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Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: Polymorphism

The distributions of genotypic frequencies were significantly different for the mild-to-moderate group and the severe group. In particular, the frequency of the T allele was 7.4% in the mild-to-moderate group and 20.4% in the severe group, and the association between severe asthma and the T allele was significant (p = 0.037; Table 3). The positive predictive value of a positive T allele for severe asthma was 55.0% and the negative predictive value was 72.4%. The relationship between bronchial hyperresponsiveness (PC20) and the CTLA-4 promoter (—318 C/T) polymorphism was also studied. PC20 was measured in 45 of the 88 asthma patients, divided into a CC genotype (wild type) group and a CT genotype +TT genotype (mutant-type) group. However, PC20 did not differ between the two groups (p = 0.758; Table 4).
CTLA-4 Exon 1 (+49 A/G) Polymorphism
No deviation from the Hardy-Weinberg equilibrium was observed in any group examined (asthma group, x2 = 3.938 and p = 0.140; control group, X2 = 0.585 and p = 0.746). The distribution of genotype frequencies was not different for the asthma group and the control group (p = 0.275; Table 5), nor for the atopic asthma group, the nonatopic asthma group, and the control group (p = 0.563; Table 6). Allergy medications allergy medications In addition, the mild-to-moderate asthma group and the severe asthma group did not differ in the distribution of genotype frequencies (p = 0.166; Table 7). However, the association between bronchial hyperresponsiveness (PC20) and the CTLA-4 exon 1 (+49 A/G) polymorphism was significant (p = 0.019; Table 8). PC20 was measured in 45 of the 88 asthma patients, classified into a GG genotype (wild-type) group and an AG genotype + AA genotype (mutant-type) group. The geometric mean (± SD) PC20 in the wild-type group was 2.19 ± 2.12 mg/mL, and in the mutant-type group was 4.51 ± 3.19 mg/mL. From these results, asthmatic patients with the GG genotype had more hyperre-sponsive airways than did those with the AG or AA genotypes.
Table 4 ——Relationship Between CTLA-4 Promoter (—318 C/T) Polymorphism and PC20

Groups Genotypes CC CT TT
Atopic asthma patients (n = 52) 38 (73.1) 13 (25.0) 1 (1.9)
Nonatopic asthma patients (n = 36) 32 (88.9) 3 (8.3) 1 (2.8)
Healthy control subjects (n = 86) 67 (77.9) 15 (7.4) 4(4.7)

Table 5—CTLA-4 Exon 1 (+49 A/G) Polymorphism in Asthmatic Patients and Healthy Control Subjects

Genotypes No. PC20mg/mL
CC 37 3.02 ± 2.75
CT + TT 8 2.68 ± 2.81

Table 6 —CTLA-4 Exon 1 (+49 A/G) Polymorphism According to Atopy

Groups Genotypes GG AG AA
Asthma patients (n = 88) 49 (55.7) 24 (27.3) 15 (17.0)
Healthy control subjects (n = 86) 49 (57.0) 29 (33.7) 8 (9.3)

Table 6 —Relationship Between CTLA-4 Exon 1 (+49 A/G) Polymorphism and PC20

Groups Genotypes GG AG AA
Atopic asthma patients (n = 52) 28 (53.8) 14 (26.9) 10(19.2)
Nonatopic asthma patients (n = 36) 21 (58.3) 10 (27.7) 5 (13.9)
Healthy control subjects (n = 86) 49 (57.0) 29 (33.7) 8 (9.3)

Table 8 —Relationship Between CTLA-4 Exon 1 (+49 A/G) Polymorphism and PC20

Genotypes No. PC20> mg/mL*
GG 30 2.19 ± 2.12
AG + AA 15 4.51 ± 3.19

Table 7 —Relationship Between CTLA-4 Exon 1 (+49 A/G) Polymorphism and PC20

Genotypes
Asthma Severity GG AG AA G Allele A Allele
Mild to moderate (n = 61) 37 (60.7) 13(21.3) 11 (18.0) 87(71.3) 35 (28.7)
Severe (n = 27) 12 (44.4) 11 (40.7) 4(14.8) 35 (64.8) 19 (35.2)