香豆素致皮肤坏死诱发的肾功能不全

• 作 者: Muniesa C. Marcoval J.eno A. 田中伟
• 机 构: Department ofDermatology,HospitalUniversitari de Bellvitge, Feixa Llarga s/n, 08907 Barcelona, Spain
• 出 处: 世界核心医学期刊文摘(皮肤病学分册)
• 发表日期: 2005年02期
• 关键词: 香豆素 肾功能不全 皮肤 肾功能衰竭 双氯芬酸 高凝状态 抗感染药物 促进因素 蛋白 并发症

Cutaneous necrosis is an infrequent complication of coumarin therapy. Skin necrosis has usually been reported in patients with congenital protein C deficiency or, less commonly, protein S deficiency. However, this complication may also occur with acquired and transient protein C and/or S deficiency. In coumarin therapy there is a relatively hypercoagulable state at the start of treatment, and most lesions appear between the third and sixth days. We describe a 75-year-old man receiving coumarin therapy (acenocumarol) for 7 years who was given a nonsteroidal anti-inflammatory agent (diclofenac) for a pain in his knee. Two days later, his renal function deteriorated and skin necrosis became evident. Biopsy showed histological changes consistent with coumarin-induced necrosis. Protein C and S levels were normal. We concluded that in our patient acute renal insufficiency aggravated by diclofenac treatment probably associated with an inadvertent withdrawal could have been the precipitating factor for transient protein C deficiency.

Cutaneous necrosis is an infrequent complication of coumarin therapy. Skin necrosis has usually been reported in patients with congenital protein C deficiency or, less commonly, protein S deficiency. However, this complication may also occur with acquired and transient protein C and / or S deficiency In coumarin therapy there is a relatively hypercoagulable state at the start of treatment, and most lesions appear between the third and sixth days. We describe a 75-year-old man receiving coumarin therapy (acenocumarol) for 7 years who was given a nonsteroidal Anti-inflammatory agent (diclofenac) for a pain in his knee. Two days later, his renal function deteriorated and skin necrosis became evident. Biopsy showed histological changes consistent with coumarin-induced necrosis. Protein C and S levels were normal. in our patient acute renal insufficiency aggravated by diclofenac treatment probably associated with an inadvertent withdrawal could have been precipitating f actor for transient protein C deficiency.