PG) is an uncommon neutrophilic dermatosis first described by Brunsting et al in 1930. 1 It is a painful, chronic ulcerating inflammatory skin condition that appears to be immune-mediated. The characteristic lesion begins as small erythematous papules that rapidly spread concentrically, coalesce, and subsequently centrally become ulcerated and necrotic. The mature lesion has a welldefined, undermined, violaceous border and is exquisitely painful. PG develops over the lower extremities in more than 70% of cases; however, any cutaneous area or mucosal surface may be affected. 2 More than 50% of PG cases are associated with systemic disease. Patients with inflammatory bowel disease (IBD) account for Ο·30% of all PG cases. 2 Other associations include rheumatoid arthritis, hematologic malignancies, and intraabdominal malignancies. 3 The precise pathogenesis of PG remains unclear. The association of PG with autoimmune disorders and successful management with a variety of local and systemic immunosuppressant agents suggests that disturbances of immune regulation play a role. Immune dysregulation, including defects in neutrophil chemotaxis, neutrophil hyperreactivity, and overexpression of cytokines such as interleukin-8 have been identified. Tumor necrosis factor alpha (TNF-β£), a powerful proinflammatory cytokine, may mediate many of these effects and, therefore, play a role in the pathogenesis