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標題: Pro-inflammatory states and IGF-I level in ischemic heart disease with low or high serum iron
作者: Lee, S.D.
Huang, C.Y.
Shu, W.T.
Chen, T.H.
Lin, J.A.
Hsu, H.H.
Lin, C.S.
Liu, C.J.
Kuo, W.W.
Chen, L.M.
關鍵字: coronary artery disease;serum iron;pro-inflammatory;cardiac markers;necrosis-factor-alpha;c-reactive protein;growth-factor-i;myocardial-infarction;risk;atherosclerosis;antioxidants;association;cholesterol
Project: Clinica Chimica Acta
期刊/報告no:: Clinica Chimica Acta, Volume 370, Issue 1-2, Page(s) 50-56.
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. Conclusion: 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. (c) 2006 Elsevier B.V. All rights reserved.
ISSN: 0009-8981
DOI: 10.1016/j.cca.2006.01.012
Appears in Collections:獸醫病理生物學所

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