Tumor necrosis factor α belongs to the family of proinflammatory cytokines and plays a major role in host immune responses to infection, tumors, and foreign proteins. It is produced mainly by mononuclear phagocytes. Various biological effects of TNF-α have been described, including initiation of acute-phase responses, increase in body temperature, stimulation of migration of dendritic cells to lymph nodes, and activation as well as attraction of neutrophils.17 Tumor necrosis factor α has been identified as a critical mediator of inflammation in several inflammatory dermatoses including cutaneous vasculitides, lupus erythematosus, eczema, and psoriasis. Infliximab (Remicade) is a humanized-murine monoclonal anti–TNF-α antibody consisting of the variable domain (Fab) of mouse IgG attached to the constant region (Fc) of human IgG1.18 The antibody binds both the soluble subunit and the membrane-bound precursor of TNF-α and thereby neutralizes the biological activity of TNF-α. After its approval by the Food and Drug Administration in 1998, its therapeutic use has been extensively studied in rheumatoid arthritis14 and inflammatory bowel diseases such as Crohn disease.11- 13 Furthermore, recent studies have shown promising results with the use of infliximab in the treatment of psoriatic arthritis,19 psoriatic skin lesions,20 and pyoderma gangrenosum (unpublished data), conditions that are characterized by a neutrophilic inflammatory infiltrate. Since there is evidence that TNF-α may be involved in the pathogenesis of SPD, and because of the association of SPD with inflammatory bowel diseases, pyoderma gangrenosum, and rheumatoid arthritis, a therapeutic trial with infliximab was performed in our patient with severe recalcitrant SPD.