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1
Department of Clinical and Experimental Medicine,
2
Department of Mother and Child, Biology and Genetics, and
3
the Institute of Clinical Chemistry, University of Verona, 37134 Verona, Italy.
aAddress correspondence to this author at: Department of Clinical and Experimental Medicine, Policlinico G.B. Rossi, 37134 Verona, Italy. Fax 39-45-580111; e-mail domenico.girelli{at}univr.it.
Background: Iron may promote coronary atherosclerotic disease (CAD) by increasing lipid peroxidation. Studies on biochemical or genetic markers of body iron stores as risk factors for CAD have yielded conflicting results.
Methods: We studied 849 individuals with a clear-cut definition of the CAD phenotype, i.e., with (CAD; n = 546) or without (CAD-free; n = 303) angiographically documented disease. We determined serum ferritin, as a biochemical estimate of iron stores, and the C282Y mutation in the HFE gene, i.e., the main cause of hemochromatosis in Caucasians. The relationships of ferritin with serum markers of either inflammation [C-reactive protein (CRP)] or lipid peroxidation (malondialdehyde) were also investigated.
Results: Mean ferritin concentrations were slightly higher in CAD vs CAD-free individuals, but this difference disappeared after adjusting for sex and CRP. Ferritin was significantly correlated with CRP (Spearman’s test, 
= 0.129; P <0.001). Heterozygotes for Cys282Tyr were 4.8% among the CAD group and 6.6% among the CAD-free group (P = 0.26). The prevalence of high concentrations of stored iron, defined as ferritin concentrations above the sex-specific upper quintiles of the control distribution, was also similar in the two groups. There was a higher prevalence of "iron depletion" in CAD-free vs CAD females (20% vs 8.8%, respectively), but this difference disappeared after adjustment for age and other cardiovascular risk factors (odds ratio, 0.66; 95% confidence interval, 0.21–2.08). No differences in iron markers were found in CAD patients with or without myocardial infarction.
Conclusions: Our results do not support a role for biochemical or genetic markers of iron stores as predictors of the risk of CAD or its thrombotic complications.
The following articles in journals at HighWire Press have cited this article:
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  L. Qi, R. M. van Dam, K. Rexrode, and F. B. Hu Heme Iron From Diet as a Risk Factor for Coronary Heart Disease in Women With Type 2 Diabetes Diabetes Care, January 1, 2007; 30(1): 101 - 106. [Abstract] [Full Text] [PDF]
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C. Bozzini, D. Girelli, O. Olivieri, N. Martinelli, A. Bassi, G. De Matteis, I. Tenuti, V. Lotto, S. Friso, F. Pizzolo, et al. Prevalence of Body Iron Excess in the Metabolic Syndrome Diabetes Care, August 1, 2005; 28(8): 2061 - 2063. [Full Text] [PDF]
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 J. R Hunt and H. Zeng Iron absorption by heterozygous carriers of the HFE C282Y mutation associated with hemochromatosis Am. J. Clinical Nutrition, October 1, 2004; 80(4): 924 - 931. [Abstract] [Full Text] [PDF]
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 I R Gunn, F K Maxwell, D Gaffney, A D McMahon, and C J Packard Haemochromatosis gene mutations and risk of coronary heart disease: a west of Scotland coronary prevention study (WOSCOPS) substudy Heart, March 1, 2004; 90(3): 304 - 306. [Abstract] [Full Text] [PDF]
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 E. Beutler, A. V. Hoffbrand, and J. D. Cook Iron Deficiency and Overload Hematology, January 1, 2003; 2003(1): 40 - 61. [Abstract] [Full Text] [PDF]
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 J. Ma and M. J. Stampfer Body Iron Stores and Coronary Heart Disease Clin. Chem., April 1, 2002; 48(4): 601 - 603. [Full Text] [PDF]
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