Measuring orexin B values in a Romanian population of children with autism spectrum disorders

Introduction: Orexins are involved in regulating appetite and circadian entrainment [1]. Enhanced orexin receptor 2 signaling, through orexin B peripheral administration, might be a protective factor for diet-induced features of the metabolic syndrome [2]. Both orexin A and orexin B contribute to the ethiopathogenesys of sleep, impulse control and appetite related disorders [3,4]. The particular sleep profiles and appetite preferences in children with autism spectrum disorder, associated with the metabolic implications of long-term atipsychotic treatment have prompted our team to search for the plasma values of orexin B in this clinical population. Aim: The aim of our study was to verify the plasma levels of orexin B in a population of children with autism spectrum disorders in comparison to neurotypical children. Materials and Methods: A total number of 24 children (aged 3 to 11) from the child and adolescent psychiatry department of the “Prof. Dr. Al. Obregia” Clinical Psychiatry Hospital were included (6 neurotypical, 6 girls). A certified child and adolescent psychiatrist established the diagnosis of autism spectrum disorder. Based on the ADOS scoring cut-off point, the children with ASD were divided into severe ASD (7 patients) and mild ASD (11 patients). Venous blood was drawn by a certified nurse, with the informed consent of both parents, approved by the local ethics committee. The plasma orexin B levels were determined using a designated ELISA kit. The data were analyzed using SPSS 22.0, by parametric (univariate ANOVA, un-paired t-test) or nonparametric tests of comparison (Kruskall Wallis test and Mann- Whitney U), based on distribution of the data (non-parametric tests were applied for samples where Shapiro-Wilk p <0.05). Results: There were no differences in the plasma levels of orexin B between control and ASD groups (p = 0.156, z = -1.467, n1 = 6, n2 = 18). There were no differences in the plasma levels of orexin B between boys and girls [t(22) = -1.114, p = 0.277] or between control children, severe and mild ASD cases [p = 0.288, χ2(2) = 2.487]. However, differences in plasma orexin B levels between the patients that were taking antipsychotic medication (7 children), those that were not (11 children) and controls (6 children) [F(2) = 3.23, p = 0.06], with an observed power of 55%. Post-hoc Dunnet's C analysis hints that the differences might be due to patiens who are not taking medication have higher levels of plasma Orexin B than control patients (95% CI for the difference = [-0.009, 0.052]). Conclusions and Discussions: These results are part of a larger study measuring various neurohormones and neuromodulators plasma levels in children with ASD versus neurotypical controls. Based on these preliminary results, specifically on the homogeneity of the plasma levels of orexin B between the groups, it does not seem to vary according to sex or diagnosis, however there seem to be higher median values in the patients with ASD than in controls, with antipsychotic medication decreasing the plasma levels of orexin B. An increase in statistical power, through increasing the sample size is necessary to verify these hypothesis and to further investigate the possible involvement of orexin B in antipshychotic induced metabolic syndrome.