In the current issue of the European Journal of Internal Medicine, Garvín-Grande et al. present a cohort analysis combined with a structured literature review delineating the clinical and immunological profile of cocaine-induced antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) [1], a distinct clinical phenotype that frequently mimics granulomatosis with polyangiitis (GPA). Cocaine-induced AAV can be considered part of the broader spectrum of cocaine/levamisole-associated autoimmune syndrome (CLAAS), which also includes cocaine-induced midline destructive lesions [2,3], and has evolved from a clinical curiosity into a relevant diagnostic challenge at the intersection between toxic exposure and autoimmunity with important implications for clinical practice.
