BACKGROUND: Chronic obstructive pulmonary disease (COPD) represents a major public health care problem worldwide due to its increasing prevalence, morbidity and mortality. Chronic obstructive pulmonary disease is known to be the fourth leading cause of death and the only cause of death, which is increasing. It is generally accepted that cigarette smoking is the most important risk factor for COPD. Nevertheless, only 10% to 20% of chronic smokers develop the severe impairment of pulmonary functions associated with COPD. This indicates the presence of genetic predisposing factors in its pathogenesis. OBJECTIVE: To test the hypothesis that genetic polymorphism of glutathione S-transferase theta 1 (GSTT1)and/or glutathione S-transferase mu 1 (GSTM1) is associated with COPD in smokers. MATERIALS AND METHODS: A case-control study was done on 34 patients with COPD and 34 matched controls. DNA was extracted from white blood cells by salting out method. GSTT1 and GSTM1 genotypes were amplified by polymerase chain reaction. The fragments were then analyzed by agarose gel electrophoresis. Statistical analysis was done using SPSS program. RESULTS: The frequency of carriers of null GSTT1 genotype was 50% among cases compared to 44.1% in the control group. Carriers of null GSTT1 were at minor risk of developing COPD when compared with carriers of the wild GSTT1 genotype (OR, 1.3; 95% CI, 0.5-3.3). In case of GSTM1, the frequency of carriers of null GSTM1 genotype was 52.9% among cases compared to 26.5% in controls. Carriers of null GSTM1 were at much higher risk of developing COPD (OR, 3.13; 95% CI, 1.1-8.6). Furthermore, the risk of developing COPD was increased among carrier of null GSTT1 & GSTM1 haplotype (OR, 3.6; 95% CI, 1.1-11.6). CONCLUSION: Carriers of null GSTM1 genotype were at high risk of developing COPD especially when they were null GSTT1 and GSTM1 haplotype.
BACKGROUND:Chronic obstructive pulmonary disease (COPD) represents a major public health care problem worldwide due to its increasing prevalence, morbidity and mortality. Chronic obstructive pulmonary disease is known to be the fourth leading cause of death and the only cause of death, which is increasing. It is generally accepted that cigarette smoking is the most important risk factor for COPD. Nevertheless, only 10% to 20% of chronic smokers develop the severe impairment of pulmonary functions associated with COPD. This indicates the presence of genetic predisposing factors in its pathogenesis. OBJECTIVE: To test the hypothesis that genetic polymorphism of glutathione S-transferase theta 1 (GSTT1)and/or glutathione S-transferase mu 1 (GSTM1) is associated with COPD in smokers. MATERIALS AND METHODS: A case-control study was done on 34 patients with COPD and 34 matched controls. DNA was extracted from white blood cells by salting out method. GSTT1 and GSTM1 genotypes were amplified by polymerase chain reaction. The fragments were then analyzed by agarose gel electrophoresis. Statistical analysis was done using SPSS program. RESULTS: The frequency of carriers of null GSTT1 genotype was 50% among cases compared to 44.1% in the control group. Carriers of null GSTT1 were at minor risk of developing COPD when compared with carriers of the wild GSTT1 genotype (OR, 1.3; 95% CI, 0.5-3.3). In case of GSTM1, the frequency of carriers of null GSTM1 genotype was 52.9% among cases compared to 26.5% in controls. Carriers of null GSTM1 were at much higher risk of developing COPD (OR, 3.13; 95% CI, 1.1-8.6). Furthermore, the risk of developing COPD was increased among carrier of null GSTT1 & GSTM1 haplotype (OR, 3.6; 95% CI, 1.1-11.6). CONCLUSION: Carriers of null GSTM1 genotype were at high risk of developing COPD especially when they were null GSTT1 and GSTM1 haplotype.