title: Pro-inflammatory states and IGF-I level in ischemic heart disease with low or high serum iron.
abstract: BACKGROUND
  Serum iron overload or iron deficiency appears to be associated with atherosclerosis and ischemic myocardial damage. Roles of low or high serum iron in patients with ischemic heart diseases are still controversial.
  
  
  METHODS
  Serum samples for biochemical and immunologic analyses were collected from the 73 normal subjects and the 90 patients with ischemic heart disease (IHD), the latter of which were selected from 142 patients and classified by low, normal and high serum iron.
  
  
  RESULTS
  Tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), high sensitive C-Reactive protein (hsCRP), and interleukin-10 (IL-10) were increased and insulin-like growth factor (IGF)-I was decreased in IHD patients with low serum iron, whereas these parameters were not changed in IHD patients with normal or high serum iron, compared with normal subjects. Total bilirubin was increased in IHD patients with high serum iron but was not changed in IHD patients with low or normal serum iron, compared with normal subjects.
  
  
  CONCLUSIONS
  The IHD patients with low serum iron were associated with a pro-inflammatory state, such as increased TNF-alpha, IL-6, and hsCRP; increased anti-inflammatory activities, such as increased IL-10; decreased cardiac protective factor, such as decreased IGF-I. These findings may imply that IHD patients with low serum irons were associated with less cardiac protection and more pro-inflammatory states than normal subjects or IHD patients with either normal or high serum iron.
authors.affiliation: School of Physical Therapy, Chung-Shan Medical University, Taichung, Taiwan.
authors.forename: Shin-Da
authors.initials: SD
authors.lastname: Lee
authors.forename: Chih-Yang
authors.initials: CY
authors.lastname: Huang
authors.forename: Wen-Tong
authors.initials: WT
authors.lastname: Shu
authors.forename: Ter-Hsin
authors.initials: TH
authors.lastname: Chen
authors.forename: James A
authors.initials: JA
authors.lastname: Lin
authors.forename: Hsi-Hsien
authors.initials: HH
authors.lastname: Hsu
authors.forename: Chung-Sheng
authors.initials: CS
authors.lastname: Lin
authors.forename: Chung-Jung
authors.initials: CJ
authors.lastname: Liu
authors.forename: Wei-Wen
authors.initials: WW
authors.lastname: Kuo
authors.forename: Li-Mien
authors.initials: LM
authors.lastname: Chen
mesh_terms: D000368:Aged; D000975:Antioxidants / Q000378:metabolism; D015415:Biomarkers; D002097:C-Reactive Protein / Q000378:metabolism; D005260:Female; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000473:pathology; D018836:Inflammation Mediators / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000032:analysis*; D015850:Interleukin-6 / Q000378:metabolism; D007501:Iron / Q000097:blood*; D050356:Lipid Metabolism; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood* / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D002097:C-Reactive Protein; D007501:Iron