Childhood infections and autism spectrum disorders and/or intellectual disability: a register-based cohort study / HÃ¥kan KARLSSON in Journal of Neurodevelopmental Disorders, 14 (2022)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 14 (2022) Titre : Childhood infections and autism spectrum disorders and/or intellectual disability: a register-based cohort study Type de document : texte imprimé Auteurs : HÃ¥kan KARLSSON, Auteur ; Hugo SJÖQVIST, Auteur ; Martin BRYNGE, Auteur ; Renee GARDNER, Auteur ; Christina DALMAN, Auteur Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/complications/diagnosis/epidemiology  Child  Cohort Studies  Female  Humans  Intellectual Disability/complications/diagnosis/epidemiology  Pregnancy  Siblings  Autism spectrum disorders  Childhood  Infection  Intellectual disability  Risk Index. décimale : PER Périodiques Résumé : OBJECTIVE: To explore the associations between childhood infections and subsequent diagnoses of autism spectrum disorder (ASD), intellectual disability (ID), and their co-occurrence. METHODS: The association between specialized care for any infection, defined by ICD-codes, and later ASD or ID was investigated in a register-based cohort of 556,732 individuals born 1987-2010, resident in Stockholm County, followed from birth to their 18th birthday or December 31, 2016. We considered as potential confounders children's characteristics, family socioeconomic factors, obstetric complications, and parental histories of treatment for infection and psychiatric disorders in survival analyses with extended Cox regression models. Residual confounding by shared familial factors was addressed in sibling analyses using within-strata estimation in Cox regression models. Sensitivity analyses with the exclusion of congenital causes of ASD/ID and documented risk for infections were also performed. RESULTS: Crude estimates indicated that infections during childhood were associated with later ASD and ID with the largest risks observed for diagnoses involving ID. Inclusion of covariates, exclusion of congenital causes of ASD/ID from the population, and sibling comparisons highlighted the potential for confounding by both heritable and non-heritable factors, though risks remained in all adjusted models. In adjusted sibling comparisons, excluding congenital causes, infections were associated with later "ASD without ID" (HR 1.24, 95%CI 1.15-1.33), "ASD with ID" (1.57, 1.35-1.82), and "ID without ASD" (2.01, 1.76-2.28). Risks associated with infections varied by age at exposure and by age at diagnosis of ASD/ID. CONCLUSIONS: Infections during childhood may contribute to a later diagnosis of ID and ASD. En ligne : https://dx.doi.org/10.1186/s11689-022-09422-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=574 [article] Childhood infections and autism spectrum disorders and/or intellectual disability: a register-based cohort study [texte imprimé] / HÃ¥kan KARLSSON, Auteur ; Hugo SJÖQVIST, Auteur ; Martin BRYNGE, Auteur ; Renee GARDNER, Auteur ; Christina DALMAN, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 14 (2022) Mots-clés : Autism Spectrum Disorder/complications/diagnosis/epidemiology  Child  Cohort Studies  Female  Humans  Intellectual Disability/complications/diagnosis/epidemiology  Pregnancy  Siblings  Autism spectrum disorders  Childhood  Infection  Intellectual disability  Risk Index. décimale : PER Périodiques Résumé : OBJECTIVE: To explore the associations between childhood infections and subsequent diagnoses of autism spectrum disorder (ASD), intellectual disability (ID), and their co-occurrence. METHODS: The association between specialized care for any infection, defined by ICD-codes, and later ASD or ID was investigated in a register-based cohort of 556,732 individuals born 1987-2010, resident in Stockholm County, followed from birth to their 18th birthday or December 31, 2016. We considered as potential confounders children's characteristics, family socioeconomic factors, obstetric complications, and parental histories of treatment for infection and psychiatric disorders in survival analyses with extended Cox regression models. Residual confounding by shared familial factors was addressed in sibling analyses using within-strata estimation in Cox regression models. Sensitivity analyses with the exclusion of congenital causes of ASD/ID and documented risk for infections were also performed. RESULTS: Crude estimates indicated that infections during childhood were associated with later ASD and ID with the largest risks observed for diagnoses involving ID. Inclusion of covariates, exclusion of congenital causes of ASD/ID from the population, and sibling comparisons highlighted the potential for confounding by both heritable and non-heritable factors, though risks remained in all adjusted models. In adjusted sibling comparisons, excluding congenital causes, infections were associated with later "ASD without ID" (HR 1.24, 95%CI 1.15-1.33), "ASD with ID" (1.57, 1.35-1.82), and "ID without ASD" (2.01, 1.76-2.28). Risks associated with infections varied by age at exposure and by age at diagnosis of ASD/ID. CONCLUSIONS: Infections during childhood may contribute to a later diagnosis of ID and ASD. En ligne : https://dx.doi.org/10.1186/s11689-022-09422-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=574

Maternal antibodies to gliadin and autism spectrum disorders in offspring-A population-based case-control study in Sweden / Renee M. GARDNER in Autism Research, 14-9 (September 2021)  

Public ISBD [article]  inAutism Research > 14-9 (September 2021) . - p.2002-2016 Titre : Maternal antibodies to gliadin and autism spectrum disorders in offspring-A population-based case-control study in Sweden Type de document : texte imprimé Auteurs : Renee M. GARDNER, Auteur ; Ida SAMUELSSON, Auteur ; Emily G. SEVERANCE, Auteur ; Hugo SJÖQVIST, Auteur ; Robert H. YOLKEN, Auteur ; Christina DALMAN, Auteur ; HÃ¥kan KARLSSON, Auteur Article en page(s) : p.2002-2016 Langues : Anglais (eng) Mots-clés : Attention Deficit Disorder with Hyperactivity  Autism Spectrum Disorder/epidemiology  Case-Control Studies  Female  Gliadin  Humans  Pregnancy  Sweden/epidemiology  attention deficit hyperactivity disorder  autism spectrum disorder  gliadin  gluten-sensitivity  intellectual disability Index. décimale : PER Périodiques Résumé : While individuals diagnosed with autism spectrum disorders (ASD) have higher levels of antibodies directed towards gliadin, a component of wheat gluten, no study has examined anti-gliadin antibodies (AGA) in etiologically relevant periods before diagnosis. The objective of this study was to investigate if maternal levels of AGA, during pregnancy and at the time of birth, are associated with ASD in offspring. We analyzed AGA in archived neonatal dried blood spots (NDBS) for 921 ASD cases and 1090 controls, and in paired maternal sera collected earlier in pregnancy for a subset of 547 cases and 428 controls. We examined associations with ASD diagnoses as a group and considering common comorbidities (intellectual disability [ID] and attention-deficit/hyperactivity disorder). We compared 206 cases to their unaffected siblings to examine the potential for confounding by shared familial factors. Odds of ASD tended to be lower among those with the highest levels (≥90th percentile) of AGA compared to those with low levels (<80th percentile; OR 0.78, 95% CI 0.56-1.09, measured in NDBS). This pattern was more apparent for ASD with comorbid ID when measured in NDBS (0.51, 0.30-0.87), with a similar trend in maternal sera (0.55, 0.24-1.29). High levels of AGA were similarly associated with lower odds of ASD in the sibling comparison. In summary, we found little association between maternal antibodies raised against components of gluten and risk of ASD in general. Exposure to high levels of AGA in the pre- and perinatal periods may be protective in terms of risk for ASD with ID. LAY SUMMARY: There is a debate among both scientists and community members as to whether an immune reaction to gluten exposure could be considered a cause of autism. We examined antibodies that are directed against gliadin, a part of gluten, in samples collected from pregnant mothers and their newborn babies. We did not see any major differences in the antibody level among those children diagnosed with ASD or their mothers compared to children who were not diagnosed with ASD. High levels of the antibodies were in fact associated with a somewhat lower risk of ASD with co-occurring intellectual disabilities, though we cannot tell from this study why that might be the case. En ligne : http://dx.doi.org/10.1002/aur.2567 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450 [article] Maternal antibodies to gliadin and autism spectrum disorders in offspring-A population-based case-control study in Sweden [texte imprimé] / Renee M. GARDNER, Auteur ; Ida SAMUELSSON, Auteur ; Emily G. SEVERANCE, Auteur ; Hugo SJÖQVIST, Auteur ; Robert H. YOLKEN, Auteur ; Christina DALMAN, Auteur ; HÃ¥kan KARLSSON, Auteur . - p.2002-2016. Langues : Anglais (eng) in Autism Research > 14-9 (September 2021) . - p.2002-2016 Mots-clés : Attention Deficit Disorder with Hyperactivity  Autism Spectrum Disorder/epidemiology  Case-Control Studies  Female  Gliadin  Humans  Pregnancy  Sweden/epidemiology  attention deficit hyperactivity disorder  autism spectrum disorder  gliadin  gluten-sensitivity  intellectual disability Index. décimale : PER Périodiques Résumé : While individuals diagnosed with autism spectrum disorders (ASD) have higher levels of antibodies directed towards gliadin, a component of wheat gluten, no study has examined anti-gliadin antibodies (AGA) in etiologically relevant periods before diagnosis. The objective of this study was to investigate if maternal levels of AGA, during pregnancy and at the time of birth, are associated with ASD in offspring. We analyzed AGA in archived neonatal dried blood spots (NDBS) for 921 ASD cases and 1090 controls, and in paired maternal sera collected earlier in pregnancy for a subset of 547 cases and 428 controls. We examined associations with ASD diagnoses as a group and considering common comorbidities (intellectual disability [ID] and attention-deficit/hyperactivity disorder). We compared 206 cases to their unaffected siblings to examine the potential for confounding by shared familial factors. Odds of ASD tended to be lower among those with the highest levels (≥90th percentile) of AGA compared to those with low levels (<80th percentile; OR 0.78, 95% CI 0.56-1.09, measured in NDBS). This pattern was more apparent for ASD with comorbid ID when measured in NDBS (0.51, 0.30-0.87), with a similar trend in maternal sera (0.55, 0.24-1.29). High levels of AGA were similarly associated with lower odds of ASD in the sibling comparison. In summary, we found little association between maternal antibodies raised against components of gluten and risk of ASD in general. Exposure to high levels of AGA in the pre- and perinatal periods may be protective in terms of risk for ASD with ID. LAY SUMMARY: There is a debate among both scientists and community members as to whether an immune reaction to gluten exposure could be considered a cause of autism. We examined antibodies that are directed against gliadin, a part of gluten, in samples collected from pregnant mothers and their newborn babies. We did not see any major differences in the antibody level among those children diagnosed with ASD or their mothers compared to children who were not diagnosed with ASD. High levels of the antibodies were in fact associated with a somewhat lower risk of ASD with co-occurring intellectual disabilities, though we cannot tell from this study why that might be the case. En ligne : http://dx.doi.org/10.1002/aur.2567 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450

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