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Risk and Severity of COPD Is Associated With the Group-Specific Component of Serum Globulin 1F Allele: dFEV1

Follow-up pulmonary function data for calculating dFEV1 was available in 86 of the 103 patients with COPD, and 21 of the 88 smoker control subjects, There was no significant difference in age, smoking history, the baseline FEV1 percentage predicted, and the distributions of Gc-globulin allele between subjects with 1-year follow-up data and those without them in either patients with COPD or control subjects. The dFEV1 of patients with COPD (48.3 ± 62.7 mL) was significantly larger than that of control subjects (17.9 ± 32.5 mL, p < 0.0001). There were 17 RDs (20%) in the group of patients with COPD, whereas there were no RDs in the smoker control group (p = 0.03). There was no significant difference in dFEV1 between Gc*1F homozygotic patients and patients with other genotypes (54.9 ± 66.4 mLvs 45.5 ± 60.7 mL, p = 0.54); likewise, there was no significant difference in the frequency of RDs between the two groups (23% vs 20%, p = 0.78). In comparison of dFEV1 between patients with COPD and Gc*1F alleles [Gc*1F( + )] and patients with COPD without Gc*1F alleles [Gc*1F( —)], there were no significant differences in age, smoking history, and the baseline FEVX percentage predicted. However, the former group showed significantly larger dFEV1 than the latter group (53.8 ± 64.8 mL vs 20.2 ± 39.9 mL, p = 0.01). All of the 17 RDs were Gc*1F( + ) patients with COPD, and no RD was seen in Gc*1F( —) patients (p = 0.04). fully

HRCT Parameters
Chest HRCT examination was performed in 85 patients with COPD. The relationship between genotypes and the value of each HRCT parameter is shown in Figures 2-4. There was no significant difference between Gc*1F homozygotes and Gc*1F heterozygotes (1F-1S and 1F-2) in any HRCT parameters (data not shown). Therefore, we compared the HRCT parameters between Gc*1F( + ) patients and Gc*1F(— ) patients. The number of subjects in each group was 72 and 13, respectively. Although the difference in the mean LAA% between the two patient groups did not reach significance (51.5 ± 13.3% vs 45.5 ± 10.5%, p = 0.07), severely emphysematous patients with LAA% > 60% showed a significant association with Gc*1F( + ) genotype (22 of 72 Gc*IF( + ) vs 1 of 13 Gc*1F( —), p = 0.01; Fig 2). There was a significant difference in the mean CT score between the two patient groups (— 929.6 ± 23.1 HU vs — 918.0 ± 16.2 HU, p = 0.027; Fig 3).
Fig2
Figure 2. LAA% obtained with HRCT in GC*1F(+) and GC*1F( —) patients with COPD. Each point represents one patient. Horizontal bars indicate mean values. Gc*1F( +) patients showed a tendency to have higher LAA% compared to Gc* 1F( —) patients (p = 0.07). The former group showed a larger frequency of patients with LAA% > 60% than the latter group (p = 0.01)
Fig3
Figure 3. Mean CT obtained with HRCT in Gc*1F( + ) and Gc*1F( —) patients with COPD. Each point represents one patient. Horizontal bars indicate mean values. Gc*1F( +) patients showed lower mean CT than Gc*1F( —) patients (p = 0.027). Gc*1F( + ) patients with mean CT < — 940 had a significantly higher frequency of occurrence than Gc*1F( —) patients (p < 0.0001). Fig4
Figure 4. CLAs obtained with HRCT in Gc*1F( + ) and Gc*1F( —) patients with COPD. Each point represents one patient. Horizontal bars indicate mean values. COPD Gc*1F( + ) patients showed larger CLAs than Gc*1F( —) patients (p = 0.004).