論文

査読有り
2016年7月

Fetal growth restriction but not preterm birth is a risk factor for severe hypospadias

PEDIATRICS INTERNATIONAL
  • Yukiko Hashimoto
  • ,
  • Masahiko Kawai
  • ,
  • Sizuyo Nagai
  • ,
  • Takashi Matsukura
  • ,
  • Fusako Niwa
  • ,
  • Takeshi Hasegawa
  • ,
  • Toshio Heike

58
7
開始ページ
573
終了ページ
577
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1111/ped.12864
出版者・発行元
WILEY-BLACKWELL

BackgroundHypospadias has multifactorial causes and occurs at a high frequency among very low-birthweight infants. Placental insufficiency is hypothesized to be one cause of hypospadias; that is, decreased human chorionic gonadotropin (hCG) secretion caused by placental insufficiency is suspected to result in abnormal male external genitalia, but there is little direct evidence to support this. The aim of this study was therefore to identify the features of hypospadias and to clarify the male genital abnormalities caused by fetal growth restriction (FGR).
MethodsWe reviewed the clinical data of boys who underwent hypospadias repair between 2005 and 2011 at Kyoto University Hospital.
ResultsTwenty boys were included in this study. Fifteen (75%) of the subjects were preterm or low-birthweight infants. Thirteen (65%) had FGR, 60% of whom had severe hypospadias regardless of gestational age. In addition, 92% of the FGR infants also had other genital anomalies, such as cryptorchidism, bifid scrotum, or micropenis. In contrast, only 14% and 43% of the non-FGR infants had severe hypospadias or genital anomalies other than hypospadias, respectively. Placental histopathology was available in eight FGR infants, in seven of whom it was suggestive of blood flow deficiency such as infarction and single umbilical artery.
ConclusionsInfants with FGR have a high incidence of hypospadias. FGR caused by placental dysfunction, but not low birthweight, is a risk factor for severe hypospadias associated with multiple genital anomalies.

リンク情報
DOI
https://doi.org/10.1111/ped.12864
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/26634292
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000380696200005&DestApp=WOS_CPL
ID情報
  • DOI : 10.1111/ped.12864
  • ISSN : 1328-8067
  • eISSN : 1442-200X
  • PubMed ID : 26634292
  • Web of Science ID : WOS:000380696200005

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