They concluded that the reason was due to the insufficient number of subjects needed to verify the hypothesis that Gc*1F homozygotes had an increased risk. These studies were based on white populations in which the frequencies of the three alleles were 0.16, 0.56, and 0.28 for Gc*1F, Gc*1S and Gc*2, respectively. It has been noted that the frequency of the Gc allele varies with ethnicity; in the Japanese population, it has been reported to be 0.49, 0.24, and 0.25 for Gc*1F, Gc*1S, and Gc*2, respectively. This distribution has a larger frequency of Gc*1F compared to that in whites. Our results and those of Ishii et al corroborate that Gc*1F homozygotes have an increased risk for COPD, at least in the Japanese population.
There are a few studies- on the relationship between genetic factors and decline of lung function. As regards Gc-globulin genotypes among smokers, there was no difference reported between the fast decliners and nondecliners. Contrary to this finding, we have shown that patients with Gc*1F allele had notably larger dFEV1 than those without it, on the basis of equal baseline FEV1 percentage predicted between the two groups. The reason for this disparity in the results is not clear; however, there seem to be several differences in the study parameters. First, we applied a different definition of rapid decline, that is, dFEV1 > 90 mL as described pre-viously, whereas the other study defined a dFEV1 > 3.0% predicted. Second, we investigated patients who already had COPD; this population would be expected to have a larger dFEV1 than smoker control subjects regardless of Gc-globulin genotypes.
In this study, the dFEV1 of the patients with COPD and Gc*1F allele was larger than that of the subjects without this allele, though the two groups showed no differences in the mean age, smoking history, and the baseline FEV1 percentage predicted. We interpret this to mean that the Gc*1F allele had some role in the deterioration of dFEV1 in patients with COPD. The reason why subjects with Gc*1F allele did not acquire the disease at a younger age compared with those without the allele may be related to other factors possibly involved in the development of COPD.