๐ ็ธฝ็ฎ้ ๏ฝ ๐ ่ฑๆๅๆ๏ผๆฌ็ฏ๏ผ ๏ฝ ๐ ๅฎๆด็ฟป่ญฏ ๏ฝ โญ ็ฒพ่ฏ็ญ่จ
PATHOGENESIS
Cutaneous small vessel vasculitis as well as other subtypes of small vessel vasculitis involving the skin are mediated by immune complexes that form in the presence of antigen excess. After their deposition within postcapillary venules, these complexes lead to complement-mediated chemotaxis of neutrophils (Fig. 24.1A). In ANCA-associated vasculitis, vessel wall damage is directly mediated by neutrophils rather than by immune complex deposition (Fig. 24.1B), hence the term โpauci-immuneโ vasculitis.