Les vascularites à ANCA chez les consommateurs de cocaïne : de la poudre aux yeux ?

ocaine use is a typical etiological trap for vasculitis. The Cocaine Induced Midline Destruction Lesions (CIMDL) is a challenge considering the mimic clinical and serological presentation with localized manifestation of the granulomatosis with polyangiitis (GPA). CIMDL lesions are characterised by painful nasal obstruction, with perforation of septum and inferior turbinates, with no ophthalmologic, auditory and systemic signs. In opposed to localised GPA, CIMDL lesions are more painful with more epistaxis. The localisation of the lesions is mainly medial, with frequent septal perforation and limited to rhinologic involvement. C-reactive protein is usually negative. Biopsy reveals a chronic inflammation, frequently ulcerated without granulomas or multinucleated giant cells. Serological biomarkers typically show ANCA-PR3 positivity, but with perinuclear pattern, as opposed to the cytoplasmic pattern in GPA. Anti-HNE Antibodies could also be detected and are highly specifics. Corticosteroids and either immunosuppressive treatment are poorly effective. The mucosal damage caused by ischemia or by crystal-induced microtrauma may predispose cocaine users to the development of chronic low-grade infection with S.Aureus. S.Aureus releases toxins known to be powerful superantigens, which can explain ANCA formation. The first aim is the complete avoidance of cocaine consumption. Local ENT treatment is indicated. Trimetoprim-Sufamethoxazole has been reported to be beneficial because it reduces the nasal carriage of S.Aureus.