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作为威尔逊病治疗并发症的铜缺乏继发脊髓病。

Myelopathy secondary to copper deficiency as a complication of treatment of Wilson's disease.

作者信息

Lozano Herrero Jesús, Muñoz Bertrán Eduardo, Ortega González Isabel, Gómez Espín Rosa, López Espín María Isabel

机构信息

Servicio de Medicina Interna, Hospital Morales Meseguer, Murcia, España.

出版信息

Gastroenterol Hepatol. 2012 Dec;35(10):704-7. doi: 10.1016/j.gastrohep.2012.03.008. Epub 2012 May 18.

Abstract

Wilson's Disease (WD) is an autosomal recessive disorder of copper metabolism resulting in a pathological accumulation of this metal, initially in the liver and later in other organs, mainly brain. Treatment with copper chelating agents and zinc salts results in a depletion of copper deposits and prevents or reverses the clinical manifestations. Copper deficiency may cause haematological and neurological changes, the latter principally being polyneuropathy and myelopathy. We report a patient with WD who developed a myelopathy associated with a deficiency of copper following prolonged treatment with D-penicillamine and zinc salts.

摘要

威尔逊病(WD)是一种常染色体隐性铜代谢紊乱疾病,会导致这种金属在体内病理性蓄积,最初蓄积于肝脏,随后累及其他器官,主要是脑。使用铜螯合剂和锌盐进行治疗可使铜沉积物减少,并预防或逆转临床表现。铜缺乏可能会引起血液学和神经学变化,后者主要表现为多发性神经病和脊髓病。我们报告了1例WD患者,该患者在长期使用D-青霉胺和锌盐治疗后发生了与铜缺乏相关的脊髓病。

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