Genetic polymorphism of glutatfflone-s- transferase and susceptibility to and severity of chronic obstructive pulmonary disease

Chronic tobacco smoking is a major risk factor in the development of COPD. However, it is estimated that only 10-20% of chronic heavy smokers will develop symptomatic COPD. This indicates the possible contribution of environmental or genetic cofactors to the development of COPD in smokers. The present work aimed to study the relationship between GST polymorphism and susceptibility to and severity of COPD in smokers. A case control study was done on 140 patients with COPD and 140 matched controls. All subjects were smokers or exsmokers. The GSTM1 and GSTT1 genotypes were identified by polymerase chain reaction in peripheral blood DNA samples. Analysis of data was done by IBM computer using SPSS program. Results shown that the proportion of GSTMl-null genotypes was significantly higher in patients with COPD than in control subjects [62.2% versus 32.2%]. The odds ratio was 3.5 [95% confidence interval [CI] = 2.1-5.7]. Moreover the patients with GSTM1 null genotype were at high risk of developing the severe type of COPD. The odds ratio was 3.2 and [95% CI = 1.5-6.7]. However the genotype frequencies of GSTTl-null genotype did not show significant difference between groups. Our data provide evidence that smokers with null genotype of GSTM1 were more susceptible to develop the severe type of COPD

lipoprotein lipase hind III polymorphism and the susceptibility to hypertension

Lipoprotein lipase [LPL] enzyme plays a central role in lipid metabolism. The primary function of LPL enzyme is the hydrolysis of the core triglycerides of circulating chylomicron and very low density lipoprotein [VLDL]. It releases monoglycerides and free fatty acids, which are taken up by skeletal muscle or adipose tissue. The present work aimed to study the association of the common variant of LPL HindlII [H+] and hypertension. Hindlll [+] variant allele of LPL were determined by polymerase chain reaction restriction fragment length polymorphism [PCR-RFLP] assay in 150 hypertensive patients and 150 normotensive as a control group. Serum lipoproteins were also observed in both groups. Allele frequencies were H+ = 0.733 and H- = 0.267 for LPL Hindlll in the hypertension group compared to H+ = 0.683 and H- = 0.317 in the control group. Individuals with homozygous [H+/+] genotype were at higher risk of developing hypertension compared to the [H-/-] genotype [Odds Ratio OR = 2.13, 95% Confidence Interval CI = 0.937-4.8]. Serum TG level were also higher in the individuals with [H+/+] genotype compared to the [H-/-] genotype, while HDL showed negative correlation with the presence of [H+/+] genotype. It can be concluded that the LPL Hindlll [H+] variant of LPL may influence the blood lipid metabolism and increase risk for hypertension