Do prune-belly syndrome and neural tube defects change testicular growth? A study on human fetuses.

ABSTRACT

BACKGROUND: There are no reports comparing testicular volume between normal fetuses, fetuses with prune-belly syndrome (PBS), and fetuses with anencephaly. The study hypothesis was that PBS and especially anencephaly alter the testicular volume during the human fetal period. AIM: The objective of the study was to compare the testicular growth in fetuses with anencephaly, with PBS, and without anomalies. STUDY DESIGN: This is a morphometric study of human fetuses. Seventy testes from fetuses without anomalies aged 11-22 weeks post-conception (WPC), 30 testes from fetuses with anencephaly aged 13-19 WPC, and eight testes from fetuses with PBS aged 13-16 WPC were studied. Testicular length, width, and thickness were evaluated with the aid of computer programs (Image Pro and ImageJ) (Figure). The fetal testicular volume was calculated using the ellipsoid formula Testicular volume (TV) = [length × thickness × width] × 0.523. The Shapiro-Wilk test was used to ascertain the normality of the data and to compare quantitative data between normal fetuses vs. fetuses with anencephaly, while the Kruskal-Wallis test was used to assess gender and laterality differences. Simple linear correlations (LCs) were calculated for testicular volume according to fetal age, weight, and crown-rump length. RESULTS: All 108 testes studied were abdominal. The right (p = 0.0310) and left (0.0470) testicular volumes were significantly smaller in fetuses with anencephaly than those in the control group. The linear regression analysis indicated that the right and the left testis volume in the control group (right r2 = 0.6665; left r2 = 0.6707) and PBS group (right r2 = 0.9937; left r2 = 0.9757) increased with fetal age (p < 0.0001). This analysis also indicated that the testicular volume in fetuses with anencephaly did not increase with fetal age (right r2 = 009816; left r2 = 0.07643). DISCUSSION: This article is the first to report testicular volume correlations with fetal parameters in fetuses with anencephalic and fetuses with PBS. Significant alterations were observed in testicular growth in the anencephalic group compared with the control group, and it was also observed that the bilateral cryptorchidism in PBS does not alter the testicular development and growth during the fetal period. The unequal WPC distribution between fetuses with PBS, fetuses with anencephaly, and controls and the small sample size are limitations of this study. Further studies should be performed to confirm this study's findings. CONCLUSIONS: Testicular growth is slower and does not show significant correlations with fetal parameters in fetuses with anencephalic. Significant differences in testicular development in fetuses with PBS was not observed.