Genetically distinct subsets within ANCA-associated vasculitis

Paul A Lyons, Tim F Rayner, Sapna Trivedi, Julia U Holle, Richard A Watts, David R W Jayne, Bo Baslund, Paul Brenchley, Annette Bruchfeld, Afzal N Chaudhry, Jan Willem Cohen Tervaert, Panos Deloukas, Conleth Feighery, Wolfgang L Gross, Loic Guillevin, Iva Gunnarsson, Lorraine Harper, Zdenka Hrušková, Mark A Little, Davide MartoranaThomas Neumann, Sophie Ohlsson, Sandosh Padmanabhan, Charles D Pusey, Alan D Salama, Jan-Stephan F Sanders, Caroline O Savage, Mårten Segelmark, Coen A Stegeman, Vladimir Tesař, Augusto Vaglio, Stefan Wieczorek, Benjamin Wilde, Jochen Zwerina, Andrew J Rees, David G Clayton, Kenneth G C Smith

    797 Citationer (Scopus)

    Abstract

    Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a severe condition encompassing two major syndromes: granulomatosis with polyangiitis (formerly known as Wegener's granulomatosis) and microscopic polyangiitis. Its cause is unknown, and there is debate about whether it is a single disease entity and what role ANCA plays in its pathogenesis. We investigated its genetic basis.
    OriginalsprogEngelsk
    TidsskriftNew England Journal of Medicine
    Vol/bind367
    Udgave nummer3
    Sider (fra-til)214-23
    Antal sider10
    ISSN0028-4793
    DOI
    StatusUdgivet - 2012

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