针对威尔逊氏病的过量铜螯合疗法会导致贫血和肝功能障碍。
Excess copper chelating therapy for Wilson disease induces anemia and liver dysfunction.
作者信息
Harada Masaru, Miyagawa Koichiro, Honma Yuichi, Hiura Masaaki, Shibata Michihiko, Matsuhashi Toru, Abe Shintaro, Harada Riko, Tabaru Akinari
机构信息
The Third Department of Internal Medicine, University of Occupational and Environmental Health, Japan School of Medicine, Japan.
出版信息
Intern Med. 2011;50(14):1461-4. doi: 10.2169/internalmedicine.50.5209. Epub 2011 Jul 15.
A 37-year-old man was diagnosed with Wilson disease at the age of 14. His first manifestations were neurological. He was treated with trientine for more than 10 years and suffered from anemia and liver dysfunction. Wilson disease is a genetic disorder characterized by accumulation of copper in the body. Excess copper is toxic, but copper is an essential trace element. Copper-binding ceruloplasmin is important for iron metabolism. Excess copper chelating treatment-induced anemia and iron deposition in the liver was suspected. Proper monitoring of copper status is important for the management of Wilson disease.
一名37岁男性在14岁时被诊断为威尔逊病。他最初的表现为神经方面的症状。他接受曲恩汀治疗超过10年，出现了贫血和肝功能障碍。威尔逊病是一种遗传性疾病，其特征是体内铜蓄积。过量的铜具有毒性，但铜是一种必需的微量元素。铜结合铜蓝蛋白对铁代谢很重要。怀疑过量铜螯合治疗导致了贫血和肝脏铁沉积。对铜状态进行适当监测对威尔逊病的管理很重要。
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