Case Presentation: Cocaine-induced plasma cell orificial mucositis (PCOM) is a rare skin disorder characterized by chronic periorificial ulcers, and in severe cases, septal or palatal perforation. This case describes a unique presentation of a patient with cocaine-induced PCOM. A 39-year-old female with monthly intranasal cocaine use presented with a progressively enlarging ulcerative defect of the upper lip and nose, originating from a minor laceration seven months prior. Examination revealed a saddle-nose deformity with a 3-cm full-thickness upper lip ulcer, and imaging showed a large soft tissue defect, anterior nasal septal perforation and sinus mucosal thickening. Laboratory workup revealed moderately elevated IgE levels, but negative infectious and autoimmune serologies. Skin biopsy demonstrated dense interstitial lymphoplasmacytic infiltrate with eosinophils, without evidence of carcinoma, findings consistent with PCOM. Diagnosis of PCOM was supported by progressive ulcerations in the setting of recent cocaine use and histopathology. Given the extent of inflammation, surgical teams deferred acute intervention but suggested immunosuppressive therapy to reduce inflammation before offering reconstructive procedures. An oral corticosteroid taper was initiated upon discharge, resulting in subsequent rapid improvement in pain and inflammation at clinic follow-up one week later.
Discussion: Cocaine-induced nasal destruction can manifest as PCOM or cocaine-induced midline destructive lesions (CIMDL), and distinguishing between them is critical due to differing treatments. Histopathologically, CIMDL is characterized by necrotizing, granulomatous, and vasculitic inflammation with neutrophilic predominance, while PCOM shows plasma cells and eosinophil-rich infiltrates. In this patient, biopsy confirmed PCOM, and infectious, autoimmune, and neoplastic causes were excluded. The pathogenesis is thought to involve hypersensitivity reaction to cocaine or its adulterants, often with elevated IgE, seen in this patient. Clinically, CIMDL causes progressive midline and nasal facial destruction, causing nasal obstruction and epistaxis. In contrast, PCOM manifests as local destructive exudative ulcers near facial orifices causing localized discomfort. Although this patient’s facial destruction was extensive and suspicious for CIMDL, histology and clinical context supported diagnosis of severe PCOM. Treatment for both conditions begins with immediate discontinuation of cocaine use, but PCOM often improves with corticosteroids, whereas CIMDL does not. This patient with PCOM was promptly started on an oral corticosteroid taper and had reported marked clinical improvement one week later on medical therapy.
Conclusions: PCOM is a rare, emerging mucosal disorder linked to cocaine use, and accurate differentiation from CIMDL by clinical and histopathological features is essential for guiding therapy. Corticosteroid treatment and cocaine cessation are effective for PCOM, in contrast to CIMDL, which does not respond to immunosuppression. In this patient’s case, prompt corticosteroid taper initiation led to rapid improvement, supporting a hypersensitivity-driven mechanism.