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Ma S, Guo X, Wang C, Yin Y, Xu G, Chen H, Qi X. Association of Barrett's esophagus with Helicobacter pylori infection: a meta-analysis. Ther Adv Chronic Dis 2022; 13:20406223221117971. [PMID: 36034104 PMCID: PMC9403448 DOI: 10.1177/20406223221117971] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/24/2022] [Accepted: 07/19/2022] [Indexed: 11/25/2022] Open
Abstract
Background and Aims: Barrett’s esophagus (BE) is the only recognized precursor for esophageal
adenocarcinoma. Helicobacter pylori (H.
pylori) infection is a major contributing factor towards upper
gastrointestinal diseases, but its relationship with BE remains
controversial. Some previous studies suggested that H.
pylori infection negatively correlated with BE, while others
did not. This may be attributed to the difference in the selection of
control groups among studies. The present meta-analysis aims to clarify
their association by combining all available data from well-designed
studies. Methods: The PubMed, EMBASE, and Cochrane
Library databases were searched. Odds ratios (ORs) with 95%
confidence intervals (CIs) were pooled by a random-effects model.
Heterogeneity was evaluated using the Cochran’s Q test and
I2 statistics. Meta-regression, subgroup,
and leave-one-out sensitivity analyses were employed to explore the sources
of heterogeneity. Results: Twenty-four studies with 1,354,369 participants were included. Meta-analysis
found that patients with BE had a significantly lower prevalence of
H. pylori infection than those without (OR = 0.53, 95%
CI = 0.45–0.64; p < 0.001). The heterogeneity was
statistically significant (I² = 79%;
p < 0.001). Meta-regression, subgroup, and leave-one-out
sensitivity analyses did not find any source of heterogeneity. Meta-analysis
of 7 studies demonstrated that CagA-positive H. pylori
infection inversely correlated with BE (OR = 0.25, 95% CI = 0.15–0.44;
p = 0.000), but not CagA-negative H.
pylori infection (OR = 1.22, 95% CI = 0.90–1.67;
p = 0.206). Meta-analysis of 4 studies also
demonstrated that H. pylori infection inversely correlated
with LSBE (OR = 0.39, 95% CI = 0.18–0.86; p = 0.019), but
not SSBE (OR = 0.73, 95% CI = 0.30–1.77; p = 0.484). Conclusion: H. pylori infection negatively correlates with BE. More
experimental studies should be necessary to elucidate the potential
mechanisms in future.
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Affiliation(s)
| | | | | | | | - Guangqin Xu
- Department of Gastroenterology, General
Hospital of Northern Theater Command, Shenyang, China
- Graduate School, Dalian Medical University,
Dalian, China
| | - Hongxin Chen
- Department of Gastroenterology, General
Hospital of Northern Theater Command, Shenyang, China
- Graduate School, Liaoning University of
Traditional Chinese Medicine, Shenyang, China
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2
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Erőss B, Farkas N, Vincze Á, Tinusz B, Szapáry L, Garami A, Balaskó M, Sarlós P, Czopf L, Alizadeh H, Rakonczay Z, Habon T, Hegyi P. Helicobacter pylori infection reduces the risk of Barrett's esophagus: A meta-analysis and systematic review. Helicobacter 2018; 23:e12504. [PMID: 29938864 PMCID: PMC6055671 DOI: 10.1111/hel.12504] [Citation(s) in RCA: 49] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
INTRODUCTION The prevalence of Helicobacter pylori infection (HPI) has been decreasing in developed countries, with an increasing prevalence of Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) at the same time. The aim of our meta-analysis was to quantify the risk of BE in the context of HPI. METHODS A systematic search was conducted in 3 databases for studies on BE with data on prevalence of HPI from inception until December 2016. Odds ratios for BE in HPI were calculated by the random effects model with subgroup analyses for geographical location, presence of dysplasia in BE, and length of the BE segment. RESULTS Seventy-two studies were included in the meta-analysis, including 84 717 BE cases and 390 749 controls. The overall analysis showed that HPI reduces the risk of BE; OR = 0.68 (95% CI: 0.58-0.79, P < .001). Subgroup analyses revealed risk reduction in Asia OR = 0.53 (95% CI: 0.33-0.84, P = .007), Australia OR = 0.56 (95% CI: 0.39-0.80, P = .002), Europe OR = 0.77 (95% CI: 0.60-0.98, P = .035), and North-America OR = 0.59 (95% CI: 0.47-0.74, P < .001). The risk was significantly reduced for dysplastic BE, OR = 0.37 (95% CI: 0.26-0.51, P < .001) for non-dysplastic BE, OR = 0.51 (95% CI: 0.35-0.75, P = .001), and for long segment BE, OR = 0.25 (95% CI: 0.11-0.59, P = .001) in case of HPI. CONCLUSIONS This extensive meta-analysis provides additional evidence that HPI is associated with reduced risk of BE. Subgroup analyses confirmed that this risk reduction is independent of geographical location. HPI is associated with significantly lower risk of dysplastic, non-dysplastic, and long segment BE.
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Affiliation(s)
- Bálint Erőss
- Institute for Translational MedicineMedical SchoolUniversity of PécsPécsHungary
| | - Nelli Farkas
- Institute of BioanalysisMedical SchoolUniversity of PécsPécsHungary
| | - Áron Vincze
- Department of GastroenterologyFirst Department of MedicineMedical SchoolUniversity of PécsPécsHungary
| | - Benedek Tinusz
- Institute for Translational MedicineMedical SchoolUniversity of PécsPécsHungary
| | - László Szapáry
- Institute for Translational MedicineMedical SchoolUniversity of PécsPécsHungary
| | - András Garami
- Institute for Translational MedicineMedical SchoolUniversity of PécsPécsHungary
| | - Márta Balaskó
- Institute for Translational MedicineMedical SchoolUniversity of PécsPécsHungary
| | - Patrícia Sarlós
- Department of GastroenterologyFirst Department of MedicineMedical SchoolUniversity of PécsPécsHungary
| | - László Czopf
- Department of CardiologyFirst Department of MedicineMedical SchoolUniversity of PécsPécsHungary
| | - Hussain Alizadeh
- Department of HematologyFirst Department of MedicineMedical SchoolUniversity of PécsPécsHungary
| | - Zoltán Rakonczay
- Department of PathophysiologyMedical SchoolUniversity of SzegedSzegedHungary
| | - Tamás Habon
- Department of CardiologyFirst Department of MedicineMedical SchoolUniversity of PécsPécsHungary
| | - Péter Hegyi
- Institute for Translational MedicineMedical SchoolUniversity of PécsPécsHungary
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Utility of endoscopy for diagnosis of barrett in a non-Western society: endoscopic and histopathologic correlation. Int Surg 2015; 100:720-5. [PMID: 25588717 DOI: 10.9738/intsurg-d-14-00167.1] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/17/2022] Open
Abstract
Barrett esophagus is metaplastic transformation of esophageal squamous epithelium to columnar cells. A total of 1370 patients who had undergone upper endoscopy because of dyspeptic complaints were enrolled in the study. Age, sex, alcohol and smoking habits, body mass index, type and duration of symptoms (heartburn, epigastric pain, nausea, vomiting), and use of proton pump inhibitors were evaluated in all patients and recorded on standardized forms. Patients were grouped as normal esophagogastric junction, long-segment Barrett esophagus, and short-segment Barrett. Biopsies were taken from at least 6 points and examined histopathologically. Of the 1370 patients involved in the study, 748 (54.6%) were female and 622 (45.4%) were male. Mean age was 47.2 ± 15.30 years. Short-segment Barrett esophagus was detected in 16 patients, and long-segment Barrett was detected in 11 patients. Although Barrett esophagus was detected in 11 cases that were suspected to have Barrett during endoscopy, histopathology was negative in all cases that were not suspected to have Barrett. Barrett esophagus prevalence was significantly higher in people who used alcohol and tobacco and who had hiatal hernia. Although Barrett esophagus was detected in 40% of cases that were suspected to have Barrett during endoscopy, histopathology was negative in all cases that were not suspected to have Barrett. Barrett was detected in 40.7% of cases that were suspected to have Barrett during endoscopy; histopathology was negative in all cases that were not suspected to have Barrett. Senstivity of endoscopy is questionable in detection of short-segment Barrett.
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4
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Fischbach LA, Nordenstedt H, Kramer JR, Gandhi S, Dick-Onuoha S, Lewis A, El-Serag HB. The association between Barrett's esophagus and Helicobacter pylori infection: a meta-analysis. Helicobacter 2012; 17:163-75. [PMID: 22515353 PMCID: PMC3335759 DOI: 10.1111/j.1523-5378.2011.00931.x] [Citation(s) in RCA: 58] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
OBJECTIVE The effect of Helicobacter pylori on Barrett's esophagus is poorly understood. We conducted a meta-analysis to summarize the existing literature examining the effect that H. pylori has on Barrett's esophagus. DESIGN We performed a comprehensive search to identify studies pertaining to the association between H. pylori and Barrett's esophagus. We conducted meta-regression analyses to identify sources of variation in the effect of H. pylori on Barrett's esophagus. RESULTS Our analysis included a total of 49 studies that examined the effect of H. pylori on Barrett's esophagus and seven studies that examined the effect of cag A positivity on Barrett's esophagus. Overall, H. pylori, and even more so cag A, tended to be protective for Barrett's esophagus in most studies; however, there was obvious heterogeneity across studies. The effect of H. pylori on Barrett's esophagus varied by geographic location and in the presence of selection and information biases. Only four studies were found without obvious selection and information bias, and these showed a protective effect of H. pylori on Barrett's esophagus (Relative risk = 0.46 [95% CI: 0.35, 0.60]). CONCLUSIONS Estimates for the effect of H. pylori on Barrett's esophagus were heterogeneous across studies. We identified selection and information bias as potential sources of this heterogeneity. Few studies without obvious selection and information bias have been conducted to examine the effect of H. pylori on Barrett's esophagus, but in these, H. pylori infection is associated with a reduced risk of Barrett's esophagus.
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Affiliation(s)
- Lori A. Fischbach
- Department of Epidemiology, University of North Texas Health Science Center, Fort Worth, TX
| | - Helena Nordenstedt
- Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, TX,Houston VA Health Services Research & Development Center of Excellence, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX
| | - Jennifer R. Kramer
- Houston VA Health Services Research & Development Center of Excellence, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX,Section of Health Services Research, Department of Medicine, Baylor College of Medicine, Houston, TX
| | - Subi Gandhi
- Department of Epidemiology, University of North Texas Health Science Center, Fort Worth, TX
| | - Sam Dick-Onuoha
- Department of Epidemiology, University of North Texas Health Science Center, Fort Worth, TX
| | - Anthony Lewis
- Department of Epidemiology, University of North Texas Health Science Center, Fort Worth, TX
| | - Hashem B. El-Serag
- Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, TX,Houston VA Health Services Research & Development Center of Excellence, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX,Section of Health Services Research, Department of Medicine, Baylor College of Medicine, Houston, TX
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5
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Reply to Letter to the Editor: Re: Comparison of COX-2, Ki-67, and BCL-2 expression in normal esophageal mucosa, Barrett’s esophagus, dysplasia, and adenocarcinoma with postablation mucosa and implications for ablative therapies (Online First). Surg Endosc 2012; 26:291-2. [DOI: 10.1007/s00464-011-1842-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/17/2022]
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6
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Helicobacter pylori infection and Barrett's esophagus: a systematic review and meta-analysis. Am J Gastroenterol 2009; 104:492-500; quiz 491, 501. [PMID: 19174811 DOI: 10.1038/ajg.2008.37] [Citation(s) in RCA: 51] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
OBJECTIVES The majority of distal esophageal adenocarcinomas are believed to arise in patients with Barrett's esophagus (BE). Helicobacter pylori (H. pylori) infection plays an etiological role in gastric carcinogenesis, but any possible role in BE is uncertain. We aimed to explore the possible relationship between H. pylori infection and BE by meta-analysis. METHODS Observational studies comparing the prevalence of H. pylori infection in patients with BE and healthy controls conducted in adult populations and published in all languages were identified through MEDLINE, EMBASE, and Cochrane database searches up to week 5, 2008. H. pylori infection had to be confirmed by histology and/or serology and/or RUT and/or culture. Studies were excluded if no raw data for outcomes of interest were available or controls were patients with disease or duplicate publications. Summary effect size was calculated as odds ratio (OR) and 95% confidence intervals (CIs) by the random-effects model using Review Manager 4.2.8. RESULTS Of 519 citations identified, a total of 12 case-control studies compared the prevalence of H. pylori infection in BE (n=550) and controls (9 studies included controls with normal endoscopy and 3 studies used healthy blood donors as control, n=2,979). There was no significant difference in the overall prevalence of H. pylori infection between BE and controls (42.9% vs. 43.9%, OR=0.74, 95% CI 0.40-1.37, P=0.34), but with significant heterogeneity. Subgroup analysis showed that the prevalence of H. pylori infection was significantly lower in BE than in endoscopically normal healthy controls (23.1% vs. 42.7%, OR=0.50, 95% CI 0.27-0.93, P=0.03) with significant heterogeneity observed between studies. The heterogeneity was eliminated by excluding a single Asian outlier study. In contrast, H. pylori infection was significantly increased in BE patients in the three studies using healthy blood donors as "normal controls" (71.2% vs. 48.1%, OR=2.21, 95% CI 1.07-4.55). In BE patients, the prevalence of H. pylori infection was significantly lower in the esophagus than in the stomach (3.3% vs. 24.7%, OR=0.14, 0.03-0.67) in three studies. CONCLUSIONS H. pylori infection and BE are inversely related when compared with endoscopically normal controls but not blood donor controls. Limited evidence suggests that there is no clear association between H. pylori infection and BE. To determine more accurately the effect size of H. pylori infection in BE, high quality prospective case-control studies with age-matched, endoscopically normal healthy controls are needed.
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Song ZZ. The influential factors of left atrial volume. Am J Gastroenterol 2008; 103:241; author reply 241. [PMID: 18184128 DOI: 10.1111/j.1572-0241.2007.01562_1.x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
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8
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Parente FR, Bargiggia SA, Anderloni A. Helicobacter pylori infection and antisecretory efficacy of proton-pump inhibitors in gastroesophageal reflux disease: a liaison dangereuse or an innocent interplay? Scand J Gastroenterol 2006; 41:1121-5. [PMID: 16990195 DOI: 10.1080/00365520600931584] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
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9
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Marshall REK, Anggiansah A, Owen WJ. Bile in the oesophagus: Clinical relevance and ambulatory detection. Br J Surg 2005. [DOI: 10.1046/j.1365-2168.1997.02648.x] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
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10
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Toruner M, Soykan I, Ensari A, Kuzu I, Yurdaydin C, Ozden A. Barrett's esophagus: prevalence and its relationship with dyspeptic symptoms. J Gastroenterol Hepatol 2004; 19:535-40. [PMID: 15086597 DOI: 10.1111/j.1440-1746.2003.03342.x] [Citation(s) in RCA: 35] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/09/2022]
Abstract
BACKGROUND AND AIM Barrett's metaplasia is a premalign condition which plays a pivotal role in the development of esophageal adenocarcinoma. It is considered a complication of chronic gastroesophageal reflux disease. Although esophageal adenocarcinoma is an uncommon cancer, its incidence is rapidly increasing. The aims of the present study were to determine the prevalence of Barrett's metaplasia in outpatients referred for gastroscopy for upper gastrointestinal symptoms, and to clarify the relationship between Barrett's metaplasia and upper gastrointestinal symptoms. METHODS Three-hundred and ninety-five consecutive dyspeptic patients, never previously investigated, underwent gastroscopy and were enrolled into the study. RESULTS Barrett's metaplasia was detected in 29 patients (7.4%). The age-specific prevalence of Barrett's metaplasia increased with age. In multivariate analysis, Barrett's metaplasia was independently and positively related to age, sex and duration of symptoms, but not with upper gastrointestinal symptoms. In univariate analysis, Barrett's metaplasia was significantly more common in patients with antral intestinal metaplasia (24%) and presence of hiatal hernia (65.5%), compared with those with normal endoscopic findings (6.2% and 39.2%, respectively, p = 0.001). CONCLUSION Symptoms do not predict Barrett's metaplasia. Barrett's metaplasia is age-related and more common in patients with a longer duration of symptoms, presence of hiatal hernia and antral intestinal metaplasia.
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Affiliation(s)
- Murat Toruner
- Department of Gastroenterology, Ankara University School of Medicine, Ibni Sina Hospital, Sihhiye 06100, Ankara, Turkey.
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11
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Zhang J, Chen XL, Wang KM, Guo XD, Zuo AL, Gong J. Relationship of gastric Helicobacter pylori infection to Barrett’s esophagus and gastro-esophageal reflux disease in Chinese. World J Gastroenterol 2004; 10:672-5. [PMID: 14991936 PMCID: PMC4716907 DOI: 10.3748/wjg.v10.i5.672] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/15/2022] Open
Abstract
AIM: To evaluate the relationship of Helicobacter pylori infection to reflux esophagitis (RE), Barrett’s esophagus (BE) and gastric intestinal metaplasia (IM).
METHODS: RE, BE and gastric IM were determined by upper endoscopy. Patients were divided into 2 groups; those with squamocolumnar junction (SCJ) beyond gastroesophageal junction (GEJ) ≥ 3 cm (group A), and those with SCJ beyond GEJ < 3 cm (group B). Biopsy specimens were obtained endoscopically from just below the SCJ, gastric antrum along the greater and lesser curvature. Pathological changes and H pylori infection were determined by HE staining, Alcian blue staining and Giemsa staining.
RESULTS: The prevalence of H pylori infection was 46.93%. There was no difference in the prevalence between males and females. The prevalence of H pylori infection decreased stepwise significantly from RE grade I to III. There was no difference in the prevalence between the two groups, and between long-segment and short-segment BE. In distal stomach, prevalence of H pylori infection was significantly higher in patients with IM than those without IM.
CONCLUSION: There is a protective role of H pylori infection to GERD. There may be no relationship between H pylori infection of stomach and BE. H pylori infection is associated with the development of IM in the distal stomach.
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Affiliation(s)
- Jun Zhang
- Department of Gastroenterology, Second Hospital, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
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12
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Raghunath A, Hungin APS, Wooff D, Childs S. Prevalence of Helicobacter pylori in patients with gastro-oesophageal reflux disease: systematic review. BMJ 2003; 326:737. [PMID: 12676842 PMCID: PMC152634 DOI: 10.1136/bmj.326.7392.737] [Citation(s) in RCA: 242] [Impact Index Per Article: 11.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 02/05/2003] [Indexed: 02/06/2023]
Abstract
OBJECTIVES To ascertain the prevalence of Helicobacter pylori in patients with gastro-oesophageal reflux disease and its association with the disease. DESIGN Systematic review of studies reporting the prevalence of H pylori in patients with and without gastro-oesophageal reflux disease. DATA SOURCES Four electronic databases, searched to November 2001, experts, pharmaceutical companies, and journals. MAIN OUTCOME MEASURE Odds ratio for prevalence of H pylori in patients with gastro-oesophageal reflux disease. RESULTS 20 studies were included. The pooled estimate of the odds ratio for prevalence of H pylori was 0.60 (95% confidence interval 0.47 to 0.78), indicating a lower prevalence in patients with gastro-oesophageal reflux disease. Substantial heterogeneity was observed between studies. Location seemed to be an important factor, with a much lower prevalence of H pylori in patients with gastro-oesophageal reflux disease in studies from the Far East, despite a higher overall prevalence of infection than western Europe and North America. Year of study was not a source of heterogeneity. CONCLUSION The prevalence of H pylori infection was significantly lower in patients with than without gastro-oesophageal reflux, with geographical location being a strong contributor to the heterogeneity between studies. Patients from the Far East with reflux disease had a lower prevalence of H pylori infection than patients from western Europe and North America, despite a higher prevalence in the general population.
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Affiliation(s)
- Anan Raghunath
- Centre for Integrated Health Care Research, Wolfson Research Institute, University of Durham, Stockton on Tees TS17 6BH.
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13
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Gisbert JP, Pajares JM. [Prevalence of Helicobacter pylori infection in gastroesophageal reflux disease and Barretts esophagus]. Med Clin (Barc) 2002; 119:217-23. [PMID: 12200010 DOI: 10.1016/s0025-7753(02)73368-x] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/26/2022]
Affiliation(s)
- Javier P Gisbert
- Servicio de Aparato Digestivo, Hospital Universitario de La Princesa, Madrid, Spain.
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14
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Sánchez-Fayos P, Martín MJ, González A, Bosch O, Polo B, Arocena C, Porres JC. [Barrett's esophagus: the biological reality of a premaligmant columnar metaplasia]. GASTROENTEROLOGIA Y HEPATOLOGIA 2002; 25:254-66. [PMID: 11975875 DOI: 10.1016/s0210-5705(02)70256-2] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 10/27/2022]
Affiliation(s)
- P Sánchez-Fayos
- Servicio de Aparato Digestivo, Fundación Jiménez Díaz, Facultad de Medicina, Universidad Autónoma de Madrid, Spain
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15
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Rubin JS, Benjamin E, Prior A, Lavy J, Ratcliffe P. The prevalence of Helicobacter pylori infection in benign laryngeal disorders. J Voice 2002; 16:87-91. [PMID: 12002892 DOI: 10.1016/s0892-1997(02)00076-0] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/26/2022]
Abstract
Helicobacter pylori (HP) is an accepted cause of chronic active gastritis and has a major causative role in peptic ulcers. It is a gastric carcinogen. Its role in nonulcer dyspepsia (NUD) is less clear, yet 50% of patients with NUD are infected with HP, and some recent literature demonstrates long-term improvement of symptoms following eradication. HP has been investigated in several other organ systems, but has not been investigated to any major degree in laryngeal disorders, a region that could be directly exposed to the bacterium from pharyngolaryngeal reflux. This study represents one arm of a larger study designed to investigate such a relationship. Of 101 patients with nonmalignant voice disorders presenting to our voice clinics, 54.5% tested positive for the H. pylori organism. Of the controls, 47.1% tested positive. When striated into age groups of < 45 years, 46-61 years, and > 62 years, and then age-matched with the controls, the likelihood of infection with the H. pylori organism was greater in both the experimental middle group, and in the middle group when combined with the elder group, than in the matched controls, and this difference demonstrated a trend approaching statistical significance. This finding is discussed in the light of other studies on HP and on gastroesophageal reflex (GER).
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Affiliation(s)
- J S Rubin
- Royal National Throat, Nose and Ear Hospital, Royal Free National Health Service Trust, London, England.
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16
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O'Connor HJ, O'Morain CA. Helicobacter pylori and gastroesophageal reflux disease: to treat or not to treat? Scand J Gastroenterol 2001. [PMID: 11444465 DOI: 10.1080/00365520116789] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Affiliation(s)
- H J O'Connor
- Dept. of Medicine, General Hospital, Tullamore, Co Offaly, Ireland.
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Abstract
Gastro-oesophageal reflux disease and its sequela, Barrett's oesophagus, are the major recognized risk factors for oesophageal adenocarcinoma, a tumour whose frequency has increased dramatically in Western countries over the past few decades. Barrett's oesophagus develops through the process of metaplasia in which one adult cell type replaces another. The metaplastic, intestinal-type cells of Barrett's oesophagus are predisposed to develop genetic changes that eventuate in cancer. This report reviews the recent controversy regarding diagnostic criteria for Barrett's oesophagus, and provides practical guidelines for identifying the condition. The risks and benefits of the proposed medical, surgical and endoscopic therapies for Barrett's oesophagus are discussed in detail, and the approach to management recently endorsed by the American College of Gastroenterology is summarized.
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Affiliation(s)
- S J Spechler
- Division of Gastroenterology (111B1), Dallas Department of Veterans Affairs Medical Center, and University of Texas Southwestern Medical Center at Dallas, 4500 South Lancaster Road, Dallas, TX, 75216, USA
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18
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Ormsby AH, Kilgore SP, Goldblum JR, Richter JE, Rice TW, Gramlich TL. The location and frequency of intestinal metaplasia at the esophagogastric junction in 223 consecutive autopsies: implications for patient treatment and preventive strategies in Barrett's esophagus. Mod Pathol 2000; 13:614-20. [PMID: 10874664 DOI: 10.1038/modpathol.3880106] [Citation(s) in RCA: 58] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]
Abstract
The frequency of intestinal metaplasia at the esophagogastric junction is as high as 36% in endoscopy studies; the majority of cases (approximately 67%) occur in short segments of esophageal columnar mucosa. The validity of these studies has been questioned, however, because of heterogenous underlying diseases prompting endoscopy. To determine the frequency and origin of intestinal metaplasia at the esophagogastric junction, we histologically evaluated the entire esophagogastric junction for the presence of intestinal metaplasia using Alcian blue/periodic acid-Schiff mucin stains in 223 consecutive autopsies. Precise localization of the Z line in relation to the esophagogastric junction and tongues of esophageal columnar-appearing mucosa were noted in each case. Mean patient age was 47 years; 69% of patients were male, and 63% were white. Twenty five of 223 cases (11%) had intestinal metaplasia at the esophagogastric junction. Only 2 of 25 cases (8%) had intestinal metaplasia in the esophagus; the remaining 23 cases (92%) had intestinal metaplasia in the gastric cardia. Male gender, advanced age, white ethnic origin, and short tongues of esophageal columnar mucosa were not associated with gastric cardia intestinal metaplasia. An association of distal gastric intestinal metaplasia (P < .01) and chronic gastritis (P < .01) with gastric cardia intestinal metaplasia suggests a role for Helicobacter pylori infection in this process. The frequency of intestinal metaplasia at the esophagogastric junction in an unselected autopsy population is low (11%) even after exhaustive histologic evaluation using Alcian blue mucin stains. Furthermore, intestinal metaplasia is confined to the gastric cardia in more than 90% of cases with no association to male gender, white ethnic origin, advanced age, or the presence of short segments of esophageal columnar-appearing mucosa at endoscopy. These results demonstrate that caution is warranted when applying the findings of endoscopy studies to the development of preventive and screening strategies aimed at identifying Barrett's esophagus in an asymptomatic general population.
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Affiliation(s)
- A H Ormsby
- Center for Swallowing and Esophageal Disorders, Cleveland Clinic Foundation, Ohio 44195, USA
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19
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Abstract
The significance of specialized intestinal metaplasia in the esophagus is its associated risk with esophageal adenocarcinoma. This tumor has increased in incidence by over 70% in 20 years. Specialized intestinal metaplasia is the most important risk factor for adenocarcinoma of the esophagus and has been reported in 9-32% of unselected patients in general endoscopy units. The annual risk of esophageal adenocarcinoma for patients with specialized intestinal metaplasia is thought to be approximately 1%, at least 30 times that of the general population. Those with long segments of specialized intestinal metaplasia are thought to be at the greatest risk. Both environmental and molecular changes have been identified in the transition from squamous epithelium through specialized intestinal metaplasia to esophageal adenocarcinoma. The most important molecular changes include impaired regulation of the cell cycle, altered function of known oncogenes and tumor-suppressor genes, changes in cell adhesion molecules, and aneuploidy. This has given rise to a metaplasia/dysplasia/carcinoma model for the evolution of esophageal carcinoma.
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Affiliation(s)
- D Aldulaimi
- Department of Medicine, University of Birmingham, Edgbaston, UK
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20
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Abstract
Adenocarcinomas at the gastroesophageal junction appear to arise from foci of intestinal metaplasia that develop either in the distal esophagus or the proximal stomach (the gastric cardia). Metaplasia is usually a consequence of chronic inflammation, and it is logical to assume that intestinal metaplasia at the gastroesophageal junction develops as a result of chronic inflammation in the epithelia that normally line the junction region. Intestinal metaplasia in the esophagus is known to be a sequela of chronic inflammation in squamous epithelium caused by gastroesophageal reflux disease, whereas intestinal metaplasia in the distal stomach is often a consequence of chronic gastritis caused by Helicobacter pylori infection. For the gastric cardia, the contributions of gastroesophageal reflux disease, H. pylori infection, and other factors to inflammation, metaplasia, and neoplasia are not clear. If physicians are to develop meaningful preventive strategies and specific therapies for tumors of the proximal stomach, a clear understanding of pathogenesis is important. Recent studies on pathogenetic factors for inflammation in cardiac epithelium (gastric carditis) have yielded contradictory results, perhaps because of fundamental differences in the techniques used by different investigators for identifying and sampling the gastric cardia. This report explores the roots of the controversy regarding the role of gastric carditis in the development of metaplasia and neoplasia at the gastroesophageal junction and suggests practical guidelines for biopsy protocols to be used in future studies that will be necessary to resolve these disputes.
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Affiliation(s)
- S J Spechler
- Division of Gastroenterology, Department of Veterans Affairs Medical Center, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA
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21
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O'Connor HJ. Review article: Helicobacter pylori and gastro-oesophageal reflux disease-clinical implications and management. Aliment Pharmacol Ther 1999; 13:117-27. [PMID: 10102940 DOI: 10.1046/j.1365-2036.1999.00460.x] [Citation(s) in RCA: 104] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
A significant proportion of patients with gastro-oesophageal reflux disease (GERD) have Helicobacter pylori infection, but it is unclear whether or not H. pylori should be treated in this clinical setting. The aim of this review was to critically assess the relationship between H. pylori and GERD and its potential implications for the management of GERD. Data for this review were gathered from the following sources up to April 1998-the biomedical database MEDLINE, a detailed review of medical journals, and a review of abstracts submitted to relevant international meetings. On average, 40% of GERD patients carry H. pylori infection, with a reported infection prevalence ranging from 16% to 88%. To date, there has been no reported controlled trial of effective H. pylori therapy in GERD. GERD has been reported to develop de novo following the cure of H. pylori in peptic ulcer disease. In the presence of H. pylori, proton pump inhibitor therapy appears to accelerate the development of atrophic corpus gastritis, a potentially precancerous condition. Conversely, proton pump inhibitor therapy seems to become less effective after cure of H. pylori. The mechanisms underlying these important contrasting phenomena are poorly understood. The relationship between H. pylori and GERD is complex, and it is difficult to give definitive guidelines on the management of H. pylori infection in GERD. Controlled trials of H. pylori therapy in GERD are urgently needed, as well as further long-term data on both the natural history of gastric histopathological changes in the H. pylori-positive GERD patient treated with proton pump inhibitors, and the impact of H. pylori status on the clinical efficacy of antisecretory therapy. Pending these data, it is perhaps advisable to advocate cure of H. pylori in young patients with proton pump inhibitor-dependent GERD who, in the absence of anti-reflux surgery, are faced with the likelihood of long-term medical therapy.
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Affiliation(s)
- H J O'Connor
- Department of Medicine, General Hospital, Tullamore, Co. Offaly, Ireland; and Faculty of Medicine, University College Dublin, Earlsfort Terrace, Dublin, 2, Ireland
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22
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Ortiz-Hidalgo C, De La Vega G, Aguirre-García J. The histopathology and biologic prognostic factors of Barrett's esophagus: a review. J Clin Gastroenterol 1998; 26:324-33. [PMID: 9649022 DOI: 10.1097/00004836-199806000-00024] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
In Barrett's esophagus, stratified squamous mucosa of the lower third of the esophagus is replaced by columnar mucosa, as a complication of chronic gastroesophageal reflux. The presence of Barrett's esophagus appears to be a major factor in the progression to adenocarcinoma of the lower third of the esophagus. Therefore it is crucial to identify the subset of patients at risk for the development of adenocarcinoma. Dysplasia is an important histologic feature to evaluate because it identifies those patients who require follow-up. The diagnosis of biopsies with lesser degrees of abnormalities, however, makes microscopic evaluation less helpful in identifying patients who need more frequent endoscopic biopsy surveillance. DNA ploidy and the use of monoclonal antibodies, such as suppressor gene product p53, oncogene cerbB-2, and Ki-67, have added dramatically to our understanding of the biology of Barrett's metaplasia and have given us objective indicators to predict the presence of an increased risk of developing cancer.
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Affiliation(s)
- C Ortiz-Hidalgo
- Department of Surgical Pathology, The American British Cowdray Hospital, Observatorio, Mexico DF, Mexico
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Henihan RD, Stuart RC, Nolan N, Gorey TF, Hennessy TP, O'Morain CA. Barrett's esophagus and the presence of Helicobacter pylori. Am J Gastroenterol 1998; 93:542-6. [PMID: 9576445 DOI: 10.1111/j.1572-0241.1998.162_b.x] [Citation(s) in RCA: 37] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
OBJECTIVE Although the role of Helicobacter pylori in the pathogenesis of peptic ulcer disease and antral gastritis has been well documented, the role of H. pylori in esophageal disease has not been clearly defined. To clarify this issue, we analyzed 141 patients with histologically confirmed esophageal disease. METHODS The study group consisted of 82 patients with Barrett's esophagus, 19 with adenocarcinoma of the esophagus arising in columnar epithelium and 40 patients with reflux esophagitis without columnar metaplasia of the esophagus. In each of these cases the presence or absence of H. pylori was assessed histologically. RESULTS H. pylori was present in 19 of 82 patients (23%) with Barrett's esophagus, but was absent in all patients with adenocarcinoma of the esophagus and in patients with reflux esophagitis without Barrett's metaplasia. H. pylori was found only in areas of gastric type metaplasia in the patients with Barrett's esophagus. All of the 19 Barrett's esophagus group with H. pylori had chronic inflammation, and in 16 the inflammation was severe. H. pylori was significantly associated with severity of inflammation in patients with Barrett's esophagus (p < 0.001). Members of the Barrett's group with evidence of moderate to severe dysplasia were negative for H. pylori. CONCLUSION These data confirm that the presence of gastric type mucosa within the esophagus is a prerequisite for H. pylori colonization, and that H. pylori may contribute to the severity of inflammation in Barrett's epithelium.
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Affiliation(s)
- R D Henihan
- Department of Surgery, Trinity College, St. James's Hospital, Dublin, Ireland
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Torrado J, Ruiz B, Garay J, Asenjo JL, Tovar JA, Cosme A, Correa P. Blood-group phenotypes, sulfomucins, and Helicobacter pylori in Barrett's esophagus. Am J Surg Pathol 1997; 21:1023-9. [PMID: 9298878 DOI: 10.1097/00000478-199709000-00006] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Barrett's esophagus, morphologically analogous to gastric intestinal metaplasia, often precedes the development of esophageal adenocarcinoma. In the stomach, expression of sulfomucins and aberrant Lewis(a) (Le[a]) antigen is an excellent predictor of premalignant progression, and Helicobacter pylori infection is a crucial determinant for the development of atrophy, metaplasia, and adenocarcinoma. In the esophagus, the significance of sulfomucin expression is controversial, the aberrant expression of Le(a) has not been explored, and the role of H pylori in the evolution of preneoplastic conditions is unknown. We investigated in 155 patients referred for endoscopy the association of Barrett's esophagus with expression of sulfomucins, Lewis, secretor, and ABO phenotypes, and H pylori infection. We report a subtype of intestinal metaplasia, present in all patients with esophageal adenocarcinoma, similar to gastric intestinal metaplasia of colonic type (type III or incomplete), that expresses sulfomucins and aberrant Le(a) in goblet and columnar cells. Lewis(a+b-), nonsecretor and blood group A phenotypes, were all positively associated with esophageal adenocarcinoma, suggesting a genetic susceptibility. H pylori infection was detected in 75% of patients with esophageal adenocarcinoma.
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Affiliation(s)
- J Torrado
- Department of Pathology, Hospital Aránzazu, San Sebastián, Spain
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Marshall RE, Anggiansah A, Owen WJ. Bile in the oesophagus: clinical relevance and ambulatory detection. Br J Surg 1997. [PMID: 9043441 DOI: 10.1002/bjs.1800840108] [Citation(s) in RCA: 26] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
BACKGROUND Experimental work in animals has implicated a role for bile in the pathogenesis of several oesophageal mucosal diseases such as oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma. Recent descriptions of a high incidence of intestinal metaplasia at the gastro-oesophageal junction in patients without a classical 3-cm Barrett's columnar-lined segment, combined with a rising incidence in oesophageal and cardia adenocarcinoma, have stimulated interest in the causes of these conditions. METHODS AND RESULTS Animal studies concerned with defining the role of the various gastroduodenal reflux constituents in oesophageal mucosal injury are summarized and evidence for bile in the pathogenesis of Barrett's oesophagus and oesophageal adenocarcinoma is reviewed. The results of various techniques for clinical measurement of oesophageal bile reflux, such as aspiration, scintigraphy and pH monitoring, are evaluated and the significance of recent studies employing ambulatory fibreoptic bilirubin monitoring is discussed. CONCLUSION There seems little doubt that bile plays a significant role in oesophageal mucosal disease, in synergy with other constituents of reflux. Although ambulatory bilirubin monitoring is new, some intriguing findings have been reported and it is hoped that this technique will continue to shed light on the role of bile in the oesophagus.
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Affiliation(s)
- R E Marshall
- Department of Surgery, Guy's Hospital, London, UK
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