Prospective Evaluation of The Prevalence of Gastric Helicobacter Pylori Infection in Patients With Gerd, Barrett's Esophagus, Barrett's Dysplasia, and Barrett's Adenocarcinoma

Weston, Allan P.; Badr, Adnan S; Topalovski, Margarita; Cherian, Rachel; Dixon, Anita; Hassanein, Ruth S.

doi:10.1111/j.1572-0241.2000.01758.x

Cited by 155 publications

(80 citation statements)

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“…16 Gastric antral biopsies were not routinely taken, and the prevalence of Helicobacter pylori colonization was unknown in the present study. H pylori colonization is associated with a decreased risk of EAC, 13,17 although data are less clear with regard to the risk of BE. 17,18 The prevalence of H pylori is higher among blacks and Hispanics than whites, 19 and this could contribute to the observed differences in BE prevalence.…”

Section: Discussionmentioning

confidence: 99%

Racial and Ethnic Disparities in the Prevalence of Barrett’s Esophagus Among Patients Who Undergo Upper Endoscopy

Abrams¹,

Fields²,

Lightdale³

et al. 2008

Clinical Gastroenterology and Hepatology

113

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Section: Discussionmentioning

confidence: 99%

Racial and Ethnic Disparities in the Prevalence of Barrett’s Esophagus Among Patients Who Undergo Upper Endoscopy

Abrams¹,

Fields²,

Lightdale³

et al. 2008

Clinical Gastroenterology and Hepatology

113

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“…Many studies have reported that the absence of H. pylori colonization is associated with a greater likelihood of developing esophageal dysplasia and adenocarcinoma [18,[20][21][22][23] . Hence, H. pylori infection appears to have a protective effect against the development of dysplasia and adenocarcinoma in BE.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, Helicobacter pylori (H. pylori) infection may play a key role in suppression of BE. Two main inhibiting roles for development of BE have been postulated in H. pylori infection: H. pylori-induced atrophic gastritis resulting in less gastric acid secretion; and neutralization of the gastric acid by ammonia produced by H. pylori independently of gastric atrophy [17][18][19][20][21][22][23] . Cag-A positive H. pylori infection is strongly associated with a reduced risk of esophageal adenocarcinoma, and the association is independent of gastric atrophy, suggesting the involvement of a mechanism other than reduced acidic gastric reflux [24][25][26] .…”

Section: Introductionmentioning

confidence: 99%

Risk factors associated with Barrett’s epithelial dysplasia

Fujita

Nakamura

Kasashima

et al. 2014

WJG

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AIM:To elucidate risk factors associated with dysplasia of short-segment Barrett's esophagus (BE). METHODS:A total of 151 BE patients who underwent endoscopic examination from 2004 to 2008 in Aoyama Hospital, Tokyo Women's Medical University, Japan and whose diagnosis was confirmed from biopsy specimens were enrolled in the study. BE was diagnosed based on endoscopic findings of gastric-appearing mucosa or apparent columnar-lined esophagus proximal to the esophagogastric junction. Dysplasia was classified into three grades -mild, moderate and severe -according to the guidelines of the Vienna Classification System for gastrointestinal epithelial neoplasia. Anthropometric and biochemical data were analyzed to identify risk factors for BE dysplasia. The prevalence of Helicobacter pylori (H. pylori ) infection and the expression of p53 by immunohistological staining were also investigated. RESULTS:Histological examination classified patients into three types: specialized columnar epithelium (SCE) (n = 65); junctional (n = 38); and gastric fundic (n = 48). The incidence of dysplasia or adenocarcinoma from BE of the SCE type was significantly higher than that of the other two types (P < 0.01). The univariate analysis revealed that sex, H. pylori infection, body weight, p53 overexpression, and low diastolic blood pressure (BP) were associated with BE dysplasia. In contrast, body mass index, waist circumference, metabolic syndrome complications, and variables related to glucose or lipid metabolism were not associated with dysplasia. Multivariate logistic analysis showed that overexpression of p53 [odds ratio (OR) = 13.1, P = 0.004], H. pylori infection (OR = 0.19, P = 0.066), and diastolic BP (OR = 0.87, P = 0.021) were independent risk factors for epithelial dysplasia in BE patients with the SCE type. CONCLUSION:Overexpression of p53 is a risk factor for dysplasia of BE, however, H. pylori infection and diastolic BP inversely associated with BE dysplasia might be protective.

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“…Barrett's esophagus and esophageal carcinoma Similar to GERD, a lower prevalence of Barrett's metaplasia and esophageal adenocarcinoma has been described in H. pylori-positive patients [Weston et al 2000]. However, in a systematic review by Nakajima and Hattori [2004] the expected annual incidence of gastric cancer in patients with corpus atrophy with persistent infection was at least 5.8-fold higher than that for esophageal adenocarcinoma after the eradication of infection at all ages.…”

Section: Gerdmentioning

confidence: 99%