[Causes and mechanisms of systemic vasculitides]

Multiple mechanisms contribute to the pathogenesis of systemic vasculitides: 1. vasculitides resulting from the deposition of circulating immune complexes, comprising polyarteritis nodosa associated with hepatitis B virus infection, cryoglobulinemia associated systemic with vasculitides, mainly the consequence of hepatitis C virus infection, and Schonlein Henoch purpura, which results from the deposition in the mesangium and vessels of IgA forming complexes; 2. vasculitides associated with anti-neutrophil cytoplasm antibodies (ANCA), comprising Wegener's granulomatosis associated with anti-proteinase 3 ANCA, and microscopic polyangiitis and Churg-Strauss syndrome, associated with anti-myeloperoxydase ANCA. The pathogenic role of ANCA has been demonstrated in vitro and in vivo in the case of anti-myéloperoxydase antibodies, whereas it has only been demonstrated in vitro in the case of anti-proteinase 3 antibodies; 3. polyarteritis nodosa unrelated to viral infection results from rheologic phenomenon that explain the localisation of vasculitis lesions at the bifurcation of arteries and the presence of microaneurysm.