Autism spectrum disorders in children of parents with inflammatory bowel disease - A nationwide cohort study in Denmark

Clinical and Experimental Gastroenterology 05/2014; 7(1):105-10. DOI: 10.2147/CEG.S59360
Source: PubMed


Inflammatory bowel disease (IBD) and autism spectrum disorders (ASD) may share genetic and environmental risk factors. We examined whether parental IBD is associated with an increased risk of ASD in offspring.

We conducted a registry-based nationwide cohort study including children born alive in Denmark from January 1, 1994 to December 31, 2009, with follow-up throughout 2010. IBD in parents and ASD in offspring were identified using inpatient and outpatient hospital diagnoses. We computed risk of ASD and crude and adjusted incidence rate ratios (aIRRs) with 95% confidence intervals (CI) using Cox proportional-hazards regression. We evaluated the risk of ASD according to maternal and paternal IBD, and separately for maternal and paternal Crohn’s disease (CD) and ulcerative colitis (UC). Children with parents free of IBD were the comparison cohort.

We identified 1,005,330 children during the study period. Among them, 11,888 (1.2%) had a parent with IBD and 8,087 (0.8%) had a diagnosis of ASD during up to 17 years of follow-up. The 10-year risks of ASD were 0.7% among children of parents with IBD and 0.9% among children of parents without IBD. The aIRR for ASD among children with parental IBD was 0.8 (95% CI: 0.6–1.0), and results were similar regardless of parent of IBD origin or whether a parent had CD or UC. The estimates were similar for different ASD subtypes.

We found no evidence of an increased risk of ASD among children born to parents with IBD.

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    ABSTRACT: The heterogeneity in the behavioral presentation of autism spectrum disorder (ASD) may be surpassed only by the level of heterogeneity in its etiology. There are diverse pathways to the singular diagnostic outcome of ASD, and several etiological risk factors have been proposed in recent years. This review paper examines the role of inflammation as one possible etiologic factor in ASD, juxtaposed in the context of research on the role of inflammation in other psychiatric disorders. Human, animal, and postmortem studies of inflammation in ASD were surveyed, and their direct and indirect contributions to developing potential inflammation-based treatments, as well as potential preventative considerations, in ASD were reviewed. Although the mechanisms that link inflammation and ASD remain unknown, there exists a sizable multidisciplinary literature suggesting inflammation as a trans-etiological process.
    06/2015; DOI:10.1007/s40489-015-0051-z

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Apr 12, 2015