ArticleThe Pan African medical journal2017
Henoch-Schonlein purpura associated with primary active Epstein-Barr virus infection: a case report.
Article in The Pan African medical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- VAERS Vasculitis Adverse Events Retrospective Study: Etiology Model of Immune Complexes Activating Fc Receptors in Kawasaki Disease and Multisystem Inflammatory Syndromes.Life (Basel, Switzerland) · 2024Article
- IgA Nephropathy: Pleiotropic impact of Epstein-Barr virus infection on immunopathogenesis and racial incidence of the disease.Frontiers in immunology · 2023Review
- Intermittent abdominal pain in IgA vasculitis.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo · 2021Article
- Epidemiology and Clinical Characteristics of Henoch-Schönlein Purpura Associated with Epstein-Barr Virus Infection.Mediterranean journal of hematology and infectious diseases · 2021Article
- Article
- Acute Acalculous Cholecystitis Associated with Epstein-Barr Infection: A Case Report and Review of the Literature.Case reports in medicine · 2020Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Henoch-Schönlein purpura (HSP) is the most common form of childhood vasculitis. Various viral and bacterial infections, drugs, vaccines, food allergy and even insect bites have been considered as triggering factors in pathogenesis of HSP. Epstein-Barr virus (EBV) infection, which is associated with HSP, have been rarely reported. Herein we present HSP patient possibly caused by EBV infection. A 8-year old boy was admitted to our department with fever, rashes on legs and arms and intermittent mild abdominal pain. Multiple purpuric rashes were on his extremities, abdomen and buttock. Laboratory investigations revealed that monospot test was positive, EBV serology tests; Anti-EA-D Ig G: 3+, Anti-VCA gp125 Ig G: 3+, Anti-VCA p19 Ig M: 2+, Anti EBNA-1 Ig M: negative, Anti EBNA-1 Ig M: negative, Anti EBNA-1 Ig G: negative. The patient was interpreted as the primary active acute EBV infection. A skin biopsy showed leucocytoclastic vasculitis. The other viral and bacterial investigations were negative. The patient was diagnosed as HSP vasculitis according to EULAR criteria and treated with intravenous hydration and ibuprofen. He was discharged after 15 days with normal laboratory findings and physical examination. We think that EBV infection may be stimulant factor for autoimmune reactions and may cause HSP vasculitis. Hence, it may be useful to investigate the EBV infection in etiology of HSP cases.
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