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Biochemical and Genetic Markers of Iron Status and the Risk of Coronary Artery Disease: An Angiography-based Study

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. We studied 849 individuals with a clear-cut definition of the CAD phenotype, i.e., with (C...

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Published in:Clinical chemistry (Baltimore, Md.) Md.), 2002-04, Vol.48 (4), p.622-628
Main Authors: Bozzini, Claudia, Girelli, Domenico, Tinazzi, Elisa, Olivieri, Oliviero, Stranieri, Chiara, Bassi, Antonella, Trabetti, Elisabetta, Faccini, Giovanni, Pignatti, Pier Franco, Corrocher, Roberto
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Language:English
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Summary: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. 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. 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, rho = 0.129; P
ISSN:0009-9147
1530-8561
DOI:10.1093/clinchem/48.4.622