Fetal growth restriction: a workshop report

Placenta. 2004 Sep-Oct;25(8-9):753-7. doi: 10.1016/j.placenta.2004.02.004.

Abstract

Intrauterine growth restriction (IUGR) is associated with significantly increased perinatal morbidity and mortality as well as cardiovascular disease and glucose intolerance in adult life. A number of disorders from genetic to metabolic, vascular, coagulative, autoimmune, as well as infectious, can influence fetal growth by damaging the placenta, leading to IUGR as a result of many possible fetal, placental and maternal disorders. Strict definitions of IUGR and of its severity are needed in order to eventually distinguish among different phenotypes, such as gestational age at onset, degree of growth restriction and presence of hypoxia. This report explores and reviews some of the most recent developments in both clinical and basic research on intrauterine growth restriction, by seeking mechanisms that involve genetic factors, utero-placental nutrient availability and vascular growth factors. New exciting findings on the genomic imprinting defects potentially associated with IUGR, and the placental anomalies associated with the decreased nutrient transport are summarized. Moreover, recent data on angiogenic growth factors as well as new information arising from application of gene chip technologies are discussed.

Publication types

  • Congress

MeSH terms

  • Adult
  • Angiogenesis Inducing Agents / metabolism
  • Female
  • Fetal Growth Retardation* / etiology
  • Fetal Growth Retardation* / metabolism
  • Fetal Growth Retardation* / pathology
  • Genomic Imprinting
  • Humans
  • International Cooperation
  • Placenta / metabolism*
  • Placenta / pathology*
  • Pregnancy

Substances

  • Angiogenesis Inducing Agents