Table 2 Types of vasculitis according to the dominant vessels affected, as defined by the Chapel Hill consensus conference8.
| Dominant vessels affected | Type of vasculitis (pathomechanism) | Specific diagnostic hallmarks |
|---|---|---|
| Small vessels | Cutaneous leucocytoclastic angiitis (unknown aetiology, drug induced/allergic) | Eventual drug history (possible serum IgE elevation), absence of cryoglobulins or IgA on histology, negative immune serology |
| Henoch‐Schönlein purpura (IgA deposition) | Increased serum IgA, usually normal serum complement, tissue IgA deposition, especially in paediatric patients, triggered by infections,9,10,11 clinical triad or tetrad of purpura, arthralgia, gastrointestinal symptoms and renal failure2,12 | |
| Mixed cryoglobulinaemia (cryoglobulin deposition) | Serum cryoglobulins, often low serum C4, tissue deposition of cryoglobulin and complement | |
| Small to medium vessels | Wegner's granulomatosis (mostly ANCA associated) | ANCA, renal and nasopharyngeal involvement |
| Churg–Strauss syndrome (mostly ANCA associated, eosinophilia) | ANCA, eosinophilia | |
| Microscopic polyangiitis (mostly ANCA associated) | ANCA | |
| Medium vessels | Polyarteritis nodosa | Clinically medium vessel affection with negative immune serology |
| Kawasaki syndrome (unknown) | ESR acceleration, C‐reactive protein increased | |
| Large vessels | Temporal arteritis (unknown) | ESR acceleration, C‐reactive protein increased |
| Takayasu arteritis (unknown) | ESR acceleration |
ANCA, antineutrophil cytoplasmic antibody; ESR, erythrocyte sedimentation rate.