Intrauterine growth restriction-etiology and consequences: What do we know about the human situation and experimental animal models?

被引:152
作者
Ergaz, Z
Avgil, M
Ornoy, A [1 ]
机构
[1] Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Anat & Cell Biol, Lab Teratol, IL-91010 Jerusalem, Israel
[2] Hadassah Med Ctr, Dept Neonatol, IL-91120 Jerusalem, Israel
关键词
IUGR; SGA; human; etiology; animal models;
D O I
10.1016/j.reprotox.2005.04.007
中图分类号
Q [生物科学];
学科分类号
07 [理学]; 0710 [生物学]; 09 [农学];
摘要
Embryonic and fetal growth depend on genetic and environmental factors, and the process is the result of the interaction between these factors. About 7-9% of live-born infants have a birth weight below normal (below the 10th percentile). The rate and extent of intrauterine growth restriction (IUGR) varies by ethnicity and socio-economic status. Some of the suspected causes of IUGR are as follows. (1) Maternal factors such as inadequate or severe malnutrition, chronic maternal diseases, birth order, multiple, births, and parental genetic factors. (2) Placental pathology, mainly placental vascular damage that may lead to placental insufficiency. This is often found in maternal diseases such as pre-eclampsia, and Thrombophilia. (3) Intrauterine infections and specific fetal syndromes, including chromosomal aberrations. (4) Non-classified causes such as adolescent's pregnancy, maternal smoking and alcohol drinking, living at high altitudes. Several existing animal models for IUGR, including uterine artery ligation or gene knock out models, although insightful of potential mechanism(s) underlying intrauterine growth restriction, are limited in that they do not reflect human causality. As the ultimate goal is prevention, we seem still to be distant from achieving this goal. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:301 / 322
页数:22
相关论文
共 206 条
[1]
Placental insufficiency leads to development of hypertension in growth-restricted offspring [J].
Alexander, BT .
HYPERTENSION, 2003, 41 (03) :457-462
[2]
1994-1996 U.S. singleton birth weight percentiles for gestational age by race, Hispanic origin, and gender. [J].
Alexander G.R. ;
Kogan M.D. ;
Himes J.H. .
Maternal and Child Health Journal, 1999, 3 (4) :225-231
[3]
Alexander GR, 1999, PAEDIATR PERINAT EP, V13, P205
[4]
Alfirevic Z, 2000, COCHRANE DB SYST REV
[5]
Standards of birth weight in twin gestations stratified by placental chorionicity [J].
Ananth, CV ;
Vintzileos, AM ;
Shen-Schwarz, S ;
Smulian, JC ;
Lai, YL .
OBSTETRICS AND GYNECOLOGY, 1998, 91 (06) :917-924
[6]
Placental transport of threonine and its utilization in the normal and growth-restricted fetus [J].
Anderson, AH ;
Fennessey, PV ;
Meschia, G ;
Wilkening, RB ;
Battaglia, FC .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 1997, 272 (05) :E892-E900
[7]
Andersson HW, 1997, ACTA OBSTET GYN SCAN, V76, P82
[8]
[Anonymous], 2001, MMWR-MORBID MORTAL W, V52, P660
[9]
Fetal ADH2*3, maternal alcohol consumption, and fetal growth [J].
Arfsten, DP ;
Silbergeld, EK ;
Loffredo, CA .
INTERNATIONAL JOURNAL OF TOXICOLOGY, 2004, 23 (01) :47-54
[10]
Endothelin 1 and leptin in the pathophysiology of intrauterine growth restriction [J].
Arslan, M ;
Yazici, G ;
Erdem, A ;
Erdem, M ;
Arslan, EO ;
Himmetoglu, O .
INTERNATIONAL JOURNAL OF GYNECOLOGY & OBSTETRICS, 2004, 84 (02) :120-126