Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • Table shows the distribution of all studied groups regarding

    2021-11-22

    Table 3 shows the distribution of all studied groups regarding mutation of GSTP1 gene polymorphism in each group. From 15 COPD smoker patients in group (A), 12 (80%) had heterozygous mutation, from 15 COPD non-smoker patients in group (B), 5 (33.3%) had heterozygous mutation, from 10 control subjects in group (C), 7 (70%) had heterozygous mutation, while 1 (10%) from 10 control subjects in group (D), a significant difference between groups A and B regarding type of mutation (P-value>0.05), highly significant difference between groups A and D (P-value<0.01) and a significant difference between groups C and D (P-value>0.05). Table 4 shows the distribution of all studied subjects regarding their smoking status compared with mutation. Twenty-five subjects have heterozygous mutation, eleven of them were smoking, eight were ex-smokers while six were non smokers. Twenty-five subjects have normal genotyping (non mutant), three of them were smoking, three were ex-smokers while nineteen were non smokers. There was a significant difference between subjects having heterozygous mutation and subjects without mutation as regards smoking status (P-value>0.05), highly significant difference between them as regards non smoking status (P-value>0.01) and non significant difference as regards ex-smoking status. Table 5 shows the distribution of all studied groups regarding their spirometry results compared with mutation. There was no significant difference between subjects having heterozygous mutation and subjects without mutation as regards spirometry results (P-value<0.05) (see Fig. 1).
    Discussion COPD is a multifactorial disease with possible genetic predisposition and involvement of various environmental factors. Among the MS023 that contribute to xenobiotic metabolism and susceptibility to COPD, GSTP1 gene is one of the most studied in diverse human populations [2]. GSTP1 was found to be mainly present in the respiratory tract and was proposed to be involved in the development of COPD [6]. Smoking alters several genes that can be associated with health problems for smokers, such as increased risk of COPD [8]. Only a relatively small proportion of smokers actually develop airway obstruction. Genetic factors are related to this susceptibility and include genes regulating the protease–antiprotease and oxidant–antioxidant interactions [9]. Oxidant stress and reactive oxygen species, resulting from an oxidant/antioxidant imbalance, are believed to play an important role in the pathogenesis of COPD. Indeed, it is well known that chronic tobacco smoking is a major risk factor for the development of COPD, and a defect in the detoxification of reactive species produced by cigarette smoke may predispose smokers to airflow obstruction and emphysema [2]. A combination of oxidative attack and changes in antiprotease activity could amplify the lung tissue damage in COPD. This underlines that the interactions between genes as well as environmental factors may play an important role in the development of this pathogenesis [2] . Lakhdar et al. [2] made a study concerning the relationship between GSTP1 polymorphism and COPD in a Tunisian population and concluded that subjects with GSTP1 Val105 allele are at higher risk of COPD. In the current study, the age of the studied patients ranged from 43 to 75years old with mean age and standard deviation of 62.40±9.32 in group A, 59.66±6.33 in group B, 38.30±5.86 in group C and 40.40±7.73 in group D. Moreover, the number of male subjects was higher than females (Table1). This result comes in agreement with Lakhdar et al. [2] who explained this result by the fact that the major population of COPD patients and chronic smokers are males in Egypt. Therefore, it is difficult to find a balanced set of female subjects for genotype studies. Secondly, there was a difference in mean age between cases and controls. In fact, younger controls were more likely to provide a blood sample than older controls, and were thereby over sampled.