This article is part of the supplement: Advances in systemic sclerosis and related fibrotic and vascular conditions
Vasculitis: mechanisms involved and clinical manifestations
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
Citation and License
Arthritis Research & Therapy 2007, 9(Suppl 2):S9 doi:10.1186/ar2193Published: 15 August 2007
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.