Prenatal alcohol exposure, blood alcohol concentrations and alcohol elimination rates for the mother, fetus and newborn

被引:113
作者
Burd, L. [1 ]
Blair, J. [1 ]
Dropps, K. [1 ]
机构
[1] Univ N Dakota, Sch Med & Hlth Sci, Dept Pediat, N Dakota Fetal Alcohol Syndrome Ctr, Grand Forks, ND 58203 USA
关键词
ethanol; fetal; exposure; maternal; metabolism; newborn; HUMAN FETAL LIVER; ETHANOL INTOXICATION; ACETALDEHYDE; PREVALENCE; INDUCTION; INFANT; CYP2E1;
D O I
10.1038/jp.2012.57
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Fetal alcohol spectrum disorders (FASDs) are a common cause of intellectual impairment and birth defects. More recently, prenatal alcohol exposure (PAE) has been found to be a risk factor for fetal mortality, stillbirth and infant and child mortality. This has led to increased concern about detection and management of PAE. One to 2h after maternal ingestion, fetal blood alcohol concentrations (BACs) reach levels nearly equivalent to maternal levels. Ethanol elimination by the fetus is impaired because of reduced metabolic capacity. Fetal exposure time is prolonged owing to the reuptake of amniotic-fluid containing ethanol by the fetus. Alcohol elimination from the fetus relies on the mother's metabolic capacity. Metabolic capacity among pregnant women varies eightfold (from 0.0025 to 0.02 gdl(-1) h(-1)), which may help explain how similar amounts of ethanol consumption during pregnancy results in widely varying phenotypic presentations of FASD. At birth physiological changes alter the neonate's metabolic capacity and it rapidly rises to a mean value of 83.5% of the mother's capacity. FA,SDs are highly recurrent and younger siblings have increased risk. Detection of prenatal alcohol use offers an important opportunity for office-based interventions to decrease exposure for the remainder of pregnancy and identification of women who need substance abuse treatment. Mothers of children with FAS have been found to drink faster, get drunk quicker and to have higher BACs. A modest increase in the prevalence of a polymorphism of alcohol dehydrogenase, which increases susceptibility to adverse outcomes from PAE has been reported. Lastly, detection of alcohol use and appropriate management would decrease risk from PAE for subsequent pregnancies. Journal of Perinalology (2012) 32, 652-659; doi:10.1038/jp.2012.57; published online 17 May 2012
引用
收藏
页码:652 / 659
页数:8
相关论文
共 41 条
[1]  
Abel ErnestL., 1998, FETAL ALCOHOL ABUSE
[2]   ALCOHOL PRODUCES SPASMS OF HUMAN UMBILICAL BLOOD-VESSELS - RELATIONSHIP TO FETAL ALCOHOL SYNDROME (FAS) [J].
ALTURA, BM ;
ALTURA, BT ;
CARELLA, A ;
CHATTERJEE, M ;
HALEVY, S ;
TEJANI, N .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1982, 86 (02) :311-312
[3]  
APERIA A, 1983, ACTA PAEDIATR SCAND, P61
[4]  
APERIA A, 1983, ACTA PAEDIATR SCAND, P70
[5]   Fatty acid ethyl esters: Quantitative biomarkers for maternal alcohol consumption [J].
Bearer, CF ;
Santiago, LM ;
O'Riordan, MA ;
Buck, K ;
Lei, SC ;
Singer, LT .
JOURNAL OF PEDIATRICS, 2005, 146 (06) :824-830
[6]  
BEATTIE JO, 1986, ALCOHOL ALCOHOLISM, V21, P163
[7]   DISPOSITION OF ETHANOL IN HUMAN MATERNAL VENOUS-BLOOD AND AMNIOTIC-FLUID [J].
BRIEN, JF ;
LOOMIS, CW ;
TRANMER, J ;
MCGRATH, M .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1983, 146 (02) :181-186
[8]   Ethanol and the placenta: A review [J].
Burd, Larry ;
Roberts, Drucilla ;
Olson, Meredith ;
Odendaal, Hein .
JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE, 2007, 20 (05) :361-375
[9]  
Carpenter SP, 1996, MOL PHARMACOL, V49, P260
[10]  
Comman-Homonoff J, J MATERN FETAL NEONA