Cocain induced Vasculitis

Active cocaine use can also trigger systemic vasculitis. Several case reports and case series describe cases that resemble the classic picture of primary idiopathic ANCA-positive vasculitis (AAV), particularly granulomatosis with polyangiitis (GPA), but occur in association with cocaine abuse. Other types of CIV have also been documented, including cases of IgA vasculitis, eosinophilic granulomatosis with polyangiitis (EGPA) and isolated central nervous system vasculitis (Chevalier X et al.1995; Aseem F et al. 2024).

Cocaine is a diffuse psychostimulant drug. Abuse can lead to potentially serious autoimmunologic manifestations that can be categorized into three overlapping clinical pictures:

• Cocaine-induced midline destructive lesions (CIMDL),
• Cocaine/levamisole-induced (LAC) vasculopathy/vasculitis
• Cocaine-induced vasculitis/vasculopathy (CIV).

In addition to nasal symptoms, patients show macular exanthema, joint involvement, pauci-immune crescentic glomerulonephritis (GN) and other specific organ manifestations. In addition, renal complications such as renal infarction, thrombotic microangiopathy and acute renal failure due to rhabdomyolysis are also associated with cocaine abuse (Lötscher F et al. 2019).

>85% ANCA positivity. ANCA + patients typically show positive PR3 antibodies in ELISA and p-ANCA in IIF or, more rarely, double positivity for PR3 and MPO-ANCA. Some studies report a higher prevalence of MPO positivity compared to other types of ANCA. A minority of CIV patients may be ANCA-negative.

Skin biopsies show a leukocytoclastic vasculitis affecting small and medium-sized skin vessels with fibrinoid necrosis of the vessel walls and perivascular neutrophilic infiltration with nuclear fragments. Direct immunofluorescence of the small vessels shows large deposits of immunoglobulin M (IgM) together with smaller amounts of IgG, IgA and C3. Renal pathologies can occur in various forms, most commonly as pauci-immune necrotizing glomerulonephritis, but also as membranous nephropathy, focal segmental glomerulosclerosis, C3-associated glormerulonephritis, mesangioproliferative/IgA-associated glomerulonephritis and immune complex-mediated glomerulonephritis (Neynaber S et al. 2008).

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