Abstract
Cocaine use is a multifaceted diagnostic pitfall in the field of systemic vasculitides. The fact that Cocaine-Induced Midline Destructive Lesions (CIMDL) can be associated with Anti-Neutrophil Cytoplasmic Antibodies (ANCA) and mimic localized granulomatosis with polyangitis is known for decades. In these cases ANCA target Proteinase 3 (PR3) and Human Neutrophil Elastase. More recently, levamisole adulterated cocaine has been implicated in a peculiar clinico-biological syndrome combining cutaneous vasculopathy and sometimes glomerulonephritis, and ANCA positivity with frequent double positivity (PR3 and myeloperoxydase). Clinician should be aware of the clinical and immunological hints to these diagnoses. The pathogenesis of such drug-induced auto-immune syndromes is poorly understood. Its studying may shed new light on the potential mechanism involved in tolerance breakdown in conventional ANCA-associated vasculitides.
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