Abstract

Abstract Introduction: Hypospadias can be defined as an abnormal urethral orifice under surface of the penis with or without chordee and with or without dorsal hood. At a critical time in sexual differentiation of the male fetus, HCG enters fetal plasma from syncytio trophoblast; acts as an LH surrogate and stimulate replication of testicular Ley dig cells and testosterone synthesis to promote male sexual differentiation. The placental insufficiency may disrupt the supply of nutrients and hcG to the fetus leading to growth retardation and hypospadias. Aim: The aim of this study was to observe and document morphological changes of placenta in children with hypospadias and compare with controls. Materials & Methods: The present study was a case control study from July 2008 to July 2011 The data base of the labor registries of the hospital indicated that there were total 3243 male births during this period. All examined for presence /absence of hypospadias by attending pediatrician. Hypospadias was detected in 17 male newborns. Control cases comprised of 68 male newborns without hypospadias of similar gestational age and birth weight collected by cluster sampling. Result: Total number of male birth during the study period was 3243, in that17 children born with hypospadias. The incidence of hypospadias in our hospital was 0.52%. Gestational age, Birth weight, Placental weight, Placental thickness, Placental volume, volume of infarcts, F.P Ratio, Cord length, were similar in children with hypospadias when compared with controls. CONCLUSION: Fetal factors like gestational age, birth weight, placental weight, Feto-placental ratio were not significantly associated with hypospadias. This study shows no role of placenta in the etiology of hypospadias in children with normal birth weight.

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