Fetal growth restriction: a workshop report

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.

Sex differences in the fetal programming of hypertension

“…Numerous epidemiological studies focused on diverse populations from various parts of the world have substantiated these initial findings and expanded them to include increased susceptibility to a number of other pathophysiological conditions such as impaired glucose tolerance, type II DM, obesity, stroke, high blood pressure and non-insulin-dependent DM (7). By far, low birth weight (LBW) which occurs when a fetus fails to achieve its genetically determined growth potential (8), and subsequent hypertension has been the most studied. Although the mechanistic pathways underlying this association remain unclear, investigators using animal models to induce a sub-optimal fetal environment are providing critical support for the fetal programming hypothesis by demonstrating that exposure to adverse conditions in utero results in offspring with marked adaptive responses and adverse adult outcomes.…”

Reduced placental prolyl hydroxylase 3 mRNA expression in pregnancies affected by fetal growth restriction

“…1,2 FGR is not a disease entity with a unique pathophysiology. 3 A variety of factors are involved, including congenital abnormalities, drug abuse, infectious diseases, and immunological and anatomical disorders. However, abnormal placentation (placental development) is observed in most cases.…”

IUGR, lipid peroxidation, and calcium ATPase activity of maternal red blood cell ghosts

“…Many factors, including maternal, fetal and placental disorders, can influence fetal growth [13]. A diminished fetal growth is generally accompanied with a decrease of important substances for the body, such as glucose and Ca 2+ [14], amino acids [15] and fatty acids [16].…”

“…In this regard, it has been demonstrated that IUGR is associated with Tables III and IV). a lower activity and expression of placental transport systems for essential amino acids, such as taurine, leucine and cationic amino acids [13]. Besides, it has also been shown that the reduced fetal weight that characterizes this condition is related to an incorrect adjustment of the placenta and poor development of the villi, conditions that lead to placental hypoxia [17] and consequently to low utero-placental perfusion and maternal-fetal transport of oxygen and nutrients [18].…”