P.1.c.018 Prevalence of gastrointestinal symptoms in young people with autism spectrum disorder

P.1.c. Basic and clinical neuroscience − Neurodevelopment P.1.c.018 Prevalence of gastrointestinal symptoms in young people with autism spectrum disorder E. Serrano-Drozdowskyj1 ° , M. Penzol1 , A. Fernandez-Diaz1 , A. Alcon1 , D. Fraguas1 , G. Alvarez-Calatayud2 , M. Parrellada1 1 Hospital General Gregorio Maranon, Children and Adolescent Psychiatry, Madrid, Spain; 2 Hospital General Gregorio Maranon, Gastroentorology Paediatric, Madrid, Spain Purpose of the study: Children and adolescents with Autism Spectrum Disorder (ASD) report more gastrointestinal (GI) problems than infants with typical development [1]. In addition, there is increasing evidence that gut-brain axis may be implicated in the pathogenesis and severity of ASD manifestations [2,3]. Despite its relevance, GI comorbidity is frequently undetected. Recent research of medical comorbidities using electronic medical records with ‘natural language processing techniques’ has enabled to identify medical comorbidities of ASD, including GI problems [4]. Given that with this method comorbid GI problems are not specifically asked, the number of cases may be underestimated. Therefore we aim to systematically assess the prevalence of GI problems in ASD and describe their clinical correlates. Methods: 326 children and adolescents (2−17 years old) consecutively referred to an ASD specialized outpatient clinic (AMITEA) between January of 2012 and June of 2014 and meeting ASD criteria (DSM-IV-TR) comprised the study sample. ASD diagnosis was based on best clinical judgment of experienced child developmental psychiatrists. Autistic Diagnostic InterviewRevised (ADI-R) and Autism Diagnostic Observation ScheduleGeneric ADOS-G were used when clinicians deemed it necessary. Diagnose of comorbid history of gastrointestinal problems were based on information reported by caregivers and classified in GI functional problems (Roma III), GI inflammatory problems, GI allergy and food intolerance. Additional demographic and clinical information (including data on Attention Deficit and Hyperactive Disorder (ADHD) and other psychiatric comorbidities, sleep problems, syndromic autism (SA), epilepsy and intellectual disability (ID)) were also collected from the clinical files at intake and follow-up visits in the clinic, using a locally devised questionnaire. Clinical and demographic features were compared between subjects with (ASD_GI) and without comorbid GI problems (ASD_NoGI). All statistical analyses were performed using SPSS (v22). Results: 326 patients (8.15±3.9 years, 82% male)[CM1] were included. 31.7% of the sample presented ID, 7.8% between moderate and severe[CM2]. 44.8% met criteria for typical Autism 43.2% for Pervasive Developmental Disorder NE[CM3], 10.7% for Asperger Syndrome; one case met criteria for Rett Syndrome and one for Childhood Disintegrative Disorder criteria. 17.8% (n = 58) presented at least one gastrointestinal problem. Of these, 53.45% have GI functional disorder (Roma III) (31% functional constipation, 10.3% functional diarrhea, 8.6% rumiation syndrome, 3.5% infant colic, 3.5% functional vomits, 3.5% aerophagia, 1 case of irritable bowel syndrome, 1 case of infant regurgitation), 13.8% had inflammatory GI problems, 7% GI allergy and 10.34% lactose intolerance. When comparing demographic and clinical variables between ASD_GI and ASD_NoGI subgroups, no significant differences where found with the exception of comorbid sleep problems. Conclusions: We found a high prevalence of GI problems in patients with ASD. This result underscores the relevance of specifically assess GI problems in ASD population. In addition,

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we found that sleep problems are more frequent in the ASD group with GI problems that those without, suggesting a pathological interrelation. According to our results, GI symptoms and its eventual influence in sleep problems should be systematically evaluated in ASD population in the clinical practice. References [1] Chaidez, V., Hansen, R.L., Hertz-Picciotto, I, 2014. Gastrointestinal problems in children with autism, developmental delays or typical development. J Autism Dev Disord 44(5), 1117–1127. [2] van De Sande, M.M., van Buul, V.J., Brouns, F.J., 2014. Autism and nutrition: the role of the gut-brain axis. Nutr Res Rev 27(2), 199–214. [3] Wang LW, Tancredi DJ, Thomas DW, 2011. The prevalence of gastrointestinal problems in children across the United States with autism spectrum disorders from families with multiple affected members. J Dev Behav Pediatr 32(5), 351−60. [4] Kohane, I.S., McMurry, A., Weber, G., MacFadden, D., Rappaport, L., Kunkel, L., Bickel, J., Wattanasin, N., Spence, S., Murphy, S., Churchill, S., 2012. The co-morbidity burden of children and young adults with autism spectrum disorders. PLoS One 7(4), e33224.

P.1.c.019 Influences of sex and estrous cycle on behavioural and neurochemical alterations induced by the neonatal administration of ketamine to rats V. Borella1 ° 1 Federal University of Cear´a, Departamento de Fisiologia e Farmacologia, Fortaleza, Brazil Schizophrenia is a neurodevelopmental disorder with sex influences in age of onset, premorbid functioning and course of illness. Estrogen, the hormone usually related to the sex differences in schizophrenia, is known to regulate oxidative pathways. Based on this, we hypothesized that the neonatal administration of ketamine to rats (postnatal days 7−11), a neurodevelopmental model of schizophrenia, would result in sex related alterations in: oxidative stress (i.e. glutathione (GSH) and lipid peroxidation). From PN7 to 11 rat pups received single daily intraperitoneal (i.p.) injections of ketamine hydrochloride (2.5 mg/kg or 5 mg/kg) (Pfizer® ) or saline (control groups) in a volume of 50 ml/8 g body weight. Injections were given with 29 G 1/2 in., 0.3 ml syringes between 8:00 and 9:00 a.m. Only one offspring from each dam was randomly used in each group, to avoid duplicate results from animals of the same litter. For behavioral determinations, animals were evaluated at PN35 (periadolescence) and/or PN75 (adulthood). Neurochemical assays were performed in brain areas of animals sacrificed at PN75. The correspondence between the human developmental periods adolescence (PN35) and adulthood (PN75) in animals was based on a previous report. To study the influence of the estrous cycle, in each experimental day, before behavioral determinations of female rats at PN75, the estrous cycle was evaluated. After the confirmation that the animals were in proestrus or diestrus, respectively, the phases in which serum estradiol levels are at the highest and lowest levels, the rats were immediately submitted to the behavioral determinations and afterwards killed for neurochemical assays. The estrous cycle was verified once more immediately after the death of the animals, in order to warranty that the animals were in the same phase of the estrous cycle in the behavioral and neurochemical evaluations. Since the neonatal administration of ketamine 2.5 caused no obvious behavioral alterations at the neurodevelopmental periods studied, we decided to show herein only the results obtained with animals neonatally challenged with ketamine 5. Our results showed that ketamine-treated male (KTmale) and female-in-diestrus (KTF-diestrus, the low estrogen