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胃手术后获得性低铜血症。

Acquired hypocupremia after gastric surgery.

作者信息

Kumar Neeraj, Ahlskog J Eric, Gross John B

机构信息

Department of Neuroogy, Mayo Clinic, Rochester, Minnesota 55905, USA.

出版信息

Clin Gastroenterol Hepatol. 2004 Dec;2(12):1074-9. doi: 10.1016/s1542-3565(04)00546-4.

DOI:10.1016/s1542-3565(04)00546-4
PMID:15625652
Abstract

BACKGROUND & AIMS: Copper absorption in humans probably occurs in the stomach and duodenum. Copper is essential for the structure and function of the nervous system and acquired copper deficiency in humans has been recognized to cause a myelopathy that resembles vitamin B12 deficiency. Acquired copper deficiency is not a well-recognized complication of gastric surgery. In Menke's disease a defect in enterocyte transport of absorbed copper results in increased copper content in the duodenal mucosa and hypocupremia.

METHODS

We report 2 patients who developed neurologic deficits with copper deficiency many years after gastric surgery. In 2 other patients with hypocupremic myelopathy but no history of gastric surgery, colonic copper was measured to determine if an absorptive defect similar to that seen in Menke's disease may be responsible for hypocupremia.

RESULTS

In all 4 patients copper deficiency was identified as the cause of the myelopathy. In 2 patients the copper deficiency occurred after gastric surgery. Eight additional patients with copper deficiency after gastric surgery were identified from the literature. Six of these 8 patients also had neurologic manifestations. Colonic mucosa copper content was increased in the 2 patients with hypocupremia without prior gastric surgery.

CONCLUSIONS

Acquired copper deficiency may be a delayed complication of gastric surgery and may result in a myelopathy similar to that seen with vitamin B12 deficiency. In some patients with acquired copper deficiency no cause for the hypocupremia may be evident and a primary absorptive defect should be considered.

摘要

背景与目的

人体对铜的吸收可能发生在胃和十二指肠。铜对于神经系统的结构和功能至关重要,并且已认识到人体后天性铜缺乏会导致一种类似于维生素B12缺乏的脊髓病。后天性铜缺乏并非胃手术中一种广为人知的并发症。在门克斯病中,吸收的铜在肠细胞转运方面存在缺陷,导致十二指肠黏膜铜含量增加和低铜血症。

方法

我们报告了2例胃手术后多年出现铜缺乏相关神经功能缺损的患者。另外2例患有低铜血症性脊髓病但无胃手术史的患者,检测了结肠铜含量,以确定是否类似于门克斯病中所见的吸收缺陷可能是低铜血症的原因。

结果

所有4例患者的铜缺乏均被确定为脊髓病的病因。其中2例患者的铜缺乏发生在胃手术后。从文献中还确定了另外8例胃手术后出现铜缺乏的患者。这8例患者中有6例也有神经学表现。2例无胃手术史的低铜血症患者的结肠黏膜铜含量增加。

结论

后天性铜缺乏可能是胃手术的一种延迟并发症,可能导致一种类似于维生素B12缺乏所见的脊髓病。在一些后天性铜缺乏患者中,低铜血症的病因可能不明显,应考虑原发性吸收缺陷。

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