A Different View on the Etiopathogenesis of Attention-deficit Hyperactivity Disorder from an Inflammation Perspective.

Abstract

ObjectiveAttention-deficit hyperactivity disorder (ADHD) has a complex etiology and genetic, environmental and biological factors are considered to play a role in the etiology of ADHD by mutually interacting. Recent studies have emphasized that inflammation may be present in the etiology of ADHD. This study aims to investigate the possible role of visfatin, IL-6, IL-1β and TNF-α molecules in the etiology of ADHD.MethodsThe study included 60 patients and 20 healthy controls between the ages of 6−18. Serum visfatin, IL-6, IL-1β and TNF-α levels were evaluated with enzyme-linked immunosorbent assay (ELISA) kits at a biochemistry laboratory.ResultsThe study showed no statistically significant difference between children with ADHD and healthy controls in terms of visfatin, IL-6, IL-1β and TNF-α levels. When ADHD subgroups (combined and predominantly inattentive types) and the control group were compared in terms of visfatin, IL-6, IL-1β and TNF-α levels, no statistically significant difference was recorded.ConclusionData on the relationship between ADHD and IL-6, IL-1β and TNF-α in this study are in compliance with the literature. However, no study was found on visfatin in ADHD. This study is the first one evaluating the ADHD-Visfatin relationship.