Rheumatology 2000; 39: 922
© 2000 British Society for Rheumatology
Letters to the Editor |
Virus-associated vasculitides
Poliklinik für Rheumatologie, Universitätsklinikum Lübeck, Medizinische Universität zu Lübeck and Rheumaklinik Bad Bramstedt, Oskar-Alexander-Strasse 26, 24576 Bad Bramstedt, Germany.
SIR, We read with interest the editorial by L. Guillevin concerning virus-associated vasculitides [1]. Unfortunately, later modifications of a seemingly persuasive concept, especially when presented as a letter, are usually not easily made public. The notion that parvovirus B19 may have a role in Wegener's granulomatosis is a good example of this. The initial case presentation raised suspicion of a relationship between parvovirus B19 infection and Wegener's granulomatosis. The case added to the few reported cases of parvovirus B19 infection and vasculitides [2]. However, 1 yr later an analysis of a series of sera from 42 patients with Wegener's granulomatosis did not support the author's previous assumption. There was no evidence of recent parvovirus B19 infections in this large series, and it was concluded that no evidence exists for a parvovirus B19 aetiology in Wegener's granulomatosis [3].
This example does not exclude the possibility that in future other infectious agents may be found as causative agents in what is still called ‘primary’ systemic vasculitides. The formerly so-called ‘essential’ cryoglobulinaemic vasculitis (CV) is a good example of this: hepatitis C virus (HCV) is now known to be the main cause of CV. However, about 10–20% of CV cases are HCV-negative and further causative agents must be sought. Regional differences seem to exist, with a higher prevalence of HCV-negative essential CV in northern Europe [4]. In contrast to earlier findings by Cacoub et al. [5], HCV-negative CV is not clinically different from HCV-associated CV [1, 6]. Interestingly, cytoplasmic pattern antineutrophil cytoplasmic antibodies (C-ANCA) and antiproteinase 3 antibodies (PR3-ANCA) have been found in patients with HCV- associated CV and in one patient with CV secondary to an infectious endocarditis due to a pacemaker system infection [6]. The patient's disease course was characterized by severe vasculitic manifestations such as rapidly progressive glomerulonephritis, which is commonly thought of as unusual symptom in CV. The patient's clinical course resembled ANCA-associated Wegener's granulomatosis or microscopic polyangiitis rather than typical CV. The C-ANCA disappeared with successful treatment of the CV, but recurred in one patient with a relapse of her CV. Thus, the occurrence of ANCA may have pathogenic implications in such patients and may represent an item of comparison between HCV- associated CV and other primary systemic vasculitides, e.g. ANCA-associated vasculitides [6, 7].
Notes
Correspondence to: P. Lamprecht. 
References
- L. Guillevin. Virus-associated vasculitides. Rheumatology1999;38:588–90.
[Free Full Text] - Nikkari S, Mertsola J, Korvenranta H, Vainionpää R, Toivanen P. Wegener's granulomatosis and parvovirus B19 infection. Arthritis Rheum1994;37:1707–10.[Medline]
- Nikkari S, Vainionpää R, Toivanen P et al. Wegener's granulomatosis and parvovirus B19 infection (letter). Arthritis Rheum1995;38:1175.
- D'Amico G. Renal involvement in hepatitis C infection: cryoglobulinemic glomerulonephritis. Kidney Int1998;54:650–71.[ISI][Medline]
- Cacoub P, Fabiani FL, Musset L et al. Mixed cryoglobulinemia and hepatitis C virus. Am J Med1994;96:124–32.[ISI][Medline]
- Lamprecht P, Gadola S, Csernok E, Herzberg C, Gross WL. PR3-ANCA in patients with cryoglobulinemic vasculitides. Clin Exp Immunol1998;112(Suppl 1):33.
- Lamprecht P, Gause A, Gross WL. Cryoglobulinemic vasculitis. Arthritis Rheum1999;42:2507–16.[ISI][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||