-hFSH, human chorionic gonadotropin (hCG), and testosterone (T) in such patients.
Design and Setting: Retrospective review in three tertiary centers in Finland between 2006 and 2016.
Patients: Five boys: ANOS1 mutation in two, homozygous PROKR2 mutation in one, FGFR1 mutation in one, and homozygous GNRHR mutation in one. Prepubertal testicular volume (TV) varied between 0.3 and 2.3 mL; three boys had micropenis, three had undergone orchidopexy.
Interventions: Two boys received r-hFSH (6 to 7 months) followed by r-hFSH plus hCG (33 to 34 months); one received T (6 months), then r-hFSH plus T (29 months) followed by hCG (25 months); two received T (3 months) followed by r-hFSH (7 months) or r-hFSH plus T (8 months).
Main Outcome Measures: TV, inhibin B, anti-M¨ullerian hormone, T, puberty, sperm count.
Results: r-hFSH doubled TV (from a mean +/- SD of 0.9 +/- 0.9 mL to 1.9 +/- 1.7 mL; P < 0.05) and increased serum inhibin B (from 15 +/- 5 ng/L to 85 +/- 40 ng/L; P < 0.05). hCG further increased TV (from 2.1 +/- 2.3 mL to 8.6 +/- 1.7 mL). Two boys with initially extremely small testis size (0.3 mL) developed sperm (maximal sperm count range, 2.8 to 13.8 million/mL), which was cryopreserved.
Conclusions: Spermatogenesis can be induced with gonadotropins even in boys with HH who have extremely small testes, and despite low-dose T treatment given in early puberty. Induction of puberty with gonadotropins allows preservation of fertility.
Objective: To evaluate the effects of r-hFSH, human chorionic gonadotropin (hCG), and testosterone (T) in such patients.
Design and Setting: Retrospective review in three tertiary centers in Finland between 2006 and 2016.
Patients: Five boys: ANOS1 mutation in two, homozygous PROKR2 mutation in one, FGFR1 mutation in one, and homozygous GNRHR mutation in one. Prepubertal testicular volume (TV) varied between 0.3 and 2.3 mL; three boys had micropenis, three had undergone orchidopexy.
Interventions: Two boys received r-hFSH (6 to 7 months) followed by r-hFSH plus hCG (33 to 34 months); one received T (6 months), then r-hFSH plus T (29 months) followed by hCG (25 months); two received T (3 months) followed by r-hFSH (7 months) or r-hFSH plus T (8 months).
Main Outcome Measures: TV, inhibin B, anti-M¨ullerian hormone, T, puberty, sperm count.
Results: r-hFSH doubled TV (from a mean +/- SD of 0.9 +/- 0.9 mL to 1.9 +/- 1.7 mL; P < 0.05) and increased serum inhibin B (from 15 +/- 5 ng/L to 85 +/- 40 ng/L; P < 0.05). hCG further increased TV (from 2.1 +/- 2.3 mL to 8.6 +/- 1.7 mL). Two boys with initially extremely small testis size (0.3 mL) developed sperm (maximal sperm count range, 2.8 to 13.8 million/mL), which was cryopreserved.
Conclusions: Spermatogenesis can be induced with gonadotropins even in boys with HH who have extremely small testes, and despite low-dose T treatment given in early puberty. Induction of puberty with gonadotropins allows preservation of fertility.
