D Sasseville1, W A Ghamdi, S A Khenaizan. 1. The Division of Dermatology, Department of Medicine, Royal Victoria Hospital, Montréal, Quebec, Canada.
Abstract
BACKGROUND: Due to advances in recombinant DNA technology, interferons are now readily available and are frequently used in all branches of medicine. These potent biologic response modifiers carry a number of systemic and local side effects. These cytokines are usually administered subcutaneously, and recent studies have described the occurrence of inflammation or necrosis at the site of injection. OBJECTIVE: We report a case of cutaneous necrosis at the sites of interferon injections in a 35-year-old man treated for chronic myeloid leukemia with high, daily doses of interferon alfa. In addition, we review the existing literature on interferon-induced cutaneous necrosis and discuss preventive strategies. CONCLUSION: Cutaneous inflammation or necrosis at interferon injection sites is not uncommon. Although interferon beta-1b is most commonly responsible for this complication, it is now increasingly reported with interferon alfa. It appears to be secondary to the proinflammatory effects of these cytokines or to their unmasking of a subtle hypercoagulable state.
BACKGROUND: Due to advances in recombinant DNA technology, interferons are now readily available and are frequently used in all branches of medicine. These potent biologic response modifiers carry a number of systemic and local side effects. These cytokines are usually administered subcutaneously, and recent studies have described the occurrence of inflammation or necrosis at the site of injection. OBJECTIVE: We report a case of cutaneous necrosis at the sites of interferon injections in a 35-year-old man treated for chronic myeloid leukemia with high, daily doses of interferon alfa. In addition, we review the existing literature on interferon-induced cutaneous necrosis and discuss preventive strategies. CONCLUSION:Cutaneous inflammation or necrosis at interferon injection sites is not uncommon. Although interferon beta-1b is most commonly responsible for this complication, it is now increasingly reported with interferon alfa. It appears to be secondary to the proinflammatory effects of these cytokines or to their unmasking of a subtle hypercoagulable state.