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

    730 Citations (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.
    Original languageEnglish
    JournalNew England Journal of Medicine
    Volume367
    Issue number3
    Pages (from-to)214-23
    Number of pages10
    ISSN0028-4793
    DOIs
    Publication statusPublished - 2012

    Keywords

    • Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
    • Case-Control Studies
    • Female
    • Genetic Predisposition to Disease
    • Genome-Wide Association Study
    • Genotyping Techniques
    • HLA-DP Antigens
    • Humans
    • Major Histocompatibility Complex
    • Male
    • Microscopic Polyangiitis
    • Myeloblastin
    • Polymorphism, Single Nucleotide
    • Risk Factors
    • Wegener Granulomatosis
    • alpha 1-Antitrypsin

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