You are here

Article Text

Article menu
Download PDFPDF
Letters
Are there specific genetic risk factors for the different forms of ANCA-associated vasculitis?
  1. Larissa Arning1,
  2. Julia Ulrike Holle2,3,
  3. Lorraine Harper4,
  4. David S Millar5,
  5. Wolfgang Ludwig Gross2,3,
  6. Jörg Thomas Epplen1,
  7. Stefan Wieczorek1
  1. 1Ruhr-University, Human Genetics, Bochum, Germany
  2. 2Department of Rheumatology, University Hospital Schleswig-Holstein, Campus Luebeck, Luebeck, Germany
  3. 3Department of Rheumatology and Immunology, Klinikum Bad Bramstedt, Bad Bramstedt, Germany
  4. 4Division of Immunity and Infection, University of Birmingham, Edgbaston, Birmingham, UK
  5. 5Institute of Medical Genetics, Cardiff University, Cardiff, UK
  1. Correspondence to Dr Stefan Wieczorek, Ruhr University, Human Genetics, MA5/39 44780 Bochum, Germany; stefan.wieczorek{at}rub.de

https://doi.org/10.1136/ard.2010.130971

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    There is continuous debate about whether Wegener's granulomatosis (WG), microscopic polyangiitis (MPA) and Churg–Strauss syndrome (CSS) represent one disease entity—‘antineutrophil cytoplasmic antibody (ANCA) associated vasculitis (AAV)’ (eg, as presented by Hogan et al1) or whether they constitute separate diseases which share common features but are otherwise heterogeneous—a view held, for example, by Hoffman and Langford.2 ANCA are a common finding in AAV, yet the majority of patients with CSS are ANCA negative. Several clinical and histopathological features unique to one disease (eg, asthma for CSS) support Hoffman's opinion. Analysis of the genetic background of the three disorders may help to differentiate between both concepts. The strongest genetic association for WG pertains to the HLA-DPB1 region,3 ,4 an association not seen in CSS.5 For MPA HLA-DPB1 …

    View Full Text

    Footnotes

    • LA, JUH contributed equally to this work.

    • Funding This work was supported by the Deutsche Forschungsgemeinschaft (KFO 170).

    • Competing interests None.

    • Ethics approval This study was conducted with the approval of the Universities of Lübeck, Germany and Birmingham, UK.

    • Provenance and peer review Not commissioned; externally peer reviewed.