Neonatal jaundice: A risk factor for infantile autism?

ArticleinPaediatric and Perinatal Epidemiology 22(6):562-8 · November 2008with16 Reads
DOI: 10.1111/j.1365-3016.2008.00973.x · Source: PubMed
In a previous study, we found that infants transferred to a neonatal ward after delivery had an almost twofold increased risk of being diagnosed with infantile autism later in childhood in spite of extensive controlling of obstetric risk factors. We therefore decided to investigate other reasons for transfer to a neonatal ward, in particular hyperbilirubinaemia and neurological abnormalities. We conducted a population-based matched case-control study of 473 children with autism and 473 matched controls born from 1990 to 1999 in Denmark. Cases were children reported with a diagnosis of infantile autism in the Danish Psychiatric Central Register. Conditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals [CI] and likelihood ratio tests were used to test for effect modification. We found an almost fourfold risk for infantile autism in infants who had hyperbilirubinaemia after birth (OR 3.7 [95% CI 1.3, 10.5]). In stratified analysis, the association appeared limited to term infants (>or=37 weeks gestation). A strong association was also observed between abnormal neurological signs after birth and infantile autism, especially hypertonicity (OR 6.7 [95% CI 1.5, 29.7]). No associations were found between infantile autism and low Apgar scores, acidosis or hypoglycaemia. Our findings suggest that hyperbilirubinaemia and neurological abnormalities in the neonatal period are important factors to consider when studying causes of infantile autism.


    • "In the current study there was no significant correlation between neonatal jaundice and autism, supporting the belief of many researchers as Gardener et al. [36]. On the other hand, few suggested that hyperbilirubinemia occurs more frequently than expected among children later diagnosed with autism [37]. Hara [38] found that seizures that occur in autistic children are most commonly of the generalized type and said that epilepsy is one of the negative factors of cognitive, adaptive and behavioral outcomes for individuals with autism. "
    [Show abstract] [Hide abstract] ABSTRACT: Background: Autism is a neurodevelopmental disorder characterized by clinical, etiologic and genetic heterogeneity. Many surveys revealed cytogenetically visible chromosomal abnormalities in 7.4% of autistic patients documented as well as several submicroscopic variants. This study had been conducted to identify some aspects that might be involved in the pathogenesis of autism which is necessary for offering proper genetic counseling to families of autistic patients and their role in the prenatal diagnosis of autism. Methods: This cross sectional study was conducted at the Child Psychiatry Clinic, Pediatric Hospital, Ain Shams University on 30 autistic patients who were subjected to the following tools: Confirmation of diagnosis using DSM-IV-TR criteria, IQ assessment using Stanford-Binet intelligence scale and assessment of severity of autistic symptoms using childhood autism rating scale (CARS). Full clinical examination, neurological examination, EEG, audiological assessment were also done. High resolution karyotyping was done for detection of numerical or structural chromosomal abnormalities as deletion, duplication, translocation of chromosomes. Results: All the results of cytogenetic analysis were normal with no detectable numerical or structural chromosomal abnormalities. Males are affected more than females, only one case had history of drug intake (progestin), two cases had history of anti-D injection and two cases had history of diabetes mellitus during pregnancy. Four cases had history of respiratory distress and seven cases had history of jaundice. Two cases had history of generalized tonic clonic convulsion and four cases had history of EEG abnormalities. Fifteen cases of our autistic patients had mild mental retardation and six cases had moderate mental retardation. Conclusion: Chromosomal abnormalities were not detected in the studied autistic children, and so the relation between the genetics and autism still needs further work up with different study methods and techniques.
    Full-text · Article · Jun 2015
    • "Rutter et al., 1999), la dépression post natale maternelle (Croen et al., 2011) ou les déprivations sensorielles (Mukaddes et al, 2007). et al., 2008), hyper bilirubinémie chez les enfants nés à terme (Maimburg et al., 2008). Il peut être illustré par Limperopoulos et al. (2007Limperopoulos et al. ( et 2008) qui montrent que le risque d'autisme chez les enfants prématurés est augmenté chez ceux qui ont également une hémorragie intracérébelleuse , détectée à l'IRM. "
    [Show abstract] [Hide abstract] ABSTRACT: Successive definitions of autism did not reduce the extent of its clinical heterogeneity. This limits progress in understanding its etiological basis and the implementation of targeted therapeutic strategies. Comorbid disorders with autism are a complex issue because their frequency is one of the core features of clinical heterogeneity. We hypothesize that they are a better etiological clue than behavioral clinical syndromes. Our first study explores the initial instinctive concerns of parents of autistic children based on 459 open-Labelled questionnaires. Parents identify a set of symptoms comorbid to autism at a very early stage in their child's development The second study lists all the pre, peri and neonatal risk factors which have a significant, although moderate, effect on autism. .The third study lists in great detail all of the major causes of autism in a clinical epidemiological sample of 183 children with a typical autism. The 36 genetic diagnoses represent 58% of all causes which leaves a significant proportion of neurodevelopmental disorders of environmental or cryptogenic origin. The clinical, genetic and environmental differences that we identified between a non-Syndromic and syndromic autism (with comorbidities) validate the hypothesis that comorbidities are linked to a more general dysfunction and contribute to distinguishing the etiologies and provide practical information on the prognosis. A dimensional approach which includes comorbid disorders is prone to establish a fine-Grained taxonomy that point to distinct etiopathological processes.
    Full-text · Article · Oct 2014 · Entropy
    • "There is a known association between excess bilirubin manifested as jaundice and autism. In a study conducted in Denmark, where sunlight availability in the winter months is scarce, infants with postnatal hyperbilirubinemia had nearly a four-fold increased risk to autism [106], and this effect was most pronounced for infants born in the winter months [107]. Treatment for jaundice involves sunlight or UV light therapy, which would lead to an increased production of cholesterol sulfate in the skin, thus ameliorating the deficit. "
    [Show abstract] [Hide abstract] ABSTRACT: In a recent paper, we proposed that a contributing factor in autism is a deficiency in cholesterol sulfate supply. In this paper, we investigate a link between preeclampsia and subsequent autism in the child, and we hypothesize that both conditions can be attributed to a severe depletion of cholesterol sulfate. Through studies on the Vaccine Adverse Event Reporting System (VAERS) database, we demonstrate a strong statistical relationship among the signs and symptoms associated with autism and those associated with preeclampsia, pernicious anemia, and serious adverse reactions to vaccines. We show that VAERS reports associated with symptoms typical of pernicious anemia produce both a set of symptoms that are highly correlated with preeclampsia and another set highly correlated with autism. We explain this observation via an argument that, in a severe reaction, the cascade of events subsequent to vaccination reflects a profuse production of nitric oxide (NO) and consequential destruction of both red blood cells (RBCs) and cobalamin. This may explain the diverse signs and symptoms associated with both preeclampsia and severe vaccine adverse reactions. We argue that excess NO synthesis, induced by the aluminum and antigen in vaccines, results in hemolysis of RBCs, which allows hemoglobin to scavenge the excess NO, converting it to nitrate. The NO is also scavenged by cobalamin, leading to its inactivation and contributing to subsequent pernicious anemia. Finally, we demonstrate that severe adverse reactions to vaccines can be associated with life-threatening conditions related to the heart and brain, as well as stillbirth, when the vaccine is administered to a woman in the third-trimester of pregnancy, as demonstrated by statistical analysis of the Gardasil records.
    Full-text · Article · Nov 2012
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