Evaluation of Endocan, endothelial nitric oxide synthase, and solubleCD89 in children with IgA vasculitis.

Background: IgA vasculitis (IGAV) is the most frequently encountered form of vasculitis in the pediatric population and typically follows a self-limiting course. In addition to well known inflammatory markers, several other inflammatory mediators, including Endocan, endothelial nitric oxide synthase (eNOS), and soluble CD89 (sCD89), have not been extensively investigated in the context of IGAV. The aim of this study was to evaluate the association between Endocan, endothelial nitric oxide synthase (eNOS), and soluble CD89 (sCD89) and established inflammatory markers (CRP, erythrocyte sedimentation rate), as well as their relationship with clinical manifestations and laboratory findings in pediatric patients diagnosed with IGAV.

Methods: Patients diagnosed with IGAV during the study period (December 2019 to May 2021) were included in the study. These patients were invited for a follow-up visit 3 months after diagnosis. Additionally, 35 healthy children, matched for age and gender and with no known diseases, were included as a control group. At both the time of diagnosis and the 3-month follow-up, blood samples were collected in EDTA tubes in addition to routine hematological and biochemical tests. The samples were centrifuged at 4000 rpm for 10 min and stored at -80 °C. Endocan, sCD89, and eNOS levels were measured using ELISA kits.

Results: The mean sCD89 level in the patient group, both during the acute and remission phases, was significantly lower than in the control group (1.42 ± 0.53 ng/mL and 1.46 ± 0.80 ng/mL vs. 1.83 ± 0.73 ng/mL; p = 0.010 and p = 0.004, respectively). However, there was no statistically significant difference in sCD89 levels between the acute and remission phases within the patient group (p = 0.376). The Endocan level during the remission phase was significantly lower in patients compared to the control group (378.4 ± 238.1 ng/mL vs. 478.9 ± 240.9 ng/mL; p = 0.014). However, no significant difference was found between the control group and the acute phase (p = 0.911). A statistically significant difference in Endocan levels was observed between the acute and remission phases in patients (p = 0.004) (Table 1). The mean eNOS level in the patient group, both during the acute and remission phases, was significantly lower than in the control group (25.29 ± 14.07 U/mL and 30.12 ± 18.10 U/mL vs. 37.71 ± 19.48 U/mL; p = 0.004 and p = 0.031, respectively). However, there was no statistically significant difference in eNOS levels between the acute and remission phases (p = 0.334).

Conclusion: The unexpectedly low levels of these vascular mediators may be due to the fact that endothelial damage in IGAV is triggered by immune complex-mediated mechanisms rather than a proinflammatory cytokine-driven process, which may result in reduced or suppressed endocan release. Secondly IGAV is primarily caused by the deposition of IgA1 immune complexes in the vessel walls. This mechanism differs from other systemic vasculitides. Key Points • This study systematically evaluated the levels of Endocan, Endothelial nitric oxide synthase (eNOS), and soluble CD89 (sCD89) in patients with IGAV. • The level of these mediators was lower than the controls unexpectedly. • It may be due to the fact that endothelial damage in IGAV is triggered by immune complex-mediated mechanisms rather than a proinflammatory cytokine-driven process, which may result in reduced or suppressed release of these mediators.