Relation Between Serum Gd-IgA1,NF-κB And Inflammatory Mediators Of Henoch-Sch(?)nlein Purpura Inchildren And Their Clinical Significance

Background and Significance Henoch-Sch(?)nlein purpura is the most common childhood systemic vasculitis, the exact etiology and pathogenesis has not yet been fully elucidated. Present study suggests that HSP is a leukocytoclastic vasculitis mediated by Ig A, and a variety of inflammatory mediatorsinvolved. Currently Ig A1 molecular abnormalities of glycosylation, overactivation of nuclear factor-κappa B, abnormal expression of inflammatory cytokines are all involved in the pathogenesis of HSP. However,the exact pathogenesis has not been fully elucidated,whether it is a link between them, it has not been determined.This study was to detect the level of serum Gd-Ig A1, NF-κB, and the former inflammatory mediators IL-8, TNF-α, intercellular adhesion molecule-1,which are regulated by NF-κB,and their relationship,in order to further elucidate the pathogenesis of HSP.Methods 1. Research Subjects and grouping: According to the clinical manifestations, seventy children who were all the first oneset, hospitalized with HSP from October 2014 to March 2015 were divided into 3 groups: general HSP group(23 cases), abdominal HSP group(Had severe abdominal pain with vomiting or blood in the stool)(26 cases); HSP nephritisgroup(21cases). 17 cases of healthy children in hospital examination is the normal control group. 2. Detection of indicators and methods Bean lectin affinity and Enzyme-linked immunosorbent assay(ELISA) to indirectlydetect serum Gd-Ig A1; serum NF-κB, IL-8, TNF-α, ICAM-1 levels was detected by ELISA. Collectperipheral venous blood 3 mlfrom HSP acute phase, recovery phase and the control group of children. Rotating speed is 3000 r / min, centrifugal radius is13.5cm, centrifuged 10 minutes;serum was separated set-80 ℃refrigerators frozen for inspection. 3. Statistical analysis Statistical analysis of this article was performed using SPSS17.0 statistical software. Normallydistributed data use mean ± standard deviation(χ ± S), several groups were analyzed by ANOVA, further pairwise comparisnusing LSD-t, skewed distribution measurement data use median(interquartile spacing) [M(P25 ~ P75)].Groups were compared by using Kruskal-Walis test. It was analyzed by Spearmancorrelation analysis analysis of two variables. P <0.05 was considered statistically significant. Results 1. HSP acute phase Gd-Ig A1, NF-κB, IL-8, TNF-α, ICAM-1 levels were significantly higher than the target recovery levels and the control group(P <0.05), NF-κB, IL-8levels in recovery phase were still higher than the control group(P <0.05). 2. Significant difference among the HSP groups. In acute phase: Gd-Ig A1, NF-κB, IL-8, TNF-α, ICAM-1 levels in nephritis group were significantly higher than normal HSP groups(P <0.05); Gd-Ig A1, NF-κB levels of nephritis groups above abdominal HSP groups(P <0.05); Gd-Ig A1, NF-κB, L-8, ICAM-1 levels in abdominal HSP groups were higher than normal HSP groups(P <0.05).In Recovery phase: in nephritis groups Gd-Ig A1, NF-κ B, TNF-α levels higher than they arein the control groups and the normal HSP groups(P <0.05),IL-8 levelsin HSPgroups were still higher than the control groups, P <0.05. 3. Acute phase Serum Gd-Ig A1 and NF-κB with HSP was positively correlated(r = 0.674, P <0.05); NF-κB and TNF-α, IL-8, ICAM-1 were positively correlated(r =0.395~0.595, P <0.05). In convalescentphase NF-κB and TNF-α was positively correlated(r =0.280, P <0.05).Conclusions Gd-Ig A1 may be activating cell NF-κB signal transduction pathway, then rising the inflammatory mediators IL-8, TNF-α and expression of ICAM-1, resulting to HSP small vascular inflammatory injury. In HSP Gd-Ig A1, NF-Κ B, IL-8, and TNF-α, ICAM-1 involving related to disease activity and organ such as alimentary tract and kidney damaged of HSP.