الفهرس 
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Abstract
The present study was a prospective case- control study conducted on 146 COPD patients, admitted to Chest Department Menoufiya University Hospital and Al-Mahalla Al-Kobra Chest Hospital in the period between December 2012 till October 2013. 130 apparently healthy subjects were included as a control group.
The aim of this study was to determine the frequency of incidence of gene polymorphisms in exon3 and exon4 of microsomal epoxide hydrolase (mEPHX1) and in GSTM1 and GSTT1 of glutathione S-transferase (GST) genes in COPD patients.
Results of this study revealed that:
1-There was an increased frequency of GSTM1 null genotypes between COPD patients than controls (72.6% versus 43.8% , p˂0.001 , OR 3.39, 95%CI=2.05-5.61) which didn’t remain significant after adjustment for age and smoking status.
2-Carriers of both null-GSTT1 and null-GSTM1 genes were at higher risk of COPD after adjustment for age and smoking status (OR 3.45, 95%CI =1.07-11.14).
3-139 His/Arg exon4 genotypes were lower in the COPD patients than controls, as a protective gene (OR 0.53, 95%CI=0.31-0.90, P=0.0017) which didn’t remain significant after adjustment for age and smoking in co-dominant model.
4-139Arg/Arg exon4 genotypes were significantly higher in COPD patients than controls (OR 4.68, 95%CI=1.02-21.53, P=0.0017) which didn’t remain after adjustment for age and smoking status in co-dominant model.
5-In the recessive model, there was increased frequency of 139Arg/Arg exon4 genotypes in COPD patients than controls with increase risk of COPD in both crude and adjusted models (crude OR 5.73, 95% CI=1.26-26.10, P=0.01) and (adjusted OR 11.10, 95% CI=1.03-119.21).
6-His allele of exon3 genotype was higher in COPD patients than controls with increase risk of COPD (OR 1.63, 95%CI=1.02-2.6, P=0.04).
7-In combination of exon3 and exon4 genotypes :
- Carriers of both113 Tyr/His exon3 and 139His/His exon4 genotypes were more frequent among COPD patients than controls in both crude and adjusted models (crude OR 2.97, 95% CI=1.3-6.78, P=0.008) and (adjusted OR 11.21, 95% CI=1.01-124.3, P=0.008).
Carriers of both113 Tyr/Tyr exon3 and 139His/Arg exon4 were higher in controls than COPD patients as protective genotypes (OR 0.52, 95%CI=0.27-0.98, P=0.04) but it didn’t remain significant after adjustment for age and smoking status.
Carriers of both113 Tyr/His exon3 and139 His/Arg exon4 genotypes had high risk in COPD patients than controls after adjustment for age and smoking status (OR 25.33, 95%CI=2.04-314.8).
Carriers of both113 His/His exon3 and 139 His/Arg exon4 genotypes had high risk in COPD patients than controls after adjustment for age and smoking status (OR 16.69, 95%CI=1.11-250.3).
Carriers of both113 Tyr/Tyr exon3 and139 Arg/Arg exon4 genotypes had higher risk of COPD in patients than controls (OR
11.47, 95%CI=1.45-90.74, P=0.004) but it didn’t remain significant after adjustment.
8-In combination of GSTM1-null and exon3 genotypes, it was found that carriers of both GSTM1-null and 113Tyr/Tyr exon3 genotypes and carriers of both GSTM1-null and 113Tyr/His exon3 genotypes were at higher risk of COPD development (OR 3.33, 95% CI=1.32-8.35, and OR 14.24, 95% CI=3.02-67.17 respectively ).
9-In combination of both GSTM1-null and exon4 genotypes, it was found that carriers of both GSTM1-null and 139 His/His exon4 genotypes and carriers of both GSTM1-null and 139 Arg/Arg exon4 genotypes were at higher risk of COPD (OR 5.58, 95% CI=2.14-14.52, and OR 23.17, 95% CI=1.74-308.46 respectively)