Maternal and fetal thrombophilia in intrauterine growth restriction in the presence or absence of maternal hypertensive disease

Reprod Sci. 2010 Sep;17(9):844-8. doi: 10.1177/1933719110371516. Epub 2010 Jul 2.

Abstract

Intrauterine growth restriction (IUGR) depends on the placental capacity to transfer oxygen and nutrients from the maternal to the fetal circulation. Placental insufficiency may be caused by impairment of the maternal or fetal circulation by a thrombotic event, possibly associated with thrombophilic disorders. The goals of our study were to define the role of maternal/fetal gain-of-function factor V Leiden and prothrombin G20210A mutations in the development of IUGR and to evaluate whether maternal pregnancy-induced hypertensive diseases would modify any such association. This is a case-control study: controls were 259 normal pregnancies, cases were 77 IUGR, 28 with and 49 without preeclampsia (PE) or pregnancy-induced hypertension (PIH). An association was found between IUGR and fetal thrombophilia (OR 2.09 CI 95% 1-4.5). The association was stronger in IUGR without PE and PIH (OR 2.9 CI 95% 1.3-6.6). This suggests a role for the fetal genotype in the development of IUGR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blood Pressure
  • Case-Control Studies
  • Chi-Square Distribution
  • Factor V / genetics*
  • Female
  • Fetal Diseases / genetics*
  • Fetal Growth Retardation / etiology*
  • Fetal Growth Retardation / genetics
  • Fetal Growth Retardation / physiopathology
  • Genotype
  • Humans
  • Hypertension, Pregnancy-Induced / physiopathology*
  • Italy
  • Logistic Models
  • Mutation
  • Odds Ratio
  • Phenotype
  • Placental Circulation
  • Pre-Eclampsia / physiopathology
  • Pregnancy
  • Pregnancy Complications, Hematologic / genetics*
  • Prothrombin / genetics*
  • Risk Assessment
  • Risk Factors
  • Thrombophilia / genetics*

Substances

  • factor V Leiden
  • Factor V
  • Prothrombin