1.28 GUT–BRAIN AXIS IN AUTISM: A POSSIBLE ROLE FOR CELIAC DISEASE GENETIC MARKERS

Objectives: The goal of this presentation is to study how the gut-brain axis could be involved in the physiopathology of autism. The main objective of our project is the identification of biological markers involved in the pathogenesis of ASD. 1) Children with autism and functional gastrointestinal...

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Veröffentlicht in:Journal of the American Academy of Child and Adolescent Psychiatry 2016-10, Vol.55 (10), p.S108-S109
Hauptverfasser: Penzol, Maria Jose, ScM, Alcon, Alicia Garcia, ScM, Gerez, Diego, BS, Alvarez-Calatayud, Guillermo, PhD, Parellada, Mara, PhD
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Sprache:eng
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Zusammenfassung:Objectives: The goal of this presentation is to study how the gut-brain axis could be involved in the physiopathology of autism. The main objective of our project is the identification of biological markers involved in the pathogenesis of ASD. 1) Children with autism and functional gastrointestinal disorder (fGID) will express a higher percentage of genetic markers for celiac disease (CD) than the general population; and 2) the group with fGID and ASD will have a higher rate of abnormal levels of serologic markers of CD than patients with ASD who have no fGID. Methods: Within a sample group of 29 children with ASD (ages 3-9 years), two groups of participants were recruited, selected based on the presence of ASD diagnosis according to DSM-5 criteria and the presence or absence of fGID (according to the ROME-III criteria). All subjects were placed on an unrestricted diet. All participants were genotyped for CD-associated human leukocyte antigen-DQ2/DQ8 alleles. All patients were tested for the recommended serologic markers of CD, including IgA transglutaminase (tTG) antibody and IgA and IgG antibodies to gliadin in serum, using the enzyme-linked immunosorbent assay kit. Comparison between groups was assessed by the chi-squared test. The statistically significance threshold was set at P < 0.05. Results: Within patients with ASD, 16 of 29 (55.2 percent) were positive for the DQ2 and/or DQ8 (10 DQ2, 7 DQ8) haplotype; there were 1 of 29 (3.4 percent) with IgG antideamidated gliadin antibodies and 0 of 29 with IgA and IgG tTG antibodies. Although we found a higher rate of the risk haplotypes DQ2 and/or DQ8 CD (9 of 14 or 64.3 percent) in patients with ASD-no fGID than patients with ASD-with fGI (7 of 15 or 46.7 percent), the difference was not statistically significant (χ2 = 0.91; sig = 0.34). Conclusions: According to our results, patients with ASD expressed higher genetic risk of developing celiac disease than the general population (30 percent, data from reference population). Risk genetic markers were not higher in the group with fGID. Research has demonstrated high rates of restricted diets prescribed in patients with ASD. Most of the diets follow the preferences of parents or professionals more than clinical profiles. This could explain poor efficacy and undesirable states of malnutrition. The results from our study could let us identify a high risk subgroup of patients and might help to personalize and optimize therapeutic interventions in patients with au
ISSN:0890-8567
1527-5418
DOI:10.1016/j.jaac.2016.09.029