Epidemiology and Clinical Characteristics of Henoch-Schönlein Purpura Associated with Epstein-Barr Virus Infection

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...

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Veröffentlicht in:Mediterranean journal of hematology and infectious diseases 2021, Vol.13 (1), p.e2021064-e2021064
Hauptverfasser: Hu, Hong-Bo, Wu, Jian-Gang, Cheng, Ying, Li, Jian-Jun
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Sprache:eng
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Zusammenfassung: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.
ISSN:2035-3006
2035-3006
DOI:10.4084/MJHID.2021.064