2001
DOI: 10.1136/jcp.54.4.332
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Influence of smoking and alcohol on gastric chemokine mRNA expression in patients with Helicobacter pylori infection

Abstract: Aim-Chemokines that play a primary role in active inflammation are increased in gastric mucosa infected with Helicobacter pylori. Cigarette smoking increases the risk of peptic ulcer disease and gastric cancer, whereas alcohol might exert an antibacterial role. The aim of this study was to examine the association between smoking or alcohol consumption and mucosal chemokine mRNA expression in H pylori associated gastritis. Methods-Gastric biopsy specimens were obtained from 46 patients with dyspepsia who were i… Show more

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Cited by 36 publications
(29 citation statements)
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“…Smoking and alcohol drinking are risk factors for gastric and duodenal ulcers as they promote the movement of bile salts from the intestine to the stomach, and increase the amount of acid produced by the stomach [26,27]. Smoking may also increase the risk of infection with H. pylori [28], which is a strong risk factor for peptic ulcers (gastric or duodenal ulcers) [26]; and has been linked to biliary tract cancers [1]. Thus, it appears biologically plausible that the combined effects of increased acid production from smoking and alcohol drinking, together with the chronic inflammation from ulcer, and possibly H. pylori infection, could increase the risk of gallbladder cancer.…”
Section: Discussionmentioning
confidence: 99%
“…Smoking and alcohol drinking are risk factors for gastric and duodenal ulcers as they promote the movement of bile salts from the intestine to the stomach, and increase the amount of acid produced by the stomach [26,27]. Smoking may also increase the risk of infection with H. pylori [28], which is a strong risk factor for peptic ulcers (gastric or duodenal ulcers) [26]; and has been linked to biliary tract cancers [1]. Thus, it appears biologically plausible that the combined effects of increased acid production from smoking and alcohol drinking, together with the chronic inflammation from ulcer, and possibly H. pylori infection, could increase the risk of gallbladder cancer.…”
Section: Discussionmentioning
confidence: 99%
“…Additionally, IL-8 and GRO-α have been demonstrated to be higher in patients (suffering from gastritis) with duodenal or peptic ulcers than in patients without these complications [50,[56][57][58][59]. Furthermore, expression of GRO-α and ENA-78 was significantly increased in H. pylori-infected mucosa of smokers compared with non-smokers [60]. However, there was no difference in GRO-α and ENA-78 expression in relation to alcohol consumption [60].…”
Section: Gastric Cancermentioning
confidence: 90%
“…Furthermore, expression of GRO-α and ENA-78 was significantly increased in H. pylori-infected mucosa of smokers compared with non-smokers [60]. However, there was no difference in GRO-α and ENA-78 expression in relation to alcohol consumption [60]. Indeed, recent studies suggest that alcohol consumption has a protective effect in patients infected with H. pylori because of its antimicrobial effect [60].…”
Section: Gastric Cancermentioning
confidence: 93%
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“…The higher risk of CAG/GC could be caused by swallowed constituents [95], inhaled toxins and other factors: increased bile reflux [143,144], increased proinflammatory chemokines [145] and impaired mucosal defense (including low vitamin C [94]) in smokers. In a study from northeastern Japan, 44% of male participants of a health check program smoked versus 2% females [113], or 45 versus 3% in Venezuela [108].…”
Section: Pathogenic Factors Of Gastritis Beyond ‘Abc'mentioning
confidence: 99%