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This article is part of the supplement: Advances in systemic sclerosis and related fibrotic and vascular conditions

Highly Accessed Review

Vasculitis: mechanisms involved and clinical manifestations

Loic Guillevin1* and Thomas Dörner2

Author affiliations

1 Service de Médecine Interne, Hôpital Cochin, rue du Faubourg Saint-Jacques, F-75014 Paris, France

2 Klinische Hämostaseologie and Rheumatologie, Charite Universitätsmedizin, Berlin and German Center for Rheumatology (DRFZ), Schumannstrasse, D-10098 Berlin, Germany

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Citation and License

Arthritis Research & Therapy 2007, 9(Suppl 2):S9  doi:10.1186/ar2193

Published: 15 August 2007

Abstract

Systemic vasculitis, an inflammatory necrotizing disease of the blood vessel walls, can occur secondary to autoimmune diseases, including connective tissue diseases. Various pathogenic mechanisms have been implicated in the induction of vasculitis, including cell-mediated inflammation, immune complex-mediated inflammation and autoantibody-mediated inflammation. This inflammatory activity is believed to contribute to accelerated atherosclerosis, and also leads to increased risk for cardiovascular events in patients with rheumatoid arthritis and systemic lupus erythematosus. Endothelial cell activation is a common pathogenic pathway in the systemic vasculitis associated with rheumatoid arthritis and systemic lupus erythematosus, with elevated levels of endothelin-1 potentially inducing vascular dysregulation.