EPIDEMIOLOGY AND CLINICAL CHARACTERISTICS OF HENOCH-SCHÖNLEIN PURPURA ASSOCIATED WITH EPSTEIN-BARR VIRUS INFECTION
Introduction: 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. Methods: We performed a five-year case-control study to evaluate the epidemiology and clinical characteristics o...
Saved in:
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
PAGEPress Publications
2021-10-01
|
| Series: | Mediterranean Journal of Hematology and Infectious Diseases |
| Online Access: | http://mjhid.org/index.php/mjhid/article/view/4714 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | Introduction: 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.
Methods: We performed a five-year case-control study to evaluate the epidemiology and clinical characteristics of HSP associated with EBV infection.
Results: 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, p = 0.027) between the two groups; C3 (t = 9.709, p < 0.001), IgA (t = 20.39, p < 0.001) and IgG (t = 6.407, p < 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, p < 0.001) and lower proportion of CD56 (t = 11.13, p < 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, p = 0.032), but their CD4/CD8 ratio (t = 10.070, p < 0.001) and CD56 proportion (t = 2.096, p = 0.037) were significantly lower.
Conclusions: 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 |