No relationship between HFE mutations and CAD (C282Y, P = 0.402; H63D, P = 0.112; S65C, P = 0.170) or CVD death (C282Y, P = 0.560; H63D, P = 0.682; S65C, P = 0.664) was demonstrated using logistic regression.
After full adjustment, the odds ratio for coronary heart disease was 1.12 (95% CI, 0.92 to 1.37) for subjects with the compound heterozygous (C282Y/H63D) genotype relative to those with the wild-type/wild-type genotype.
A weighted Cox proportional hazards model was used to estimate crude, age-adjusted and multivariate adjusted hazard ratios for C282Y and H63D carriership in relation to coronary heart disease.
The C282Y and H63D gene mutations were tested in 338 Caucasians with type 2 diabetes: 156 cases with CAD</span> an</span>d 182 subjects with no history of CAD.
We examined the relation between two HFE mutations (C282Y and H63D), indicators of iron homeostasis, and the prevalence of coronary heart disease in a large population of white adults.