Hu Hong-Bo, Wu Jian-Gang, Cheng Ying, Li Jian-Jun
Department of Laboratory, Maternal and Child Health Hospital of Hubei Province, China.
Department of Infectious Disease, The first people's Hospital of Guangshui, China.
Mediterr J Hematol Infect Dis. 2021 Nov 1;13(1):e2021064. doi: 10.4084/MJHID.2021.064. eCollection 2021.
Henoch-Schönlein purpura (HSP) is an immune-mediated vasculitis, and the formation of immune complexes may be triggered by exposure to Epstein-Barr virus (EBV) infection.
We performed a five-year case-control study to evaluate the epidemiology and clinical characteristics of HSP associated with EBV infection.
The incidence of EBV-triggered HSP was 4.2%, while EBV infection in children with HSP was 0.9%; The EBV-triggered HSP cases had a significantly higher frequency of abdominal pain than the (MP)-triggered HSP group (χ2 = 8.024, p = 0.005); Significant differences were observed in the duration of abdominal pain (Z = -1.935, = 0.027) between the two groups; C3 (t = 9.709, < 0.001), IgA (t = 20.39, < 0.001) and IgG (t = 6.407, < 0.001) were significantly increased in the EBV infection group than those in the healthy control group. Notably, significantly higher proportion of CD19 (t = 6.773, < 0.001) and lower proportion of CD56 (t = 11.13, < 0.001) was found in EBV infection group compared with healthy control group. The IgA level was higher than that of the non-infectious group (t = 2.162, = 0.032), but their CD4/CD8 ratio (t = 10.070, < 0.001) and CD56 proportion (t = 2.096, = 0.037) were significantly lower.
Both cellular and humoral immunity were involved in the pathogenesis of EBV-triggered HSP, leading to increased production of inflammatory mediators and immunoglobulins. Those events may cause or promote the development of systemic vessel vasculitis.
过敏性紫癜(HSP)是一种免疫介导的血管炎,免疫复合物的形成可能由暴露于爱泼斯坦-巴尔病毒(EBV)感染引发。
我们进行了一项为期五年的病例对照研究,以评估与EBV感染相关的HSP的流行病学和临床特征。
EBV引发的HSP发病率为4.2%,而HSP患儿中EBV感染率为0.9%;EBV引发的HSP病例腹痛频率显著高于(MP)引发的HSP组(χ2 = 8.024,p = 0.005);两组间腹痛持续时间存在显著差异(Z = -1.935,p = 0.027);EBV感染组的C3(t = 9.709,p < 0.001)、IgA(t = 20.39,p < 0.001)和IgG(t = 6.407,p < 0.001)显著高于健康对照组。值得注意的是,与健康对照组相比,EBV感染组中CD19比例显著更高(t = 6.773,p < 0.001),而CD56比例显著更低(t = 11.13,p < 0.001)。IgA水平高于非感染组(t = 2.162,p = 0.032),但其CD4/CD8比值(t = 10.070,p < 0.001)和CD56比例(t = 2.096,p = 0.037)显著更低。
细胞免疫和体液免疫均参与EBV引发的HSP的发病机制,导致炎症介质和免疫球蛋白产生增加。这些事件可能导致或促进系统性血管炎的发展。