521 PLACENTAL INSUFFICIENCY AND HYPOSPADIAS
Article Outline
INTRODUCTION AND OBJECTIVES
Fetal Testosterone secretion is under the influence of placental human chorionic gonadotropin during first 14 weeks of gestation. Placental insufficiency may disrupt the supply of nutrients and human chorionic gonadotropin to the fetus leading to growth retardation and hypospadias. To validate this hypothesis we analyzed male neonates with hypospadias for growth parameters and placental examination
METHODS
All newborns in our hospital were examined for evidence of hypospadias. Neonates with hypospadias were examined in detail. The mothers of these neonates answered a questionnaire after consent. The placenta of these study neonates was obtained for macroscopic and microscopic examination. Neonates without hypospadias and of similar birth weight born within a week of the study neonate were used as controls. The control neonates were similarly examined in detail and mothers of these control neonates similarly answered the questionnaire after consent. The placenta of these control neonates was similarly obtained for examination.
RESULTS
6 male neonates were born with hypospadias during the study period Sept 2008 to Aug 2009. The mean birth weight was 2.85 kg. There were no other obvious anomalies noted in any of these children. 4 of these neonates had proximal hypospadias. Placenta to fetal ratio and gestational age were significantly higher in neonates with hypospadias. Histopathologic examination of the placenta obtained from the neonates with hypospadias revealed pronounced degenerative changes, infarction and calcifications
CONCLUSIONS
Significant association between the occurrence of hypospadias with higher placenta to fetal ratio and placental abnormalities suggest that placental dysfunction in early gestation may play an important role in the occurrence of hypospadias
Source of Funding: None
PII: S0022-5347(10)00976-6
doi:10.1016/j.juro.2010.02.720
© 2010 American Urological Association Education and Research, Inc. Published by Elsevier Inc All rights reserved.

