Abstract

The three major categories of systemic vasculitis are large vessel vasculitis (chronic granulomatous arteritis), medium vessel vasculitis (necrotizing arteritis), and small vessel vasculitis (necrotizing polyangiitis). This chapter will focus on medium vessel vasculitis (necrotizing arteritis) and small vessel vasculitis that are not known to be caused by direct vessel wall invasion by infectious pathogens. These vasculitides are mediated by immunologic mechanisms that, in many if not most, involve autoimmunity.The two major variants of medium vessel vasculitis are polyarteritis nodosa and Kawasaki’s disease. Small vessel vasculitis is divided into immune complex-mediated vasculitis and pauci-immune vasculitis associated with, and probably caused by, anti-neutrophil cytoplasmic autoantibodies (ANCA). Immune complex vasculitis reviewed in this chapter includes IgA vasculitis (Henoch–Schönlein purpura) and cryoglobulinemic vasculitis. ANCA-associated vasculitis reviewed includes microscopic polyangiitis, granulomatosis with polyangiitis (Wegener’s granulomatosis), and eosinophilic granulomatosis with polyangiitis (Churg–Strauss syndrome).

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call