title: Clinicopathological analysis of hematological disorders in tube-fed patients with copper deficiency.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Second Department of Internal Medicine, Nagasaki University School of Medicine.
authors.forename: Chun Chuan
authors.initials: CC
authors.lastname: Chen
authors.forename: Fuminao
authors.initials: F
authors.lastname: Takeshima
authors.forename: Takashige
authors.initials: T
authors.lastname: Miyazaki
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Murase
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ohtani
authors.forename: Hajime
authors.initials: H
authors.lastname: Isomoto
authors.forename: Saburo
authors.initials: S
authors.lastname: Shikuwa
authors.forename: Katsuhisa
authors.initials: K
authors.lastname: Omagari
authors.forename: Yohei
authors.initials: Y
authors.lastname: Mizuta
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Ozono
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kohno
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000740:Anemia / Q000097:blood / Q000178:diet therapy / Q000209:etiology*; D001853:Bone Marrow / Q000187:drug effects / Q000473:pathology; D002570:Ceruloplasmin / Q000187:drug effects / Q000378:metabolism; D003300:Copper / Q000008:administration & dosage / Q000097:blood / Q000172:deficiency*; D003677:Deficiency Diseases / Q000150:complications* / Q000473:pathology; D019587:Dietary Supplements; D004750:Enteral Nutrition; D005260:Female; D006801:Humans; D007970:Leukopenia / Q000097:blood / Q000178:diet therapy / Q000209:etiology*; D008297:Male; D012016:Reference Values; D016896:Treatment Outcome
chemical_list: D003300:Copper; D002570:Ceruloplasmin