Neuroinflammation Process as a Key Etiopathogenetic Factor in the Evolution of Autism Spectrum Disorders in Child Patients

Abstract

Background: the prevalence of autism spectrum disorders (ASD) is increasing every year, however, diagnostic and therapeutic options are still limited. Aim: identification the patterns of the neuroinflammation process in the etiopathogenesis of ASD of child patients. Patients and methods: clinical, anamnestic and laboratory data of 85 child patients with a confirmed ASD diagnosis. Each patient was assessed for the level of neurospecific proteins (neuron-specific enolase (NSE), S100b protein), the indices of the “Neuro-immuno-test” panel (leukocyte elastase (LE) and α1-proteinase inhibitor (α1-PI) activity, autoantibodies to S100b protein and myelin basic protein) in the blood before and after a standardized three-month-course of treatment. The reference interval of the laboratory was taken as normal values. The clinical picture was assessed according to the Childhood Autism Rating Scale (CARS). The correlation calculations were carried out in the MS Excel program. Results: in this work we describe the dynamics of the neuroinflammation process parameters in children with autism-like syndrome and psycho-speech development delay on the basis of complex anti-inflammatory therapy. The results of the research prove the increase in NSE and S100b protein quantity among 85% of patients before the treatment. More than 60% of patients had the increase of the parameters of the Neuro-test panel. The severity levels of symptoms among patients according to the scales used specified moderate and severe autism. The quantity of neurospecific proteins and immunological parameters correlated with CARS scale scores. Positive dynamics of clinical symptoms and studied parameters decrease were observed while therapy. The use of the parameters allows to evaluate objectively the severity levels of the patient’s immunomitochondrial status and shows a congruent change on the basis of etiopathogenetic therapy.