Fetal abnormality and maternal ethanol metabolism.
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We investigated the transfer of three antioxidants - melatonin, S-adenosyl methionine (SAM) and various forms of vitamin E - across the term, normal human placenta. The transport technique involved the single, isolated placental cotyledon system in vitro. Melatonin crossed the placental rapidly, equally to the freely diffusible marker, antipyrine. There was no biotransformation of the agent. SAM was transferred slowly, similarly to passively transported L-glucose as a marker. There was a breakdown of SAM to at least one other derivative; the process appeared to be nonenzymatic. Vitamin E was transferred slowly, at a rate only 10% of L-glucose. The natural RRR (nonracemic) form of vitamin E was transported best. Free vitamin, rather than the acetate seems to be transferred best, a finding that will require further study.
A sample of 12 children (seven males, five females; mean age 6 years 7 months, SD 2 years 6 months, range 2 years 4 months to 12 years 1 month) with moderate-to-severe foetal alcohol syndrome (FAS) and another sample of 26 children (12 males, 14 females; mean age of 6 years 2 months SD 2 years 10 months, range 2 years 6 months to 12 years 8 months) with mild FAS or foetal alcohol effects (FAE) as well as a sample of 15 age- and sex-matched control children with unspecific intellectual disability were compared using the Developmental Behaviour Checklist (DBC). There were significant differences (p=0.01) between the groups on five of six subscales of the DBC with controls scoring lower on the disruptive, self-absorbed, anxiety, antisocial behaviour, and communication disturbance scales. The DBC profiles of the two foetal alcohol exposed groups did not differ from each other. It is concluded that quantitative behaviour measurement provides insights into specific behavioural phenotypes of FAS/FAE.
The purpose of this review is to familiarize physical therapists with the diagnostic, clinical, and behavioral characteristics associated with fetal alcohol syndrome (FAS) and other alcohol-related birth defects. Through review of FAS research studies of both humans and animals, the prevalence, pharmacokinetics, and clinical features of this syndrome are described. Deficits in the areas of cognitive, behavioral, and motor development are also described. Particular attention is given to neuromotor differences and orthopedic abnormalities associated with FAS that may require consultation or intervention from physical therapists.
PURPOSE: To describe the experiences of foster parents who are living with a child diagnosed with Fetal Alcohol Syndrome (FAS). DESIGN AND METHOD: A qualitative approach was selected due to the paucity of knowledge on the topic. Eight foster mothers living with children with FAS were studied. These foster parents had parented a collective total of 17 children with FAS, ranging between the ages of 2 and 16. Each in-depth interview was unstructured and consisted of open-ended questions. Data were analyzed using content analysis. RESULTS: Foster parents described many difficult issues needing attention in children with FAS. Cognitive concerns included diminished memory/comprehension, lack of understanding of consequences, and the absence of fear. Behavioral management was a problem due to the frequent occurrence of hyperactivity, aggressiveness, destructiveness, and high pain tolerance. Parents also described problems in coping with daily realities of life with a child with FAS including the necessity of providing consistency, coping strategies, and fears for the child's future. CLINICAL IMPLICATIONS: Nurses need to understand the complex problems that face affected children and their families. Understanding the daily realities of living with children with FAS allows nurses to realistically assess childrens' abilities, maximize their development, and provide for their needs more effectively, as well as assisting families to cope with the behavior and cognitive issues so apparent in children with FAS.
In Australia the issue of fetal alcohol syndrome (FAS) has not been the subject of policy development or of extensive research. There is a lack of knowledge, both in the general community and by health professionals, of the nature of the risks associated with heavy alcohol consumption during pregnancy and the factors that increase this risk. This paper reviews the literature surrounding FAS with the aim of providing the reader an understanding of the diagnostic features and epidemiology of FAS and of the developmental sequelae associated with this syndrome.
After documenting the wide range of psychopathology and impairment of intellectual functioning in earlier contributions, the present report from long-term observations of an extended cohort of children with Fetal Alcohol Syndrome (FAS) deals with correlates of psychopathology and intelligence in these children. At preschool age, severity of morphological damage, the type of milieu, sex and IQ were significant predictors of psychopathology. In another subgroup of school-aged children, these associations were less strong; only severity of morphological damage and IQ still correlated to some extent significantly with psychopathology. Intelligence was significantly impaired in those children with severe morphological damage who were raised in institutions.
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This research aimed to develop a Fetal Alcohol Behavior Scale (FABS) that describes the behavioral essence of fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE), regardless of age, race, sex, and IQ. Using a reference sample of 472 diagnosed patients with FAS or FAE, ages 2 to 51, five studies are described. The FABS demonstrates high item-to-scale reliability (Cronbach's alpha = 0.91) and good test-retest reliability (r = 0.69) over an average interval of 5 years. It identifies many of the subjects with known or presumed prenatal alcohol exposure in detection studies using both prison and general samples. FABS scores also predict dependent living among adult patients with FAS/FAE. The FABS is uncorrelated with IQ, sex, age, race, and diagnosis (FAS versus FAE). We outline areas of further work to define the specificity and utility of this FABS.
On day 20 of gestation, after ethanol feeding (27% ethanol calories, 25% protein), placental weights, DNA, RNA and water content were greater than in controls pair-fed an isocaloric diet without ethanol or those ad lib fed a pellet diet of similar composition. Rat litter size and fetal body, liver and brain weights were similar in all groups. In vivo fetal amino acid accumulation was significantly lower after alcohol exposure despite similar placental uptake. These results indicate that both placental hyperplasia and abnormal fetal amino acid uptake occur at a low alcohol dose when fetal body weight is unaffected.
Persons with fetal alcohol syndrome (FAS) who are not mentally retarded often have difficulty qualifying for special educational and vocational services. In this pilot study, 16 nonretarded young adults with FAS were divided into two groups--one with average to above-average IQ and one with borderline to low-average IQ. Participants in both groups manifested clear deficits on neuropsychological measures sensitive to complex attention, verbal learning, and executive function. The frequency and severity of cognitive impairment demonstrated in both FAS groups were greater than what would have been predicted on the basis of IQ alone. The implications of these findings for identification and management of cognitive impairment in individuals with FAS are discussed.
Ethanol consumption during pregnancy can cause fetal alcohol syndrome (FAS). Although the exact mechanism is unknown, nutritional alterations caused by ethanol exposure may be an etiologic factor in FAS. The congenital heart defects seen in FAS are similar to those found in vitamin A teratogenesis. Because ethanol ingestion alters vitamin A metabolism, we hypothesized that the cardiac manifestations seen in FAS result from an alteration in vitamin A metabolism or function in the developing fetus. Twenty-day gestation fetal rat hearts from ethanol-exposed and control pregnancies were analyzed for 1) levels of endogenous retinol, retinyl palmitate, and retinoic acid by quantitative HPLC; 2) binding activity levels of both retinol by cellular retinol binding protein and retinoic acid by cellular retinoic acid binding protein using specific competitive binding assays; and 3) relative abundance of cellular retinol binding protein and retinoic acid receptor alpha, beta, and gamma subtype message as expressed in mRNA. Levels of retinol and retinyl palmitate were significantly higher (p < 0.01) and the level of retinoic acid was significantly lower (p < 0.02) in the ethanol-exposed fetal hearts. Binding activity levels of cellular retinol binding protein and cellular retinoic acid binding protein were not different in the two groups. The message for retinoic acid receptor alpha (3.7 kb) was increased (p < 0.01) and the message for retinoic acid receptor beta was decreased (p < 0.05) in the ethanol-exposed hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
This article examines the portrayal of pregnancy and alcohol in thirty-six national network evening news broadcasts (ABC, CBS, NBC). Early coverage focused on white, middle-class women, as scientific authorities and government officials warned against drinking during pregnancy. After 1987, however, women who drank during pregnancy were depicted as members of minority groups and as a danger to society. The thematic transition began before warning labels appeared on alcoholic beverages and gained strength from official government efforts to prevent fetal alcohol syndrome. The greatest impetus for the revised discourse, however, was the eruption of a "moral panic" over crack cocaine use. By linking fetal harm to substance abuse, the panic suggested it was in the public's interest to control the behavior of pregnant women.
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BACKGROUND: Fetal alcohol syndrome (FAS), which involves the triad of features reflecting facial dysmorphology, growth retardation and intellectual impairments, encompasses a relatively small proportion of the children affected prenatally by alcohol. Unfortunately, in the absence of facial dysmorphology, the diagnosis is difficult in the majority of children, who are considered to have alcohol-related neurodevelopmental disorder (ARND). Because accepted clinical methods are not pathognomonic, a novel profile approach was used to examine neuropsychological abilities and disabilities to identify children with ARND who do not meet the diagnostic criteria of FAS. OBJECTIVE: To establish a set of criteria, to be validated in future studies, for characterizing the neuropsychological profile of children with ARND. By describing the procedures at this preliminary stage of our work, the goal is to draw attention to this neglected topic and to suggest a model that can be replicated and validated by others, and to provide the first systematic clinical report on diagnosing ARND in Canada. PROCEDURES: On the basis of the literature, parents' descriptions and the authors' own experience with ARND, a profile of neuropsychological characteristics, including both deficits and assets, that are associated with prenatal alcohol exposure was hypothesized. A group of children was then evaluated, mostly adoptees or children in foster care, who were referred for learning and behavioural problems potentially associated with gestational exposure. Their results were submitted to a profile analysis by comparing their deficits and assets according to a list describing a hypothetical ARND profile to determine whether each child fit or did not fit the ARND profile. Groups were compared for background characteristics, FAS symptomatology, and results on specific neuropsychological and behavioural tests. Finally, the characteristics most strongly differentiating the two groups were identified. SETTING: Hospital-based outpatient program. PARTICIPANTS: Fifty-two children aged four to 18 years who were referred for a diagnostic assessment related to suspected or known prenatal alcohol exposure. OUTCOME MEASURES: Each child's assessment results were compared against a list of 21 deficits and six assets by two independent raters. Children with an average of more than 60% deficits and 50% assets were considered to have ARND, while the remainder were not. RESULTS: Twenty-eight children (54%) were assigned to the ARND group and 24 to the non-ARND group. The groups did not differ in physical features or home background characteristics, with the exception of higher parental intelligence quotient in the non-ARND group. The ARND group was more likely to have repeated a grade or received special education and scored lower on standardized measures of intelligence, language and memory abilities. Frequency of behaviour or social problems were equivalent in both groups. CONCLUSIONS: A profile approach used to identify children with ARND discriminates problems in neuropsychological but not behavioural domains. Because elevated scores on behavioural tasks in both ARND and non-ARND groups were clinically significant, more research is needed to identify what behavioural problems are unique to children with ARND compared with other clinic-referred children.
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