Authors
Lyons, Paul ARayner, Tim F
Trivedi, Sapna
Holle, Julia U
Watts, Richard A
Jayne, David R W
Baslund, Bo
Brenchley, Paul
Bruchfeld, Annette
Chaudhry, Afzal N
Cohen Tervaert, Jan Willem
Deloukas, Panos
Feighery, Conleth
Gross, Wolfgang L
Guillevin, Loic
Gunnarsson, Iva
Harper, Lorraine
Hrušková, Zdenka
Little, Mark A
Martorana, Davide
Neumann, Thomas
Ohlsson, Sophie
Padmanabhan, Sandosh
Pusey, Charles D
Salama, Alan D
Sanders, Jan-Stephan F
Savage, Caroline O
Segelmark, Mårten
Stegeman, Coen A
Tesař, Vladimir
Vaglio, Augusto
Wieczorek, Stefan
Wilde, Benjamin
Zwerina, Jochen
Rees, Andrew J
Clayton, David G
Smith, Kenneth G C
Affiliation
Cambridge Institute for Medical Research, and Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom. kgcs2@cam.ac.ukIssue Date
2012-07-19MeSH
Anti-Neutrophil Cytoplasmic Antibody-Associated VasculitisCase-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
Metadata
Show full item recordCitation
Genetically distinct subsets within ANCA-associated vasculitis. 2012, 367 (3):214-23 N. Engl. J. Med.Publisher
The New England journal of medicineJournal
The New England journal of medicineDOI
10.1056/NEJMoa1108735PubMed ID
22808956Abstract
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.Item Type
Article In PressLanguage
enISSN
1533-4406ae974a485f413a2113503eed53cd6c53
10.1056/NEJMoa1108735
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