Chen Chun Chuan, Takeshima Fuminao, Miyazaki Takashige, Murase Kunihiko, Ohtani Hiroshi, Isomoto Hajime, Shikuwa Saburo, Omagari Katsuhisa, Mizuta Yohei, Ozono Yoshiyuki, Kohno Shigeru
Second Department of Internal Medicine, Nagasaki University School of Medicine.
Intern Med. 2007;46(12):839-44. doi: 10.2169/internalmedicine.46.6264. Epub 2007 Jun 15.
Anemia and leukopenia caused by copper deficiency are well-documented consequences of long-term total parenteral nutrition. We measured the serum copper levels of bed-ridden patients receiving enteral feeding, and evaluated optical and ultrastructural features of bone marrow before and after copper supplementation.
Serum samples were obtained from 15 bed-ridden elderly patients receiving tube feeding (TF) and 10 age-matched bed-ridden patients who took food orally (CO), and the copper ceruloplasmin concentration of each sample was measured. Bone marrow samples were obtained from patients who exhibited copper deficiency and leukopenia and/or anemia before and after the copper supplementation, for use in light and electron microscopic analysis.
The tube-fed patients had significantly lower mean serum copper and ceruloplasmin concentrations than the control patients. Seven of the 15 tube-fed patients had reduced serum copper concentrations and leukopenia. Six of those 7 patients also had anemia. Copper sulfate was administered to those 7 patients by enteral tube; their copper concentration, anemia and leukopenia improved within 1 month after they were administered copper sulfate. In the bone marrow examination before copper supplementation, light microscopy showed cytoplasmic vacuolization in both myeloid and erythroid precursors, and electron microscopy showed electron-dense deposits in mitochondria and cytoplasm of erythroid and myeloid cells. After copper supplementation, these pathological changes disappeared.
Bicytopenia is likely to occur in tube-fed patients with copper deficiency. Copper deficiency appears to be associated with cytoplasmic vacuolization and electron-dense deposits in mitochondria in erythroid and myeloid cells.
长期全胃肠外营养导致铜缺乏引起贫血和白细胞减少已有充分文献记载。我们测定了接受肠内喂养的卧床患者的血清铜水平,并评估了补充铜前后骨髓的光学和超微结构特征。
从15例接受管饲(TF)的卧床老年患者和10例年龄匹配的经口进食卧床患者(CO)中采集血清样本,测定每个样本的铜蓝蛋白浓度。从出现铜缺乏和白细胞减少和/或贫血的患者补充铜前后采集骨髓样本,用于光镜和电镜分析。
管饲患者的平均血清铜和铜蓝蛋白浓度显著低于对照患者。15例管饲患者中有7例血清铜浓度降低和白细胞减少。这7例患者中有6例也有贫血。通过肠内管给这7例患者施用硫酸铜;在施用硫酸铜后1个月内,他们的铜浓度、贫血和白细胞减少情况得到改善。在补充铜之前的骨髓检查中,光镜显示髓系和红系前体细胞均有细胞质空泡化,电镜显示红系和髓系细胞的线粒体和细胞质中有电子致密沉积物。补充铜后,这些病理变化消失。
铜缺乏的管饲患者可能会出现双血细胞减少。铜缺乏似乎与红系和髓系细胞线粒体中的细胞质空泡化和电子致密沉积物有关。