The role of interleukin-1β in pyoderma gangrenosum

IL: interleukin PAPA: pyogenic arthritis, pyoderma gangrenosum, and acne PASH: pyoderma gangrenosum, acne, and suppurative hidradenitis PG: pyoderma gangrenosum TNF: tumor necrosis factor UC: ulcerative colitis INTRODUCTION Pyoderma gangrenosum (PG) is a rare, inflammatory, and necrotizing disease that belongs to the group of neutrophilic dermatosis. The pathogenesis of PG remains unknown. In the last 2 years, some researchers found a significant increase in interleukin (IL)-1b and in the IL-1b receptor in skin samples of PG patients. Most PG cases respond to immunomodulators and immunosuppressants. However, there are no clear gold standards for PG treatment. Systemic corticosteroids and cyclosporine are considered first-line treatments. Azathioprine, mycophenolate mofetil, cyclophosphamide, and methotrexate are considered second-line therapies. Antietumor necrosis factor-a (TNF-a) biological agents show efficacy for a wide range of inflammatory conditions, including inflammatory bowel disease, rheumatoid arthritis, and psoriasis. Several studies report PG being successfully treated with infliximab (including 1 randomized, controlled trial), etanercept, and adalimumab. Infliximab is a chimeric IgG monoclonal antibody that blocks the inflammatory cytokine TNF-a. Adalimumab is a fully human monoclonal antibody IgG1 against TNF-a. Etanercept is a human TNF receptor fusion protein that inhibits the binding of TNF-a to TNF receptors on cells’ surfaces. Because a significant contribution of IL-1 to the pathogenesis of PG has been confirmed, biologic agents that inhibit IL-1 represent a therapeutic option in PG. Our patient had ulcerative PG for 24 years. Her disease was refractory to systemic corticosteroids,