doi: 10.1161/01.hcg.0000342161.52290.1d
Correction |
Correction
The article "Mutations in the HFE Gene and Cardiovascular Disease Risk: An Individual Patient Data Meta-Analysis of 53 880 Subjects" by van der A et al, which appeared in the October 2008 issue (Circ Cardiovasc Genet. 2008:1:43–50), contained an error in the Clinical Perspective. The corrected Clinical Perspective is below. It has also been corrected in the online version of the article.CLINICAL PERSPECTIVE
In the early 1980s, Sullivan proposed that an increase in body iron levels and subsequent oxidative stress may play a role in the occurrence of cardiovascular disease. Until 1996, blood markers of iron status and dietary iron intake were mostly studied as indicators of iron exposure, but from that year on, new opportunities were opened due to the discovery of the hemochromatosis-related gene HFE. The 2 most important mutations in the HFE gene, 282C3Y and 63H3D, have been associated with varying degrees of iron overload. However, their role as risk factors for cardiovascular disease remains subject to debate. In this individual patient data meta-analysis based on >10 000 documented cases of coronary heart disease (of which almost 6000 were acute myocardial infarction) from 11 observational studies, we found no evidence for a material role of HFE genotypes in cardiovascular disease risk. However, the power of our study does not exclude weak genetic effects on coronary heart disease (odds ratio, 1.23) or acute myocardial infarction (odds ratio, 1.30) by the C282Y/H63D genotype.
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