Excess Copper Chelating Therapy for Wilson Disease Induces Anemia and Liver Dysfunction

被引：11

作者：

Harada, Masaru ^{[1
]}

Miyagawa, Koichiro ^{[1
]}

Honma, Yuichi ^{[1
]}

Hiura, Masaaki ^{[1
]}

Shibata, Michihiko ^{[1
]}

Matsuhashi, Toru ^{[1
]}

Abe, Shintaro ^{[1
]}

Harada, Riko ^{[1
]}

Tabaru, Akinari ^{[1
]}

机构：

[1] Univ Occupat & Environm Hlth, Japan Sch Med, Dept Internal Med 3, Tokyo, Japan

来源：

INTERNAL MEDICINE | 2011年 / 50卷 / 14期

关键词：

ceruloplasmin; chelating therapy; hemochromatosis; Wilson disease; ACQUIRED SIDEROBLASTIC ANEMIA; LATE ENDOSOMES; IRON; GENE; CERULOPLASMIN; ATP7B; ACERULOPLASMINEMIA; FERROPORTIN; DIAGNOSIS; HEPCIDIN;

D O I：

10.2169/internalmedicine.50.5209

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页码：1461 / 1464

页数：4

共 45 条

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[24] Long-Term Urinary Copper Excretion and Exchangeable Copper in Children With Wilson Disease Under Chelation Therapy
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[25] Copper-chelating therapeutic effect in Wilson disease with different clinical phenotypes and polymorphisms of ATP7B gene
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[27] Copper metabolism after living donor liver transplantation for hepatic failure of Wilson's disease from a gene mutated donor
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