Increased serum levels of tumour necrosis factor-like weak inducer of apoptosis in children with autism spectrum disorder

Abstract

Introduction: A previous study has evaluated the association between serum tumour necrosis factor-like weak apoptosis inducer (TWEAK) levels and autism spectrum disorder (ASD). In line with this investigation, the present study aimed to measure serum TWEAK levels to determine whether their eventual alteration might have etiopathogenetic significance in children with ASD. Methods: A total of 40 treatment-naive children with ASD and 40 healthy children as controls were included in the present study. The Schedule for Affective Disorders and Schizophrenia for School-Aged Children—Present and Lifetime Version, DSM-5 was used by a psychiatrist to screen the healthy controls for psychiatric disorders after a physical examination by a paediatrician. The clinical severity of the ASD symptoms was assessed by the Childhood Autism Rating Scale. Venous blood samples were collected, and serum TWEAK levels were measured. Results: This study included 80 children in total, with 40 (50.0%) in the patient group and 40 (50.0%) in the healthy control group. Thirty four (85.0%) of the participants in the patient group, and 31 (77.5%) in the healthy control group, were male, and the remainder were female. The distribution of the gender ratio was statistically similar between groups (p = 0.568). The volunteers were between 36 and 59 months old. The average age in the patient group was 46.0 ± 6.5, while that in the healthy control group was 45.2 ± 6.7. The ages were also statistically similar between groups (p = 0.615). The TWEAK values of the patient group were found to be statistically higher than those of the healthy control group (p < 0.001). Discussion: This study examined whether serum TWEAK levels were related to ASD in childhood. Our findings indicate that children with ASD have higher TWEAK levels when compared to other children. The findings further indicate that serum TWEAK levels could be related to ASD etiopathogenesis independent of ASD symptom severity.