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Serum inhibin B concentrations in pubertal boys conceived by ICSI: first results
F Belva1, M Bonduelle, R C Painter
1Center for Medical Genetics, UZ Brussel, Laarbeeklaan 101, Brussels, Belgium. florence.belva@uzbrussel.be
Insights
Boys born after intracytoplasmic sperm injection (ICSI) show normal increases in serum inhibin B, a marker of sperm production, by age 14. Paternal fertility status did not impact ICSI boys' inhibin B levels.
Area of Science:
- Reproductive Endocrinology
- Pediatric Endocrinology
- Andrology
Background:
- Limited data exist on gonadal function in children conceived via intracytoplasmic sperm injection (ICSI).
- Assessing testicular function in boys born after ICSI is crucial, especially when fathers have compromised spermatogenesis.
Purpose of the Study:
- To evaluate the gonadal function in boys born after ICSI.
- To assess serum inhibin B levels as a marker for spermatogenesis in ICSI-conceived adolescents.
- To investigate the impact of paternal spermatogenesis on offspring's gonadal function.
Main Methods:
- Recruited 50 pubertal adolescents born following ICSI.
- Measured cross-sectional serum inhibin B levels in all 50 participants.
- Conducted longitudinal assessment of serum inhibin B in 25 boys at ages 8 and 14.
Main Results:
- Serum inhibin B levels significantly increased from age 8 to 14 (P < 0.001).
- Over 75% of ICSI boys showed at least a 30% increase in inhibin B between ages 8 and 14.
- Most 14-year-old ICSI boys had normal serum inhibin B levels, irrespective of paternal fertility status.
Conclusions:
- The majority of ICSI boys exhibit significant increases in serum inhibin B, reaching normal pubertal levels by age 14.
- Paternal spermatogenesis severity does not appear to negatively affect serum inhibin B levels in ICSI adolescents.
- Long-term follow-up is necessary to confirm the reproductive capacity of ICSI teenagers into adulthood.
Background:
Currently, no published data exist about the gonadal function of children born after ICSI. To evaluate potential risk of testicular seminal dysfunction in boys born to fathers with compromised spermatogenesis, serum inhibin B (as a marker for spermatogenesis) was assessed.
Methods:
We recruited 50 pubertal adolescents from the oldest cohort of infants born following ICSI. Cross-sectional serum inhibin B levels of all 50 ICSI adolescents, and longitudinal serum inhibin B (assessed at 8 and 14 years) in 25 boys, are reported.
Results:
A statistically significant increase in inhibin B levels was observed between 8 (mean 69 ng/l, SD ± 35) and 14 years (mean 145 ng/l, SD ± 41; P < 0.001). In three quarters of the ICSI boys an increase in serum inhibin B levels of at least 30% between 8 and 14 years was observed. In all but 4 of the 14-year-old ICSI boys serum inhibin B was normal. Serum inhibin B levels in boys from fathers with severe oligozoospermia did not differ from concentrations in boys from fathers without severe oligozoospermia (154 ± 51 and 142 ± 47 ng/l, respectively; P = 0.4).
Conclusions:
The majority of ICSI boys have a significant increase in serum inhibin B, attaining normal values for pubertal status at the age of 14 years. ICSI adolescents from fathers with severely compromised spermatogenesis do not have lower inhibin B levels than those with fathers with normal spermatograms. Further follow-up of the spermatogenic potential of ICSI teenagers up to young adulthood is mandatory to confirm a normal reproductive capacity.
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