Chronic alcoholic gastritis. Roles of alcohol and Helicobacter pylori

Uppal, Rajiv; Lateef, Syed K.; Korsten, Mark A.; Paronetto, Fiorenzo; Lieber, Charles S.

doi:10.1001/archinte.151.4.760

Cited by 25 publications

(17 citation statements)

References 25 publications

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“…However, current evidence does not convincingly support the conclusion that alcoholic beverages directly cause erosive lesions [29]. Many studies examining the effect of alcohol on gastric mucosa antedated the awareness of H. pylori [5].…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori and Gastric Erosions

et al. 2000

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Background/Aims: Helicobacter pylori is considered to be the primary cause of most forms of gastritis, but its role as a causative agent in gastric erosions is unclear. The aim of this study was to estimate the prevalence of gastric erosions and H. pylori infection in asymptomatic volunteers. Methods: 175 asymptomatic subjects underwent upper gastrointestinal endoscopy. Antral biopsies were taken for bacterial cultures, histology and quick urease (CLO) test. A ¹³C-urea breath test was performed after endoscopy. NSAID intake, alcohol consumption and smoking habits were also recorded in each subject. Results: 33 (19%) of 175 asymptomatic volunteers had macroscopic lesions on upper gastrointestinal endoscopy, 7 were H. pylori positive, 26 were H. pylori negative. Gastric erosions occurred in 8% (14 subjects) of all volunteers. 10 subjects were H. pylori negative and 4 H. pylori positive. In 11 volunteers, gastric erosions were restricted to the prepyloric antrum. Only 1 of 14 subjects had a history of NSAID intake and 6 subjects were alcohol abstainers. Conclusion: We conclude that gastric erosions occur in a considerable amount of asymptomatic volunteers. They are predominantly localized in the prepyloric antrum and are most likely not associated with H. pylori infection, NSAID intake, smoking or alcohol consumption.

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori and Gastric Erosions

et al. 2000

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“…Chronic infection with Helicobacter pylori and not alcohol itself seems to be the major causative agent of chronic gastritis in alcoholic patients [78,79] .…”

Section: Chronic Gastritismentioning

confidence: 99%

Alcohol-Related Diseases of the Esophagus and Stomach

Franke

Teyssen²,

Singer³

2005

Dig Dis

179

104

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The present review summarizes the clinically relevant effects of acute and chronic alcohol consumption on motility, mucosal inflammation and cancer of the esophagus and the stomach. Alcohol consumption results in a significant increase in the morbidity of these two organs, the most important probably being the significant increase in the development of esophageal cancer. This review refers to epidemiologic and systematic experimental data to elucidate the clinical impact of alcohol consumption as well as the underlying alcohol-induced pathophysiologic mechanisms for these esophageal and gastric diseases. Much research is still needed to clarify the effects of alcohol itself and the byproducts that result during the production of the different types of alcoholic beverages on dismotility and mucosal injury to the esophagus and stomach.

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“…the mucosal injury found in the majority of alcoholics [6][7][8]. In some studies an increased incidence of chronic gastritis in alcoholics has been dem onstrated [6,9] whereas other studies [8,10] did not reveal any evidence of alcohol play ing a role in the etiology of chronic gastritis. Furthermore, no association between alcohol consumption and the prevalence of peptic ulceration has been found [11,12].…”

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confidence: 99%

Effect of Alcohol Consumption on the Risk of Helicobacter pylori Infection

Höök‐Nikanne

1991

Digestion

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To investigate the effect of alcohol consumption on the risk of Helicobacter pylori infection, standardized questionnaires on drinking habits were used to interview 451 patients, whose H. pylori status was determined both by culture and serology. Reported alcohol consumption did not increase the risk of H. pylori infection (a 1.0 odds ratio, CI₉₅ 0.6–1.6). However, when the patients were divided into two age-groups, those under 35 years who reported to use alcohol seemed to have a slightly higher risk of H. pylori infection (a 3.3 odds ratio CI₉₅ 0.9–12.2) compared to those over 35 years (a 1.0 odds ratio, CI₉₅ 0.5–2.2). This phenomenon did not reach statistical significance. The type of alcohol consumed did not affect the age-adjusted risk of H. pylori infection. If pathologically defined chronic gastritis was found, the risk for H. pylori was high (a 26.7 odds ratio, CI₉₅ 12.1–59.0, for those under 35 years, and a 12.8 odds ratio, CI95 6.7–24.3, for those over 35 years of age).

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Chronic alcoholic gastritis. Roles of alcohol and Helicobacter pylori

Cited by 25 publications

References 25 publications

<i>Helicobacter pylori</i> and Gastric Erosions

<i>Helicobacter pylori</i> and Gastric Erosions

Alcohol-Related Diseases of the Esophagus and Stomach

Effect of Alcohol Consumption on the Risk of <i>Helicobacter pylori </i>Infection

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