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Results for “Fetal Alcohol Spectrum Disorders”

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At least 253 records · Page 14Linked to original sources
PubMed1986

Selenium in pregnancy: effect of maternal drinking.

To study the effect of drinking alcohol during pregnancy on serum selenium, selenium concentrations were measured in 41 women (ten abstinent, 31 problem drinkers) throughout pregnancy as well as in 24 nonpregnant abstinent women. In abstinent pregnant women, serum selenium decreased with advancing gestational age, a pattern not affected by moderate maternal drinking (42 to 126 g of ethanol weekly, N = 14). Seventeen women drank heavily (more than 140 g of ethanol weekly), and nine of them (53%) gave birth to infants with fetal alcohol syndrome. The women with infants having fetal alcohol syndrome had higher (P less than 0.05) selenium levels than the abstinent controls both at the 25th to 32nd (63.3 +/- 6.2 versus 56.6 +/- 4.4 micrograms/L) and at the 33rd to 40th gestational weeks (58.6 +/- 3.4 versus 53.5 +/- 5.9 micrograms/L). The selenium levels in umbilical serum were 20 and 33% lower than in maternal serum of abstinent and drinking women, respectively. However, alcohol-damaged newborns did not demonstrate any further decrease in selenium levels. Thus, heavy maternal drinking is accompanied by increased maternal and decreased umbilical concentration of selenium.

Alcohol Drinking↗
PubMed1979

In utero opiate dependence and sudden infant death syndrome.

Infants born to smoking, alcoholic, and drug-dependent women appear to suffer increased prenatal and postnatal growth deficiency, vascular changes, and hypoxic episodes as a result of decreased oxygen carrying capacity in the blood, depression with overdose, and withdrawal symptoms. The author reviews these associations and suggests further research to clarify their role in the sudden infant death syndrome.

Alcoholism↗
PubMed1985

Prenatal effects of alcohol on growth: a brief overview.

Intrauterine growth retardation is the most reliable consequence of prenatal exposure to alcohol in both humans and animals. The decrease in fetal growth is caused by alcohol, not by congeners present in alcoholic beverages. The most likely hypothesis whereby alcohol decreases growth is via hypoxia, which interferes with cellular processes that require oxygen to function adequately, e.g., placental transport and protein synthesis. The third trimester of pregnancy is when alcohol exerts its greatest impact on fetal growth.

Animals↗
PubMed1985

Growth analysis in clinical genetics.

The number of genetic and environmental determinants of human growth is very large and their interplay is responsible for the enormously complex phenomenon of prenatal and postnatal growth and simultaneous differentiation in function. Genetic factors participate substantially in determining size at birth, but become more and increasingly important in the realization of inherent potential after the age of two years. Thus, prenatal growth is determined by a greater number of environmental factors than postnatal growth, including parity, pregnancy spacing, maternal age, size, blood pressure, race, health, smoking, alcohol intake, twinning, intrauterine constraint, etc. Galilei's scale effect sets the upper limit of human size, and our surface area determines our metabolic rate and to some extent our life span. Age and rate of pubertal maturation varies with sex, race, and health of the individual, and may be dramatically influenced by numerous environmental and genetic disturbances. One of the most consistent and dramatic effects of autosomal aneuploidy on development is permanent reduction of growth rate, beginning very early in embryonic development. This effect on growth can be interpreted as an abnormality of developmental homeostasis or canalization. Reduced buffering or canalization of growth has been demonstrated in the DS and constitutes most elegant confirmation of the Waddington-Shapiro hypothesis; it ought to be demonstrable also in most if not all of the gonosomal aneuploidies. Thus, an ultrasonographic analysis of embryonic and fetal growth ought to be normal practice in all, not just high--risk pregnancies, and serve as valuable indicator of fetal developmental abnormality if IUGR is found. Because of difference in prognosis and possible difference in obstetric management, ultrasonographers ought to make a distinction in practice between (proportionate) IUGR and (disproportionate) CSOS. Depending on age of onset and severity, reduced prenatal movement can lead to the fetal akinesia sequence including growth retardation of all or part of the fetus. Neurohypotrophy shows that normal innervation is required for normal growth and function of limbs.

Aneuploidy↗
PubMed1985

[Histoautoradiographic study of synthesis of neuronal proteins of the brain in response to exposure to damaging factors during the prenatal period].

The incorporation of 3H-leucine into the neuronal proteins of the hemispherical cortex and hyppocampus was studied in rats aged 1 and 3 months which were exposed to hypoxia and ethanol in the antenatal period. The test one-month-old animals showed activation of protein synthesis in neurons and in layers III and V of the cortex and hyppocampus. At the age of 3 months the rats showed inhibited incorporation of the label into neuronal proteins of the studied structures of the brain which was more expressed in animals which had suffered intrauterine hypoxia.

Animals↗
PubMed1985

Alcohol and foetal damage.

Heavy alcohol consumption (more than 80 g per day) in pregnancy is associated with the foetal alcohol syndrome. More moderate consumption is reported to result in increased rates of spontaneous abortion, still birth and congenital malformation as well as growth retardation. There may be functional deficits in early childhood. In the light of current knowledge abstinence from alcohol before and during pregnancy is advisable.

Alcohol Drinking↗
PubMed1979

The teratogenic effect of acetaldehyde: implications for the study of the fetal alcohol syndrome.

Pregnant mice were injected intravenously with either saline alone (controls) or 1% or 2% acetaldehyde in saline, on days 7, 8 and 9 of gestation. The uterine contents were examined either on day 10 or on day 19. Acetaldehyde-treated females had more resorptions both at mid-gestation and at term, though no significant difference in maternal weight gain was observed. Experimental embryos examined on day 10 were smaller, and had a higher incidence of developmental delay, as compared to controls. Anomalies of closure of the cranial and caudal regions of the neural tube were the most commonly noted defects. When examined on day 19, acetaldehyde-treated fetuses were significantly smaller and weighed less than controls. These results suggest a role for acetaldehyde in the production of some of the teratogenic effects of ethanol manifested in the fetal alcohol syndrome.

Abnormalities, Drug-Induced↗
PubMed1979

Alcohol embryopathy and diabetic fetopathy in the same newborn.

Both alcohol embryopathy and diabetic fetopathy were observed in the same female child. The mother was known to be alcoholic as well as diabetic. At birth the signs of diabetic fetopathy predominated: the child showed edematous subcutaneous fat, birth weight was 3650 g. The heart was enlarged. The patient's blood sugar levels ranged from 0 to 1.4 mMol/1 (0-25 mg/dl). Features of alcohol embryopathy were typical craniofacial dysmorphy, hypotonia of muscles and hyperexcitability. Later on the features of alcohol embryopathy predominated: the child became dystrophic with pronounced microcephaly, and the craniofacial dysmorphy clearly resembled other patients with alcohol embryopathy. This observation is in favour of the hypothesis, that alcohol induces cell hypoplasia in the embryo resulting in postnatal growth retardation. Maternal and consequently embryonic and fetal hyperglycemia induced cell hypertrophy in the embryo and fetus, which compensated the effect of alcohol on birth weight in our patient.

Abnormalities, Multiple↗
PubMed1981

Fetal alcohol syndrome: a review.

Presented is a review of the clinical manifestations of fetal alcohol syndrome (FAS), the mode of action in this syndrome, the maternal malnutrition that may occur, and consideration that may prevent the development of FAS in the fetus. Several factors are discussed that may help explain the abnormalities noted in infants with FAS. Education regarding the dangers of alcohol abuse for pregnant women is essential in prevent the development of fetal alcohol syndrome and other alcohol-related birth defects.

Alcoholism↗
PubMed1983

Victims of addiction.

Explore the source record for details and available documents.

Education, Nursing, Continuing↗
PubMed1984

Foetal alcohol syndrome.

Foetal alcohol syndrome (FAS) is the combination of growth retardation, neurological impairment and abnormal facies shown by some infants born to alcoholic women. It seems likely that FAS only indicates a small proportion of the total damage inflicted on the foetus by maternal drinking. Levels of alcohol consumption below the equivalent of 30 ml per day of absolute alcohol probably do not have a significant effect on the foetus. But there is an increased incidence of either growth retardation or behavioural and congenital abnormalities amongst the infants of women who drink heavily in pregnancy but who are not alcoholic. Such children are sometimes described as showing foetal alcohol effects and such effects are probably commoner than complete FAS. The way in which alcohol damages the foetus is unknown. Genetic and nutritional factors in mother or child may determine the response to alcohol. Smoking appears to potentiate the effects of alcohol on the foetus. Drugs may also alter the foetal response to alcohol. The prevalence of children damaged by maternal drinking is impossible to estimate. Foetal alcohol effects overlap with many other congenital and developmental abnormalities. FAS is more common than 1 in 2500 births in Liverpool and may even approach the incidence of 1 or 2 cases per 1000 births seen in U.S.A. and Scandinavia.

Abnormalities, Drug-Induced↗