Page 405 - The Vasculitides, Volume 1: General Considerations and Systemic Vasculitis
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Dermatologic Aspects of Systemic Vasculitis                   379

Table 4. Pathogenic Mechanisms of Vasculitis and Their Clinical Diagnostic and
                                     Histologic Correlates1

Pathogenic Mechanism Vasculitic Syndrome Vasculitis Pattern

Type I (Anaphylactic)  Eosinophilic vasculitis Eosinophilic small-vessel vasculitis

Type II (Cytotoxic-    EGPA           Eosinophilic small- and medium vessel vasculitis

cytolytic antibody)                   Neutrophilic mostly small- and medium vessel

                       GPA            vasculitis

                                      Neutrophilic mostly small- and medium vessel

                       MPA            vasculitis

Type III (Immune       HSP            Neutrophilic small-vessel vasculitis

complex)               CLA            Neutrophilic small-vessel vasculitis

                       CV Neutrophilic mostly small- and medium vessel

                                      vasculitis

                       PAN            Neutrophilic medium-vessel vasculitis

Type IV (Delayed       GCA            Granulomatous medium-vessel vasculitis

hypersensitivity)      Chronic GVHD   Lymphocytic small-vessel vasculitis

Abbreviations: CLA, Cutaneous leukocytoclastic angiitis; CV, Cryoglobulinemic vasculitis; EGPA,

Eosinophilic granulomatosis with polyangiitis; GCA, Giant cell arteritis; GPA, Granulomatosis

with polyangiitis; GVHD, Graft-versus-host disease; HSP, Henoch-Sch?nlein purpura; MPA,
Microscopic polyangiitis, PAN, Polyarteritis nodosa. 1 Adapted from [1].

                             STAGE 1                                STAGE 2

                             STAGE 3                                STAGE 4

Figure 10. The four morphologic stages of cutaneoFuigsupreol1y0arteritis nodosa with end-stage healed arteritis
or endarteritis nodosa. The acute stage is characterized by endothelial loss and fibrin thrombi with
neutrophil infiltration without obvious internal elastic lamina disruption and medial fibrinoid necrosis.
The subacute stage shows mixed cellular infiltration and unique intimal target-like fibrinoid necrosis
and leakage extending through the disrupted internal elastic lamina sites to the media. The reparative
stage shows intimal fibroblastic proliferation and perivascular neovascularization with predominant
histiocyte and lymphocyte infiltration. The healed stage reveals minimal cellular inflammation and
occlusive intimal thickening.

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