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Parvovirus B19 infection in Behçet's disease
  1. S KIRAZ,
  2. M A ÖZTÜRK,
  3. I ERTENLI,
  4. M ÇALGÜNERI
  1. Hacettepe University School of Medicine
  2. Department of Rheumatology
  3. Ankara, Turkey
  1. Dr M A Öztürk, Ostim mahallesi 89. sokak AK-84 sitesi A-2 blok no: 8, TR-06170, Yenimahalle, Ankara-Turkey makifozturk{at}yahoo.com

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We read with great interest the article by Kerr which reviewed present knowledge about the possible association of parvovirus B19 infection with various connective tissue and autoimmune disorders.1 The author concluded that data implicating B19 virus infection in the aetiopathogenesis of rheumatic diseases are insufficient and conflicting. Although a significant number of studies support a possible role for the virus in the pathogenesis of rheumatoid arthritis, juvenile idiopathic arthritis, systemic lupus erythematosus, and vasculitis, the author believes that B19 infection is only one of a number of triggers.

Behçet's disease (BD) is a multisystem disorder originally described by the Turkish dermatologist Hulusi Behçet.2Although its cause is unknown, vasculitis is widely accepted as the underlying pathological process.3 As stated by the author, various case reports have been published demonstrating the presence of B19 virus in patients with vasculitic syndromes.4 5 Viral infections have also been postulated as triggering factors in BD. Therefore, in a previous study that was not cited in the report by Kerr, we investigated a possible role of B19 virus in BD.6We assessed antibodies against parvovirus B19 in serum samples from 41 patients with BD and from 40 age and sex matched controls. Six patients with BD (15%) had anti-B19 IgM antibodies while no IgM antibodies were detected in the control group (p=0.03). However, anti-B19 IgG antibodies were present in 23 patients with BD and 25 controls. There was also no correlation between the presence of anti-B19 IgM antibodies and articular and vascular manifestations of BD (p=0.9 and p=0.5, respectively). Therefore, we concluded that our findings did not strongly support the involvement of B19 in the pathogenesis of BD, and we also concluded that serological evidence of acute B19 infection in six patients with BD might have been coincidental. However, the presence of anti-B19 IgM antibodies in patients with BD might provide evidence for the place of B19 infection in the pathobiology of BD. As far as we know our previous report is the only published study investigating the association of B19 virus infection and BD. Therefore, further studies will be clearly needed to clarify this unresolved issue.

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