PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Fetal Alcohol Spectrum Disorders”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1985

Effects of maternal alcohol intoxication on fetal circulation and myocardial function: an experimental study in the ovine fetus.

To determine whether acute alcohol ingestion during pregnancy could affect fetal myocardial function, studies were carried in six chronically catheterized fetal sheep during maternal alcohol infusion. Absolute ethyl alcohol (0.8 ml/kg) was administered to the mother over 10 minutes via the jugular vein. These infusions were repeated every 30 minutes during 3 hours, and peak maternal and fetal blood concentrations close to 200 mg/dl alcohol were reached. Fetal PCO2 decreased from a baseline of 43.15 +/- 3.75 to 36.13 +/- 2.6 torr 1 hour after the start of alcohol infusion (P less than 0.05). Similarly, pH rose from 7.37 +/- 0.027 to 7.44 +/- 0.015 (P less than 0.05). Both values returned to baseline level at the end of alcohol infusion. PO2 remained within physiologic limits. The systolic time intervals of the fetal heart showed a rapid and prolonged modification. The pre-ejection period from 58 +/- 8 to 66 +/- 4 msec (P less than 0.05) during the infusion; this change was related to an increase in the isometric contraction period. The ratio of the pre-ejection period over the ejection time was also significantly increased (P less than 0.01), and remained elevated until the end of the experiment (12 hours). A rise in fetal systolic and diastolic pressures was observed at about 2 hours after the start of the alcohol infusion, and lasted 4 hours. This study suggests that an episode of maternal alcohol intoxication causes rapid depression of fetal myocardial contractility that is maintained several hours after cessation of alcohol ingestion.

Alcoholic Intoxication↗
PubMed1999

Optic nerve morphology may reveal adverse events during prenatal and perinatal life--digital image analysis.

OBJECTIVE: To evaluate optic nerve morphology in children with various conditions caused by adverse events during prenatal and/or perinatal life and to investigate whether optic nerve morphology can reveal brain lesions associated with these conditions, as well as provide insight into the etiology and timing of the prenatal and perinatal damage. METHODS AND PATIENTS: A digital image analysis technique was used to analyze fundus photographs. One hundred healthy Swedish individuals of various ages from childhood to adolescence constituted a reference group. The following patient groups were chosen to represent various clinical conditions affecting the newborn or fetus at different stages of development: children born preterm (N = 39), children with fetal alcohol syndrome (FAS [N = 16]), children with periventricular leukomalacia (PVL [N = 17]), and children with septo-optic dysplasia (SOD [N = 6]). RESULTS: Preterm children without known brain lesions demonstrated normal optic disk morphology but abnormal retinal vascular pattern; children born preterm with an acquired brain lesion late in gestation (PVL) demonstrated normal disk size with enlarged cups in addition to the abnormal vascular pattern. Children with prenatal alcohol exposure (FAS) had a subnormal optic disk area with increased tortuosity of both arteries and veins, whereas children born at term with an early acquired brain lesion (SOD) had a markedly reduced optic disk area with isolated tortuosity of the retinal veins. CONCLUSIONS: Evaluation of optic nerve morphology, by digital image analysis, demonstrated that differences in ocular fundus morphology were correlated with differences in etiology and timing of the adverse event occurring in prenatal and perinatal life. In addition, digital image analysis may be a helpful tool for understanding variations in optic nerve and retinal vessel morphology and their relationship with central nervous pathology.

Adolescent↗
PubMed1981

Zinc status of pregnant alcoholic women: a determinant of fetal outcome.

The zinc status of 25 alcoholic and 25 non-alcoholic pregnant women was measured and correlated with fetal outcome. The volume index of alcohol consumption and the Michigan Alcoholic Screening Test were used to define alcoholic women. The alcoholic women had significantly lower plasma-zinc levels that the non-alcoholic women (50.7 versus 72.2 micrograms/dl). Fetal cord-plasma zinc levels were also lower in the offspring of alcoholic women (65.5 versus 81.3 micrograms/dl). Manifestation of fetal dysmorphogenesis appears to relate to zinc status.

Alcoholism↗
PubMed2002

Vasoactive intestinal peptide mRNA and immunoreactivity are decreased in fetal alcohol syndrome model.

Vasoactive intestinal peptide (VIP) regulates growth in the early post-implantation embryo. Previous work has demonstrated that peptide agonists (SALLRSIPA and NAPVSIPQ) from downstream mediators that are regulated by VIP were able to prevent the alcohol-induced fetal death, growth restriction and microcephaly associated with fetal alcohol syndrome. Here we evaluated the role of VIP in this mouse model of fetal alcohol syndrome, to determine if fetal or maternal levels of VIP are altered. In addition, we evaluated whether peptide treatment would alter the effects of alcohol on VIP levels. Treatment groups included control, alcohol, and alcohol+peptides. VIP levels were measured with enzyme immunoassay [EIA] (Peninsula Laboratories, Belmont, CA). Quantitation of VIP expression was measured with rt-PCR using mimic cDNA primers. Embryo/decidual VIP levels were similar in control and alcohol-treated groups 6 h after treatment. However, in the embryo/deciduas at 12 and 24 h, VIP levels were below the EIA's detection limit in the alcohol-treated groups, and significantly lower than the control or peptide-pretreated groups (p<0.05). Maternal cortex VIP levels were undetectable and significantly lower in the alcohol-treated group than control or peptide+alcohol group at 6 and 12 h (p<0.001). VIP mRNA expression was quantitated in the embryo and deciduas, with a significant decline noted at 6 h to 58% of control levels (p=0.02). Pretreatment with the peptides attenuated the alcohol-induced decrease in VIP mRNA. These studies demonstrate that treatment with alcohol can decrease the expression and immunoreactivity of VIP in both maternal and fetal tissues. This alcohol-induced loss of a recognized regulator of embryonic growth and differentiation may contribute to the sequelae of toxicity observed in fetal alcohol syndrome.

Animals↗
PubMed2006

[Value of 3D-4D sonography in fetal and gynecological ultrasound examination: principles and indications].

Three-dimensional ultrasound has become an essential tool for visualization of fetal structures in the past few years. The recent improvements in transducers and signal processing provide new information, particularly in obstetrics and gynecology sonography. The present paper will present the most recent advances in volume acquisition and presentation modes followed by results of fetal organ visualization in normal and abnormal cases as well as applications in gynecology.

Adult↗
PubMedDate not supplied

Alcohol, tobacco and marijuana use among pregnant teenagers: 6-year follow-up of offspring growth effects.

This prospective study evaluated the relations between maternal alcohol, tobacco and marijuana use during pregnancy and children's growth at 6 years. In this cohort of pregnant teenagers and their offspring, mothers were recruited from an urban prenatal clinic between 1990 and 1995, and observed from their fourth prenatal month. At the delivery assessment, there were 413 live-born singletons. At the 6-year visit, 345 children and mothers were evaluated. Prenatal alcohol and marijuana exposure were significantly associated with growth deficits, after controlling statistically for other prenatal substance use, current maternal substance use, current environmental tobacco exposure (ETS) and sociodemographic and growth-related covariates. There was a significant negative association between the second and third trimester alcohol exposure and offspring height. Third trimester alcohol exposure predicted reduced skinfold thickness. Exposure to any prenatal marijuana in the second trimester was significantly associated with shorter stature. First trimester tobacco exposure was associated with increased skinfold thickness among the 6-year-olds. The effects of prenatal alcohol exposure on growth at birth persisted in older children despite a low level of exposure during gestation. Effects of prenatal marijuana exposure on reduced height were not anticipated and occurred only when use was categorized as any/none. These data are consistent with an emerging body of evidence indicating that, by contrast to the growth deficits associated with smoking during pregnancy, which are evident at birth, the shorter stature associated with prenatal alcohol exposure continues to be evident during childhood.

Adolescent↗
PubMed2004

Effect of maternal diabetes and ethanol interactions on embryo development in the mouse.

The aim of this study was to determine the possible fetal effects of interaction between maternal diabetes and acute doses of alcohol. Pregnant TO mice were made diabetic by a single injection of streptozotocin (STZ) on gestation day (GD) 2. Single dose of 0.003 or 0.03 ml/g body weight of fresh ethanol (25% v/v of absolute alcohol in normal saline) was injected into groups of diabetic and nondiabetic animals on GD 7 or 8. One group of diabetic animals had a daily dose of 6-8 IU of insulin subcutaneously. Fetuses were collected on GD 18. There was a significant increase in the incidence of implantation failure in the diabetes plus ethanol groups and insulin control group. Ethanol injection on GD 7 accentuated diabetes-related embryonic resorption and intrauterine growth retardation (IUGR). This effect was less marked in the diabetic group treated with ethanol on GD 8. Diabetes alone produced a greater incidence of IUGR than ethanol alone. Midfacial hypoplasia and minor anomalies were found more frequently in the combination treatment groups. Holoprosencephaly and thymus hypoplasia observed in diabetic groups were found to be reduced in frequency in the diabetes plus ethanol groups, suggesting an antagonistic type of ethanol-diabetes interaction, stage-dependently. Since severely malformed embryos are known to be resorbed/killed in utero in mice, this reduction might reflect the magnitude of early death of severely malformed embryos. These data suggest that the interaction effects are possibly related to alterations in fundamental developmental processes of early embryos.

Abnormalities, Drug-Induced↗
PubMed2000

Exposure of rats to a high but not low dose of ethanol during early postnatal life increases the rate of loss of optic nerve axons and decreases the rate of myelination.

Visual system abnormalities are commonly encountered in the fetal alcohol syndrome although the level of exposure at which they become manifest is uncertain. In this study we have examined the effects of either low (ETLD) or high dose (ETHD) ethanol, given between postnatal days 4-9, on the axons of the rat optic nerve. Rats were exposed to ethanol vapour in a special chamber for a period of 3 h per day during the treatment period. The blood alcohol concentration in the ETLD animals averaged approximately 171 mg/dl and in the ETHD animals approximately 430 mg/dl at the end of the treatment on any given day. Groups of 10 and 30-d-old mother-reared control (MRC), separation control (SC), ETLD and ETHD rats were anaesthetised with an intraperitoneal injection of ketamine and xylazine, and killed by intracardiac perfusion with phosphate-buffered glutaraldehyde. In the 10-d-old rat optic nerves there was a total of approximately 145,000-165,000 axons in MRC, SC and ETLD animals. About 4% of these fibres were myelinated. The differences between these groups were not statistically significant. However, the 10-d-old ETHD animals had only about 75,000 optic nerve axons (P < 0.05) of which about 2.8 % were myelinated. By 30 d of age there was a total of between 75,000-90,000 optic nerve axons, irrespective of the group examined. The proportion of axons which were myelinated at this age was still significantly lower (P < 0.001) in the ETHD animals (approximately 77 %) than in the other groups (about 98 %). It is concluded that the normal stages of development and maturation of the rat optic nerve axons, as assessed in this study, can be severely compromised by exposure to a relatively high (but not low) dose of ethanol between postnatal d 4 and 9.

Analysis of Variance↗
PubMed1982

Magnesium and zinc deficiency and growth retardation in offspring of alcoholic rats.

Alcohol ingestion during pregnancy is known to cause fetal malformation and growth retardation. We investigated the effect of alcohol on mineral content and fetal development in rats fed 24% (v/v) alcohol eight weeks prior to and during pregnancy. Rats ingesting alcohol produced fewer fetuses (6.3 +/- 0.3 vs 9.6 +/- 0.3 in control) with lower fetal weight (3.48 +/- 0.09 vs 4.12 +/- 0.08 gm in control) and heavier placentas (0.66 +/- 0.05 vs 0.50 +/- 0.01 gm in control). The fetuses of alcoholic rats contained lower zinc (423.8 +/- 4.5 vs 459.9 +/- 5.4 microEq/100 gm dry weight in control) and magnesium (12.4 +/- 0.1 vs 12.7 +/- 0.1 mEq/100 gm dry weight in control) in the total carcass.

Alcoholism↗
PubMedDate not supplied

Fetal ADH2*3, maternal alcohol consumption, and fetal growth.

There is some evidence suggesting the allele for alcohol dehydrogenase 2*3 (ADH2*3) is associated with a protective effect against alcohol-related intrauterine growth retardation (IUGR). This study was conducted to explore the affect of the ADH2*3 allele on fetal growth. Bloodspots (n = 1016) belonging to individual infants of a subgroup of the Baltimore-Washington Infant Study (BWIS) were assayed for the presence of the ADH2*3 allele by a polymerase chain reaction (PCR)-based method. Infants genotyped for ADH2*3 were those for whom bloodspots were identified and obtained from the Maryland Newborn Screening Program. The effect of ADH2*3 and maternal alcohol consumption on intrauterine growth was explored by multivariable linear regression analysis. Twenty-six percent of the 306 blood spots belonging to African-American infants were positive for ADH2*3 (4% were homozygous and 22% were heterozygous). Only a small percentage of bloodspots for Caucasian (1.3%) were positive for the ADH2*3 allele. Consequently, further analysis concentrated on gene-exposure interactions for African-American infants. It was found that the incidence of being small-for-gestation-age (SGA) was lower for ADH2*3-positive infants (2.5% versus 8.8%; p = .08). SGA infants had elevated odds for being ADH2*3 negative (OR: 3.15, 95% C.I.: 0.70-14.26) and for being born to mothers that consumed alcohol during pregnancy (OR: 2.31, 95% C.I.: 0.77-6.91). A negative trend between maternal alcohol consumption and mean offspring birthweight was found; however, ADH2*3 did not have a significant impact on mean birthweight for infants born to mothers that drank during pregnancy. These results could be interpreted as possible support for the hypothesis that ADH2 genotype in the infant may impact risk for alcohol-related IUGR. However, this study has limitations in that it is a "nested study of convenience" and involves a relatively small number of infants born to mothers reporting moderate to heavy alcohol use during pregnancy.

Adult↗
PubMed2004

Differential gene profiles in developing embryo and fetus after in utero exposure to ethanol.

Alcohol consumption during pregnancy results in morphological abnormalities in the fetuses of humans and experimental animals, and is referred to as fetal alcohol syndrome (FAS). However, the molecular mechanism underlying FAS has not been completely elucidated. The aim of the present study was to investigate the potential molecular mechanisms of ethanol-induced FAS in the developing embryo and fetus. cDNA microarray analysis was used to screen for altered gene profiles. Ethanol at a teratogenic dosage (3.8 g/kg, twice a day) was administered intraperitoneally to pregnant C57Bl/6J mice from gestation day (GD) 6 to 8. Morphologic observations showed excessive malformations of the craniofacial regions (reduction of the face, the absence of eyes, nose, jaw, and mandible, underdevelopment of vibrissae areas, cleft lip, and palate) in ethanol-exposed embryos (GD 10) and fetusus (GD 15). cDNA microarray analysis showed alterations in several gene profiles, including the "palate, lung, and nasal epithelium clone (plunc), "neurofilament, " and "pale ear. " Of these genes, the expressions of plunc were confirmed by reverse-transcription polymerase chain reaction (RT-PCR) and whole-mount in situ hybridization. The plunc was highly expressed in the craniofacial region, specifically in upper airways and nasopharyngeal epithelium. RT-PCR analysis revealed that normal plunc mRNA expression levels were present in GD 15 fetuses, but not in GD 10 embryos. Interestingly, ethanol significantly downregulated the plunc expression in GD 15 fetuses. Our results suggest that ethanol-induced FAS is due in part to the downregulation of plunc expression in the fetus, and this gene may be a candidate biological marker for FAS.

Animals↗
PubMed1990

Hepatic glutathione, metallothionein and zinc in the rat on gestational day 19 during chronic ethanol administration.

Ethanol, under certain conditions, alters the metabolism of sulfur amino acids, metallothionein (MT) and zinc. If chronic ethanol administration during pregnancy decreases the availability of sulfur amino acids or Zn, this deficiency could contribute to growth retardation of the fetuses, one of the features of fetal alcohol syndrome. The purpose of this study was to discern whether chronic ethanol administration to pregnant rats alters glutathione (GSH), MT or Zn content of selected tissues of the dams and fetuses. Sprague-Dawley rats were fed from gestational days 5 to 19 either the control diet ad libitum (AF), the ethanol diet ad libitum (EF) or the control diet using the pair-feeding technique (PF). On the 19th day of gestation, total hepatic GSH was significantly lower for the EF and PF dams than for the AF dams. Hepatic MT contents were similar for the AF and EF dams, and hepatic MT content was significantly greater for the PF dams than the AF and EF dams. The three groups did not differ regarding hepatic Zn content of dams or fetuses. In summary, on the 19th day of gestation, chronic ethanol feeding of pregnant rats did not lower the maternal hepatic GSH level below that of PF dams, did not induce hepatic MT in the dams and did not prevent fetuses from achieving body weights and hepatic Zn concentrations equal to those of controls.

Animals↗
PubMed2001

Expression of vascular endothelial growth factor receptors 1, 2 and 3 in placentas from normal and complicated pregnancies.

Extensive angiogenesis and invasion of the maternal decidua by trophoblasts are essential for the development and function of the placenta. Vascular endothelial growth factors (VEGF), placenta growth factor (PlGF) and their receptors VEGFR-1/Flt-1, VEGFR-2/KDR and VEGFR-3/Flt4 have important roles in vasculogenesis and angiogenesis. We have studied the localization of these proteins by immunohistochemistry and Western blotting in the placenta and of PlGF in maternal serum, and their association with diabetes, pre-eclampsia, fetal growth restriction (FGR) and fetal alcohol syndrome (FAS). VEGFR-1 and VEGFR-3 were detected mainly in the syncytiotrophoblastic layer whereas VEGFR-2 was detected in the vascular endothelial cells of the placenta. VEGFR-1, but not the other receptors, showed increased expression in placental syncytiotrophoblasts from 50% of patients with severe pre-eclampsia and FGR when compared with normal placentas. PlGF was undetectable in 38 of 44 samples of amniotic fluid of mothers with normal and complicated pregnancies. However, maternal serum PlGF concentrations were significantly lower in pre-eclamptic patients and in those with FGR when compared to diabetic women or healthy controls. These results suggest that low maternal serum PlGF and increased placental expression of its receptor VEGFR-1 are associated with pre-eclampsia and FGR.

Female↗
PubMed2004

Protection from ethanol-induced limb malformations by the superoxide dismutase/catalase mimetic, EUK-134.

Based on previous in vitro studies that have illustrated prevention of ethanol-induced cell death by antioxidants, using an in vivo model, we have tested the anti-teratogenic potential of a potent synthetic superoxide dismutase plus catalase mimetic, EUK-134. The developing limb of C57BL/6J mice, which is sensitive to ethanol-induced reduction defects, served as the model system. On their ninth day of pregnancy, C57BL/6J mice were administered ethanol (two intraperitoneal doses of 2.9 g/kg given 4 h apart) alone or in combination with EUK-134 (two doses of 10 mg/kg). Pregnant control mice were similarly treated with either vehicle or EUK-134, alone. Within 15 h of the initial ethanol exposure, excessive apoptotic cell death was observed in the apical ectodermal ridge (AER) of the newly forming forelimb buds. Forelimb defects, including postaxial ectrodactyly, metacarpal, and ulnar deficiencies, occurred in 67.3% of the ethanol-exposed fetuses that were examined at 18 days of gestation. The right forelimbs were preferentially affected. No limb malformations were observed in control fetuses. Cell death in the AER of embryos concurrently exposed to ethanol and EUK-134 was notably reduced compared with that in embryos from ethanol-treated dams. Additionally, the antioxidant treatment reduced the incidence of forelimb malformations to 35.9%. This work illustrates that antioxidants can significantly improve the adverse developmental outcome that results from ethanol exposure in utero, diminishing the incidence and severity of major malformations that result from exposure to this important human teratogen.

Animals↗
PubMed1998

Alcohol and fetal damage.

Since the identification of fetal alcohol syndrome in the end of the 1960s, substantial evidence has accumulated on a number of adverse effects that alcohol consumption during pregnancy may have on the fetus. Long-term effects on child development has also been observed. Although the various types of effects are well documented, less is known about threshold levels of consumption, under which there is no risk of damage. Few studies have assessed the risk associated with high episodic drinking. From a theoretical point of view, binge drinking in critical stages in organ formation may constitute a particularly high risk for adverse outcomes.

Alcohol Drinking↗
PubMed1986

The spectrum of fetal abuse in pregnant women.

Physical assault by a woman or her partner upon their unborn child has received minimal attention in the psychiatric or obstetric literature. The spectrum concept facilitates the application of knowledge about one type of fetal abuse (e.g., physical assault in response to fetal movements) to other types (e.g., neglect or failure to protect the fetus from chemical assault by alcohol, nicotine, or drugs). Three illustrative case histories are presented, including two cases of assault by the mother via the anterior abdominal wall. Fetal abuse may be one antecedent of child abuse, and this paper attempts to transpose the known correlates of child abuse into an antenatal time framework. The resultant preliminary etiological model also draws upon research findings from neonaticide, the psychology of pregnancy, and the psychology of aggression. In addition, recent research on the maternal-paternal-fetal triad is reviewed in an attempt to delineate under what circumstances ambivalence in the parental-fetal relationship may find expression as fetal abuse. The characteristics of individuals most at risk of perpetrating fetal abuse are outlined.

Adolescent↗