cutaneous leukocytoclastic angiitis

• Occurs 7–10 days after certain medications
• (penicillins, cephalosporins, sulfonamides, phenytoin, allopurinol) or
• infections (eg, HCV, HIV).
• Palpable purpura, no visceral involvement.

Immune complex–mediated leukocytoclastic vasculitis; late involvement indicates systemic vasculitis.

(Arthritis Rheumatol 2018;70:171)

• Most common type of vasculitis; heterogeneous group of clinical syndromes due to IC deposition in capillaries, venules, and arterioles; includes hypersensitivity vasculitis
• Etiol: drugs (PCN, ASA, amphetamines, levamisole, thiazides, chemicals, immunizations, etc.); infection (Strep, Staph, endocarditis, TB, hepatitis); malignancy (paraneoplastic)
• Clinical manifestations: abrupt onset of palpable purpura and transient arthralgias after exposure to the offending agent; visceral involvement rare but can be severe
• Dx studies: ↑ ESR, ↓ complement levels, eosinophilia; ✓ U/A; skin biopsy → leukocytoclastic vasculitis w/o IgA deposition in skin (to distinguish from IgA vasculitis); if etiology not clear, consider ANCA, cryoglobulins, hepatitis serologies, ANA, RF
• Treatment: withdrawal of offending agent ± rapid prednisone taper