The global burden of anti-neutrophil cytoplasmic antibody vasculitis
نویسندگان
چکیده
منابع مشابه
Genetic aspects of anti-neutrophil cytoplasmic antibody-associated vasculitis.
The genetics of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a complex area of investigation because of the low frequency of AAVs, the rarity of familial cases and the complexity of disease phenotypes. However, recent studies have been able to gather significant numbers of patients, and multicentre collaborative efforts have allowed the performance of two genome-wi...
متن کامل[Treatment of anti-neutrophil cytoplasmic antibody related vasculitis].
ANCA-associated vasculitides are a well-known clinico-pathological group of systemic diseases comprising microscopic poliangiitis, granulomatosis with poliangiitis and eosinophilic granulomatosis with poliangiitis. This article shows contemporary treatment of this diseases with extensive literature review. Stepwise treatment of ANCA-associated vasculitides is divided into induction therapy and ...
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Enormous progress has been made during the last 25 years in our understanding of the aetiopathogenesis of the anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitides (AAV). This has led to improvements in early diagnosis, treatment and secondary prevention of these diseases. Nevertheless, there are still unmet needs in the AAV. With respect to diagnosis and follow-up, sensitive ...
متن کاملAnti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, Large Vessel Vasculitis and Kawasaki Disease in Japan
Based on studies comparing the prevalence of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) between Japan and Europe, we have learned that the difference may be due to genetic background and environmental factors, but not to diagnosis or ELISA system for myeloperoxidase and proteinase-3 ANCA. In Japan, microscopic polyangiitis is the most common among AAV, but Wegener’s...
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ژورنال
عنوان ژورنال: Rheumatology
سال: 2016
ISSN: 1462-0324,1462-0332
DOI: 10.1093/rheumatology/kew438