Systemic CD163 and IL-17 A in functional gastrointestinal disorders: a case control study in Egyptian adolescents

Abstract Background Functional gastrointestinal disorders (FGIDs), now classified as disorders of gut–brain interaction (DGBIs), are common among adolescents and significantly affect quality of life. Despite their high prevalence, the pathophysiology of these disorders remains incompletely understood, particularly regarding the role of systemic immune activation. This study aimed to evaluate the clinical, anthropometric, laboratory, and immunological characteristics of adolescents with DGBIs (FGIDs according to Rome IV criteria) and to assess the presence of systemic immune activation through the measurement of CD163 and IL-17 A. A cross-sectional case–control study was conducted involving 181 adolescents aged 10–18 years, comprising 99 patients diagnosed with FGIDs according to Rome IV criteria and 82 healthy controls. All participants underwent clinical evaluation, anthropometric assessment, and laboratory investigations. Serum CD163 and IL-17 A concentrations were measured once for each participant using enzyme-linked immunosorbent assay (ELISA). Results DGBIs/FGIDs were significantly more prevalent among female participants ( p = 0.023). Hemoglobin levels were significantly lower in the FGID group ( p = 0.037). Functional gastrointestinal symptoms, including irritable bowel syndrome and functional abdominal pain disorders, were significantly more common among patients with FGIDs ( p ≤ 0.005). No statistically significant differences were found in serum CD163 or IL-17 A levels between the two groups. Conclusion No significant differences in serum CD163 or IL-17 A levels were detected between adolescents with DGBIs/FGIDs and healthy controls in the present study population. These findings are based on single-time-point serum measurements and do not exclude localized mucosal immune alterations or subtle systemic immune changes. Further larger-scale, longitudinal, and tissue-based studies are warranted to better define the role of immune mechanisms in pediatric DGBIs/FGIDs.