Griffiths J D, Campbell L J, Woodruff I W, Cruickshank D, Matthews J P, Hunt D, Campbell D G, Cowling D C
Am J Clin Pathol. 1985 Nov;84(5):649-54. doi: 10.1093/ajcp/84.5.649.
Fifty six patients admitted consecutively to the coronary care unit with ischemic chest pain participated in a controlled prospective study of acute changes in iron metabolism. Following myocardial infarction there were significant reductions of plasma iron by 8.1 mumol/L (P = 0.002), total iron binding capacity by 12.9 mumol/L (P = 0.003), and plasma transferrin by 0.70 g/L (P = 0.007). In contrast, there was a significant elevation of serum ferritin by 218 micrograms/L (P = 0.0005). The magnitude and duration of these acute changes in iron metabolism was greater in patients with higher peak serum creating kinase levels, suggesting that these changes are influenced by the extent of tissue necrosis. Comparison with the control group showed that alteration in dietary iron intake was not a significant factor. The possible mechanisms of these acute changes and their similarity to those observed in the anemia of chronic disease are discussed.
56例因缺血性胸痛连续入住冠心病监护病房的患者参与了一项关于铁代谢急性变化的对照前瞻性研究。心肌梗死后，血浆铁显著降低8.1 μmol/L（P = 0.002），总铁结合力降低12.9 μmol/L（P = 0.003），血浆转铁蛋白降低0.70 g/L（P = 0.007）。相比之下，血清铁蛋白显著升高218 μg/L（P = 0.0005）。血清肌酸激酶峰值较高的患者，这些铁代谢急性变化的幅度和持续时间更大，提示这些变化受组织坏死程度的影响。与对照组比较表明，饮食中铁摄入量的改变并非重要因素。本文讨论了这些急性变化的可能机制及其与慢性病贫血中所见变化的相似性。
