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Mülder DT, Hahn AI, Huang RJ, Zhou MJ, Blake B, Omofuma O, Murphy JD, Gutiérrez-Torres DS, Zauber AG, O'Mahony JF, Camargo MC, Ladabaum U, Yeh JM, Hur C, Lansdorp-Vogelaar I, Meester R, Laszkowska M. Prevalence of Gastric Precursor Lesions in Countries With Differential Gastric Cancer Burden: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol 2024; 22:1605-1617.e46. [PMID: 38438000 PMCID: PMC11272442 DOI: 10.1016/j.cgh.2024.02.023] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/09/2024] [Revised: 02/20/2024] [Accepted: 02/22/2024] [Indexed: 03/06/2024]
Abstract
BACKGROUND & AIMS The prevalence of precursor lesions for gastric cancer (GC) and the differential burden between countries of varying GC risk is not well-understood. We conducted a systematic review and meta-analysis to estimate the global prevalence of precursor lesions. METHODS We estimated the prevalence of atrophic gastritis (AG), gastric intestinal metaplasia (IM), and dysplasia in regions with low, medium, and high GC incidence. Because IM is an advanced manifestation of AG, we assessed the prevalence of less advanced precursors, regardless of the presence of more advanced lesions. Prevalence was sub-stratified by Helicobacter pylori infection, symptomatology, and period (<2000, 2000-2010, and >2010). RESULTS Among the 582 articles that underwent full-text review, 166 studies met inclusion criteria. The global prevalence estimates of AG, IM, and dysplasia were 25.4%, 16.2%, and 2.0%, respectively, on the basis of 126 studies that reported the prevalence of less advanced precursors, regardless of the presence of more advanced lesions. The prevalence of all precursor lesions was higher in high and medium compared with low GC incidence countries (P < .01). Prevalence of AG and IM was significantly higher among H pylori-infected individuals (P < .01) but not statistically different between symptomatic and asymptomatic individuals (P > .17). All precursors demonstrated a secular decrease in prevalence over time. CONCLUSIONS Gastric precursor lesions have differences in prevalence in regions with differential GC incidence and are associated with H pylori infection. Because of the substantial prevalence of precursor lesions in both symptomatic and asymptomatic individuals, symptomatic evaluation may not be sufficient to identify individuals at risk. These estimates provide important insights for tailoring GC prevention strategies.
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Affiliation(s)
- Duco T Mülder
- Department of Public Health, Erasmus Medical Center, Rotterdam, Netherlands
| | - Anne I Hahn
- Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York
| | - Robert J Huang
- Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California
| | - Margaret J Zhou
- Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California
| | - Benjamin Blake
- Weill Cornell Medical College of Cornell University, New York, New York
| | - Omonefe Omofuma
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland
| | - John D Murphy
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland
| | | | - Ann G Zauber
- Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York
| | - James F O'Mahony
- Department of Public Health, Erasmus Medical Center, Rotterdam, Netherlands; School of Economics, University College Dublin, Dublin, Ireland
| | - M Constanza Camargo
- Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland
| | - Uri Ladabaum
- Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California
| | - Jennifer M Yeh
- Department of Pediatrics, Harvard Medical School, Boston Children's Hospital, Boston, Massachusetts
| | - Chin Hur
- Division of General Medicine, Department of Medicine, Columbia University Irving Medical Center, New York, New York; Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, New York
| | | | - Reinier Meester
- Department of Public Health, Erasmus Medical Center, Rotterdam, Netherlands; Health Economics & Outcomes Research, Freenome Holdings Inc, San Francisco, California
| | - Monika Laszkowska
- Gastroenterology, Hepatology, and Nutrition Service, Department of Subspecialty Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.
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2
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Hatta W, Koike T, Asano N, Hatayama Y, Ogata Y, Saito M, Jin X, Uno K, Imatani A, Masamune A. The Impact of Tobacco Smoking and Alcohol Consumption on the Development of Gastric Cancers. Int J Mol Sci 2024; 25:7854. [PMID: 39063094 PMCID: PMC11276971 DOI: 10.3390/ijms25147854] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/21/2024] [Revised: 07/09/2024] [Accepted: 07/12/2024] [Indexed: 07/23/2024] Open
Abstract
Chronic infection of Helicobacter pylori is considered the principal cause of gastric cancers, but evidence has accumulated regarding the impact of tobacco smoking and alcohol consumption on the development of gastric cancers. Several possible mechanisms, including the activation of nicotinic acetylcholine receptors, have been proposed for smoking-induced gastric carcinogenesis. On the other hand, local acetaldehyde exposure and ethanol-induced mucosal inflammation have been proposed as the mechanisms involved in the development of gastric cancers in heavy alcohol drinkers. In addition, genetic polymorphisms are also considered to play a pivotal role in smoking-related and alcohol-related gastric carcinogenesis. In this review, we will discuss the molecular mechanisms involved in the development of gastric cancers in relation to tobacco smoking and alcohol consumption.
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Affiliation(s)
- Waku Hatta
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Tomoyuki Koike
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Naoki Asano
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
- Division of Cancer Stem Cell, Miyagi Cancer Center Research Institute, 47-1 Nodayama, Medeshima-Shiode, Natori 981-1293, Miyagi, Japan
- Division of Carcinogenesis and Senescence Biology, Tohoku University Graduate School of Medicine, Natori 981-1293, Miyagi, Japan
| | - Yutaka Hatayama
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Yohei Ogata
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Masahiro Saito
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Xiaoyi Jin
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Kaname Uno
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Akira Imatani
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
| | - Atsushi Masamune
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Miyagi, Japan; (T.K.); (Y.H.); (Y.O.); (M.S.); (X.J.); (K.U.); (A.I.); (A.M.)
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Rugge M, Genta RM, Malfertheiner P, Dinis-Ribeiro M, El-Serag H, Graham DY, Kuipers EJ, Leung WK, Park JY, Rokkas T, Schulz C, El-Omar EM. RE.GA.IN.: the Real-world Gastritis Initiative-updating the updates. Gut 2024; 73:407-441. [PMID: 38383142 DOI: 10.1136/gutjnl-2023-331164] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/18/2023] [Accepted: 12/18/2023] [Indexed: 02/23/2024]
Abstract
At the end of the last century, a far-sighted 'working party' held in Sydney, Australia addressed the clinicopathological issues related to gastric inflammatory diseases. A few years later, an international conference held in Houston, Texas, USA critically updated the seminal Sydney classification. In line with these initiatives, Kyoto Global Consensus Report, flanked by the Maastricht-Florence conferences, added new clinical evidence to the gastritis clinicopathological puzzle.The most relevant topics related to the gastric inflammatory diseases have been addressed by the Real-world Gastritis Initiative (RE.GA.IN.), from disease definitions to the clinical diagnosis and prognosis. This paper reports the conclusions of the RE.GA.IN. consensus process, which culminated in Venice in November 2022 after more than 8 months of intense global scientific deliberations. A forum of gastritis scholars from five continents participated in the multidisciplinary RE.GA.IN. consensus. After lively debates on the most controversial aspects of the gastritis spectrum, the RE.GA.IN. Faculty amalgamated complementary knowledge to distil patient-centred, evidence-based statements to assist health professionals in their real-world clinical practice. The sections of this report focus on: the epidemiology of gastritis; Helicobacter pylori as dominant aetiology of environmental gastritis and as the most important determinant of the gastric oncogenetic field; the evolving knowledge on gastric autoimmunity; the clinicopathological relevance of gastric microbiota; the new diagnostic horizons of endoscopy; and the clinical priority of histologically reporting gastritis in terms of staging. The ultimate goal of RE.GA.IN. was and remains the promotion of further improvement in the clinical management of patients with gastritis.
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Affiliation(s)
- Massimo Rugge
- Department of Medicine-DIMED, University of Padova, Padua, Italy
- Azienda Zero, Veneto Tumour Registry, Padua, Italy
| | - Robert M Genta
- Gastrointestinal Pathology, Inform Diagnostics Research Institute, Dallas, Texas, USA
- Pathology, Baylor College of Medicine, Houston, Texas, USA
| | - Peter Malfertheiner
- Medizinische Klinik und Poliklinik II, Ludwig Maximilian Universität Klinikum München, Munich, Germany
- Klinik für Gastroenterologie, Hepatologie und Infektiologie, Otto-von-Guericke Universität Magdeburg, Magdeburg, Germany
| | - Mario Dinis-Ribeiro
- Porto Comprehensive Cancer Center & RISE@CI-IPO, University of Porto, Porto, Portugal
- Gastroenterology Department, Portuguese Institute of Oncology of Porto, Porto, Portugal
| | - Hashem El-Serag
- Gastroenterology and Hepatology, Baylor College of Medicine, Houston, Texas, USA
- Houston VA Health Services Research & Development Center of Excellence, Michael E DeBakey Veterans Affairs Medical Center, Houston, Texas, USA
| | - David Y Graham
- Department of Medicine, Michael E DeBakey Veterans Affairs Medical Center, Houston, Texas, USA
| | - Ernst J Kuipers
- Erasmus University Medical Center, Rotterdam, The Netherlands
| | | | - Jin Young Park
- International Agency for Research on Cancer, Lyon, France
| | - Theodore Rokkas
- Gastroenterology, Henry Dunant Hospital Center, Athens, Greece
| | | | - Emad M El-Omar
- Microbiome Research Centre, University of New South Wales, Sydney, New South Wales, Australia
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Pham C, Nguyen Wenker T, El-Serag HB. Epidemiology of Gastric Intestinal Metaplasia and Gastric Cancer. FOREGUT: THE JOURNAL OF THE AMERICAN FOREGUT SOCIETY 2023; 3:80-88. [DOI: 10.1177/26345161231154024] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2025]
Abstract
Gastric cancer remains one of the most common cancers globally. The pathogenesis of intestinal-type gastric cancer involves pre-malignant stages, including gastric intestinal metaplasia (GIM), the replacement of native gastric foveolar and/or glandular epithelium by intestinal-type epithelium. GIM prevalence is highly variable based on geography and race/ethnicity partly due to the varying prevalence of H. pylori, a potent risk factor. However, gastric cancer incidence does not mirror that of H. pylori, demonstrating a complex interaction between H. pylori and risk factors. We will discuss the epidemiology of GIM and gastric cancer, including incidence trends, risk factors, and implications for future management.
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Affiliation(s)
- Codey Pham
- Department of Medicine, Baylor College of Medicine, Houston, TX, USA
| | - Theresa Nguyen Wenker
- Department of Medicine, Baylor College of Medicine, Houston, TX, USA
- Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E DeBakey Veterans Affairs Medical Center, Houston, TX, USA
| | - Hashem B El-Serag
- Department of Medicine, Baylor College of Medicine, Houston, TX, USA
- Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E DeBakey Veterans Affairs Medical Center, Houston, TX, USA
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Sekar R, Preethi M, Mohammed J. Quantification of Helicobacter pylori and its oncoproteins in oral cavity. A cross sectional study. Oral Dis 2022; 29:1868-1874. [PMID: 35092112 DOI: 10.1111/odi.14141] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/21/2021] [Revised: 12/30/2021] [Accepted: 01/20/2022] [Indexed: 11/30/2022]
Abstract
OBJECTIVE To identify Helicobacter pylori (H.pylori) and related oncogenic and virulent proteins (CagA and VacA) in patients with gingivitis, periodontitis, oral cancer and gastric cancer. METHODS Subgingival plaque samples were collected from 90 individuals with either gingivitis/ periodontitis (group A, n=30), oral cancer (group B, n=30) and gastric cancer (group C, n=30). H.pylori was identified by real time- polymerase chain reaction (RT-PCR). The virulent organisms were detected by identification of proteins CagA and VacA through Enzyme Linked Immuno Sorbent Assay (ELISA). RESULTS We identified the presence of H.pylori in subgingival plaque samples among a large majority (76/90) of our study cohort. The proportions of CagA and VacA identified among H.pylori individuals with periodontal inflammation and oral cancer were lower than those diagnosed with gastric cancer. Furthermore, the relative risk of oral cancer based on the presence of the organism was no different to those with gingivitis/periodontitis. CONCLUSION The findings of our study does not indicate significant association between the organism and oral cancer but preludes that the oral cavity could act as a potential niche for H.pylori. The possibility for CagA and VacA proteins to be pathogenic in oral cavity is highly possible and to be researched extensively.
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Affiliation(s)
- Ramya Sekar
- Department of Oral and Maxillofacial Pathology, Meenakshi Ammal Dental College and Hospital, Maduravoyal, Chennai, 600 095, India
| | - Murali Preethi
- Department of Oral and Maxillofacial Pathology, Meenakshi Ammal Dental College and Hospital, Maduravoyal, Chennai, 600 095, India
| | - Junaid Mohammed
- School of Population and Global Health, University of Western Australia, Clifton Street Building, Clifton street, Nedlands, 6009, Western Australia, Australia.,Telethon Kids Institute, University of Western Australia, Nedlands, 6009, Western Australia, Australia
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Associations of Duration, Intensity, and Quantity of Smoking With Risk of Gastric Intestinal Metaplasia. J Clin Gastroenterol 2022; 56:e71-e76. [PMID: 33337636 PMCID: PMC8875544 DOI: 10.1097/mcg.0000000000001479] [Citation(s) in RCA: 10] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/14/2020] [Accepted: 11/09/2020] [Indexed: 12/12/2022]
Abstract
GOAL Determine whether various dimensions of smoking increase risk for gastric intestinal metaplasia. BACKGROUND Cigarette smoking has been implicated in the etiology of gastric cancer, but it is not clear if smoking is a risk factor for gastric intestinal metaplasia, a precursor lesion of gastric cancer. MATERIALS AND METHODS We compared data from 385 gastric intestinal metaplasia cases and 1577 controls without gastric intestinal metaplasia recruited into a cross-sectional study at the Michael E. DeBakey VA Medical Center in Houston, Texas. All participants completed standardized questionnaires and underwent a study endoscopy with gastric mapping biopsies. Gastric intestinal metaplasia cases included participants with intestinal metaplasia on any noncardia gastric biopsy. We calculated odds ratios and associated 95% confidence intervals using multivariable logistic regression models. RESULTS Compared with never smokers, current smokers had 2-fold increased risk for gastric intestinal metaplasia (odds ratio, 2.05; 95% confidence interval, 1.47-2.85). Among ever smokers, increasing duration and total dose were significantly associated with increased risk for gastric intestinal metaplasia (P-trend, 0.004 and 0.01, respectively). Among former smokers, risk for gastric intestinal metaplasia decreased over time and was no different to never smokers after 15 years smoking cessation. Cases with gastric intestinal metaplasia were more likely than controls to have Helicobacter pylori infection (53.2% vs. 21.7%); however, smoking effect on gastric intestinal metaplasia was not different by H. pylori infection status. CONCLUSIONS Cigarette smoking is a risk factor for gastric intestinal metaplasia. Risk of gastric intestinal metaplasia among former smokers remained significantly elevated until 15 years postcessation.
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Holmes HM, Jove AG, Tan MC, El-Serag HB, Thrift AP. Alcohol consumption and the risk of gastric intestinal metaplasia in a U.S. Veterans population. PLoS One 2021; 16:e0260019. [PMID: 34780551 PMCID: PMC8592489 DOI: 10.1371/journal.pone.0260019] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/13/2021] [Accepted: 11/01/2021] [Indexed: 12/31/2022] Open
Abstract
Background Chronic alcohol use is a risk factor for non-cardia gastric adenocarcinoma. However, it is less well understood whether alcohol use is a risk factor for premalignant mucosal changes, namely gastric intestinal metaplasia. We examined the association between various parameters of alcohol use and risk of gastric intestinal metaplasia. Methods We used data from 2084 participants (including 403 with gastric intestinal metaplasia) recruited between February 2008-August 2013 into a cross-sectional study at the Michael E. DeBakey Veterans Affairs Medical Center in Houston, Texas. All participants underwent a study upper endoscopy with systematic gastric mapping biopsies. Cases had intestinal metaplasia on any non-cardia gastric biopsy. Participants self-reported lifetime history of alcohol consumption, along with other lifestyle risk factors, through a study survey. We calculated odds ratios (OR) and 95% confidence intervals (95% CI) for categories of average alcohol consumption using multivariable logistic regression, and restricted cubic spline regression to explore the potential shape of a dose-response relationship. Results Compared to lifelong non-drinkers, individuals who consumed on average ≥28 drinks per week had no elevated risk for gastric intestinal metaplasia (adjusted OR, 1.27; 95% CI, 0.74–2.19). Based on a spline regression curve and its 95% CI, there was also no demonstrable association between cumulative lifetime alcohol consumption and risk of gastric intestinal metaplasia. Similarly, we found no association between beverage type (beer, wine, liquor/spirits) and risk for gastric intestinal metaplasia. Conclusions Neither amount of alcohol consumed nor specific beverage type was associated with risk of gastric intestinal metaplasia.
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Affiliation(s)
- Hudson M Holmes
- Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America
| | - Andre G Jove
- Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America
| | - Mimi C Tan
- Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America
| | - Hashem B El-Serag
- Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America.,Houston VA HSR&D Center for Innovations in Quality, Effectiveness and Safety, Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas, United States of America
| | - Aaron P Thrift
- Section of Epidemiology and Population Sciences, Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America.,Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, Texas, United States of America
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Tan MC, Mallepally N, Ho Q, Liu Y, El-Serag HB, Thrift AP. Dietary Factors and Gastric Intestinal Metaplasia Risk Among US Veterans. Dig Dis Sci 2021; 66:1600-1610. [PMID: 32535778 PMCID: PMC8845052 DOI: 10.1007/s10620-020-06399-9] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/13/2019] [Accepted: 06/03/2020] [Indexed: 02/06/2023]
Abstract
BACKGROUND Studies on diet and gastric intestinal metaplasia (GIM) risk are lacking in US populations. AIM To determine the associations of dietary factors and risk of GIM among a US population with typical American diet. METHODS We analyzed data from a cross-sectional study of veterans attending primary care and endoscopy clinics at the Houston VA Medical Center. Patients completed a 110-item Block Food Frequency Questionnaire then underwent upper endoscopy with gastric mapping biopsies. We compared cases defined by GIM on ≥ 1 non-cardia gastric biopsy to controls without GIM. Associations of dietary factors and GIM were estimated using logistic regression models as odds ratios (OR) and 95% confidence intervals (CI). RESULTS Among 423 GIM cases and 1796 controls, cases were older (62.1 vs. 59.9 years) and more likely to be male (97.2% vs. 90.8%) and non-White (58.6% vs. 39.0%). GIM cases had lower fat intake (percent kcal from fat tertile 1: 43.6% vs. 33.4%) and higher carbohydrate intake (percent kcal from carbohydrate T3: 41.8% vs. 33.3%) than controls. Adjusting for age, gender, race, smoking, and Helicobacter pylori, percent kcal from carbohydrates (T3 vs. T1: OR 1.35, 95% CI 1.08-1.67), fruit intake (T3 vs. T1: OR 1.28, 95% CI 1.02-1.61), and fiber intake (T3 vs. T1: OR 1.37, 95% CI 1.04-1.80) were associated with GIM. In subgroup analyses, these associations were primarily seen in non-White patients. CONCLUSIONS Few dietary factors, including high carbohydrate intake, are associated with increased risk of GIM in US populations, independent of H. pylori or smoking.
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Affiliation(s)
- Mimi C Tan
- Section of Gastroenterology and Hepatology, Baylor College of Medicine, Baylor College of Medicine, One Baylor Plaza, MS: BCM 285, Houston, TX, 77030-3498, USA.
| | | | - Quynh Ho
- Section of Gastroenterology and Hepatology, Baylor College of Medicine, Baylor College of Medicine, One Baylor Plaza, MS: BCM 285, Houston, TX, 77030-3498, USA
- University of St. Thomas, Houston, TX, USA
| | - Yan Liu
- Section of Gastroenterology and Hepatology, Baylor College of Medicine, Baylor College of Medicine, One Baylor Plaza, MS: BCM 285, Houston, TX, 77030-3498, USA
- Houston VA HSR&D Center for Innovations in Quality, Effectiveness and Safety, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, USA
| | - Hashem B El-Serag
- Department of Medicine, Baylor College of Medicine, Houston, TX, USA
- Houston VA HSR&D Center for Innovations in Quality, Effectiveness and Safety, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, USA
| | - Aaron P Thrift
- Section of Epidemiology and Population Sciences, Department of Medicine, Baylor College of Medicine, Houston, TX, USA
- Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA
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Koulis A, Busuttil RA, Boussioutas A. Premalignant lesions of the stomach and management of early neoplastic lesions. RESEARCH AND CLINICAL APPLICATIONS OF TARGETING GASTRIC NEOPLASMS 2021:185-216. [DOI: 10.1016/b978-0-323-85563-1.00013-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/06/2025]
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Huang HL, Leung CY, Saito E, Katanoda K, Hur C, Kong CY, Nomura S, Shibuya K. Effect and cost-effectiveness of national gastric cancer screening in Japan: a microsimulation modeling study. BMC Med 2020; 18:257. [PMID: 32921305 PMCID: PMC7489209 DOI: 10.1186/s12916-020-01729-0] [Citation(s) in RCA: 35] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/28/2020] [Accepted: 08/03/2020] [Indexed: 02/06/2023] Open
Abstract
BACKGROUND A national endoscopic screening program for gastric cancer was rolled out in Japan in 2015. We used a microsimulation model to estimate the cost-effectiveness of current screening guidelines and alternative screening strategies in Japan. METHODS We developed a microsimulation model that simulated a virtual population corresponding to the Japanese population in risk factor profile and life expectancy. We evaluated 15 endoscopic screening scenarios with various starting ages, stopping ages, and screening intervals. The primary outcomes were quality-adjusted life-years (QALYs), costs, and incremental cost-effectiveness ratio. Cost-effective screening strategies were determined using a willingness-to-pay threshold of $50,000 per QALY gained. One-way sensitivity and probabilistic sensitivity analyses were done to explore model uncertainty. RESULTS Using the threshold of $50,000 per QALY, a triennial screening program for individuals aged 50 to 75 years was the cost-effective strategy, with an incremental cost-effectiveness ratio of $45,665. Compared with no endoscopic screening, this strategy is predicted to prevent 63% of gastric cancer mortality and confer 27.2 QALYs gained per 1000 individuals over a lifetime period. Current screening guidelines were not on the cost-effectiveness efficient frontier. The results were robust on one-way sensitivity analyses and probabilistic sensitivity analysis. CONCLUSIONS This modeling study suggests that the endoscopic screening program in Japan would be cost-effective when implemented between age 50 and 75 years, with the screening repeated every 3 years. These findings underscore the need for further evaluation of the current gastric cancer screening recommendations.
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Affiliation(s)
- Hsi-Lan Huang
- Department of Global Health Policy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
- Division of Cancer Statistics Integration, Center for Cancer Control and Information Services, National Cancer Center, Tokyo, Japan
| | - Chi Yan Leung
- Department of Global Health Policy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
- Division of Cancer Statistics Integration, Center for Cancer Control and Information Services, National Cancer Center, Tokyo, Japan.
| | - Eiko Saito
- Division of Cancer Statistics Integration, Center for Cancer Control and Information Services, National Cancer Center, Tokyo, Japan
| | - Kota Katanoda
- Division of Cancer Statistics Integration, Center for Cancer Control and Information Services, National Cancer Center, Tokyo, Japan
| | - Chin Hur
- Department of Medicine, Columbia University Irving Medical Center, New York City, USA
- Institute for Technology Assessment, Massachusetts General Hospital, Boston, MA, USA
| | - Chung Yin Kong
- Institute for Technology Assessment, Massachusetts General Hospital, Boston, MA, USA
- Department of Radiology, Harvard Medical School, Boston, MA, USA
| | - Shuhei Nomura
- Department of Global Health Policy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
- Department of Health Policy and Management, School of Medicine, Keio University, Tokyo, Japan
- Epidemiology and Prevention Group, Center for Public Health Sciences, National Cancer Center, Tokyo, Japan
| | - Kenji Shibuya
- Department of Global Health Policy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
- University Institute for Population Health, King's College London, London, UK
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El Khadir M, Boukhris Alaoui S, Benajah DA, Ibrahimi SA, Chbani L, El Abkari M, Bennani B. VacA genotypes and cagA-EPIYA-C motifs of Helicobacter pylori and gastric histopathological lesions. Int J Cancer 2020; 147:3206-3214. [PMID: 32542674 DOI: 10.1002/ijc.33158] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/20/2020] [Revised: 05/23/2020] [Accepted: 06/02/2020] [Indexed: 02/06/2023]
Abstract
Helicobacter pylori infection induces inflammation of the gastric mucosa, which may progress to precancerous lesions and gastric cancer. The gastric histo-pathological damages may be associated with some virulence genes of the bacterium, notably vacA and cagA genes. To establish correlations between these genes and the lesions, biopsies from 1303 adults consenting patients that were previously analyzed by PCR to characterize vacA-s vacA-m, vacA-i regions and cagA 3' region polymorphism, were used. The highest average age was obtained in patients with intestinal metaplasia (53.65 ± 15.26 years) and gastric cancer (53.60 ± 14.32 years). Thus, these lesions are more frequent in elderly and male subjects. Tobacco smoking was significantly associated with neutrophilic activity (P = .02). No significant association was obtained between patients with chronic inflammation and vacA and cagA H. pylori genotypes. However, a significant association has been obtained between this lesion and cagA+ in aged patients (P = .02), while intestinal metaplasia was significantly associated with vacAi1 and vacAm1 separately (P < .01 and .01). Also, a significant association was obtained between intestinal metaplasia and strains with one EPIYA-C motif in young patients (P = .001). Interestingly, a significant association was obtained between gastric cancer and cagA+, vacAi1, vacAm1 H. pylori genotypes and also with two EPIYA-C motifs independently of age groups (all P < .05). The results of our study show that H. pylori vacAi1 could be more potent than the other H. pylori virulent factors for predicting the precancerous gastric lesions, confirming that this gene may be helpful to identify patients at high risk for gastric cancer.
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Affiliation(s)
- Mounia El Khadir
- Laboratoire de Pathologie Humaine Biomédecine et Environnement, Faculté de Médecine et de Pharmacie de Fès (FMPF), Université Sidi Mohammed Ben Abdellah (USMBA), Fès, Morocco
| | - Samia Boukhris Alaoui
- Laboratoire de Pathologie Humaine Biomédecine et Environnement, Faculté de Médecine et de Pharmacie de Fès (FMPF), Université Sidi Mohammed Ben Abdellah (USMBA), Fès, Morocco
| | - Dafr-Allah Benajah
- Laboratoire de Pathologie Humaine Biomédecine et Environnement, Faculté de Médecine et de Pharmacie de Fès (FMPF), Université Sidi Mohammed Ben Abdellah (USMBA), Fès, Morocco.,Service d'Hépato Gastro-entérologie CHU Hassan II, Fès, Morocco
| | - Sidi Adil Ibrahimi
- Laboratoire de Pathologie Humaine Biomédecine et Environnement, Faculté de Médecine et de Pharmacie de Fès (FMPF), Université Sidi Mohammed Ben Abdellah (USMBA), Fès, Morocco.,Service d'Hépato Gastro-entérologie CHU Hassan II, Fès, Morocco
| | - Laila Chbani
- Service d'Anatomie Pathologique CHU Hassan II, Fès, Morocco
| | - Mohamed El Abkari
- Laboratoire de Pathologie Humaine Biomédecine et Environnement, Faculté de Médecine et de Pharmacie de Fès (FMPF), Université Sidi Mohammed Ben Abdellah (USMBA), Fès, Morocco.,Service d'Hépato Gastro-entérologie CHU Hassan II, Fès, Morocco
| | - Bahia Bennani
- Laboratoire de Pathologie Humaine Biomédecine et Environnement, Faculté de Médecine et de Pharmacie de Fès (FMPF), Université Sidi Mohammed Ben Abdellah (USMBA), Fès, Morocco
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Abstract
OBJECTIVES The risk of noncardia gastric cancer is increased in the presence of gastric intestinal metaplasia. We aimed to identify demographic and lifestyle factors independently associated with the risk of gastric intestinal metaplasia. METHODS We used data from a cross-sectional study of patients attending primary care and endoscopy clinics at the Michael E. DeBakey VA Medical Center in Houston, Texas, between February 2008 and August 2013. All patients completed standardized questionnaires and underwent endoscopy with gastric mapping biopsies. Gastric intestinal metaplasia cases included patients with intestinal metaplasia on any noncardia gastric biopsy; we defined extensive gastric intestinal metaplasia as antrum and corpus involvement. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariate logistic regression models. RESULTS We identified 423 cases with gastric intestinal metaplasia and 1,796 controls without gastric intestinal metaplasia. Older age (vs <60 years: 60-69 years AdjOR, 1.50; 95% CI, 1.17-1.93; ≥70 years AdjOR, 2.12; 95% CI, 1.48-3.04), male sex (AdjOR, 2.76; 95% CI, 1.50-5.10), nonwhite race/ethnicity (vs non-Hispanic white: Hispanic, AdjOR, 2.66; 95% CI, 1.89-3.76; black, AdjOR, 2.36; 95% CI, 1.85-3.02), and current smoking status (AdjOR, 1.78; 95% CI, 1.29-2.48) were independently associated with gastric intestinal metaplasia. These risk factors remained statistically significantly associated with gastric intestinal metaplasia after adjusting for Helicobacter pylori infection, and their effect sizes were larger for associations with extensive gastric intestinal metaplasia compared with focal gastric intestinal metaplasia. DISCUSSION Older age, male sex, nonwhite race/ethnicity, and current smoking status were the nonendoscopic factors independently associated with gastric intestinal metaplasia in a predominantly nonimmigrant US population.
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Trieu JA, Bilal M, Saraireh H, Wang AY. Update on the Diagnosis and Management of Gastric Intestinal Metaplasia in the USA. Dig Dis Sci 2019; 64:1079-1088. [PMID: 30771043 DOI: 10.1007/s10620-019-05526-5] [Citation(s) in RCA: 15] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]
Abstract
Gastric intestinal metaplasia (GIM) is a premalignant condition that can lead to intestinal-type gastric adenocarcinoma. It is characterized by a change in the gastric mucosa to a small-intestinal phenotype. Infection with Helicobacter pylori is the most common factor associated with GIM. Although GIM is typically a histologic diagnosis, various techniques have been developed to enable the endoscopic identification of GIM. There are presently no widely accepted guidelines on screening and surveillance strategies in patients with GIM in the USA. The aim of this review is to provide an update regarding the problem, diagnosis, and management of GIM in the USA.
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Affiliation(s)
- Judy A Trieu
- Department of Internal Medicine, The University of Texas Medical Branch, 301 University Blvd, Galveston, TX, 77555, USA
| | - Mohammad Bilal
- Division of Gastroenterology and Hepatology, The University of Texas Medical Branch, 301 University Blvd, Galveston, TX, 77555, USA.
| | - Hamzeh Saraireh
- Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University, 1200 East Broad Street, P.O. Box 98034, Richmond, VA, 23298, USA
| | - Andrew Y Wang
- Division of Gastroenterology and Hepatology, University of Virginia, P.O. Box 800708, Charlottesville, VA, 22908, USA
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14
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Ghatak S, Yadav RP, Lalrohlui F, Chakraborty P, Ghosh S, Ghosh S, Das M, Pautu JL, Zohmingthanga J, Senthil Kumar N. Xenobiotic Pathway Gene Polymorphisms Associated with Gastric Cancer in High Risk Mizo-Mongoloid Population, Northeast India. Helicobacter 2016; 21:523-535. [PMID: 27006283 DOI: 10.1111/hel.12308] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/20/2022]
Abstract
BACKGROUND The aim of this study was to evaluate the risk of gastric cancer associated with individual or combined glutathione S-transferases (GSTs) polymorphism and their interaction with environmental factors. MATERIALS AND METHODS Genotyping by PCR was carried out for 80 cases and controls each for GSTM1, GSTT1, and GSTP1 polymorphism and mapped for gene-environment association studies. The samples were subjected to pathogen detection and GSTP1 expression for analyzing their association with different genotypes. Logistic regression analyses were conducted to compute the influence of both genetic and environmental factors for gastric cancer. MDR analysis was performed to assess the risk of gastric cancer by studying the gene-gene and gene-environment effect on the basis of GST genotyping and GSTP1 gene expression. RESULTS Infection with Helicobacter pylori and CagA+ strains was more frequent in patients with GSTM1/T1 null genotype. Intake of high fermented fat and smoked meat was found to be significantly associated with gastric cancer. The G/G, A/G (rs1695), and T/T (rs1138272) were found to be significantly associated with low expression of GSTP1 gene in cancer tissue. CONCLUSION Presence of H. pylori with CagA genotype showed significant individual effect with GSTT1 polymorphism as well as strong synergistic effect in gastric cancer risk. Majority of the gastric cancer samples showed significant negative expression in G/G, A/G (rs1695), and T/T (rs1138272) genotypes. This study shows that GST gene polymorphism was significantly relevant for determining the individual susceptibility to gastric cancer.
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Affiliation(s)
- Souvik Ghatak
- Department of Biotechnology, Mizoram University, Aizawl, Mizoram, India
| | | | - Freda Lalrohlui
- Department of Biotechnology, Mizoram University, Aizawl, Mizoram, India
| | - Payel Chakraborty
- Department of Biotechnology, Mizoram University, Aizawl, Mizoram, India
| | - Soumee Ghosh
- Department of Zoology, University of Calcutta, Kolkata, West Bengal, India
| | - Sudakshina Ghosh
- Department of Zoology, University of Calcutta, Kolkata, West Bengal, India
| | - Madhusudan Das
- Department of Zoology, University of Calcutta, Kolkata, West Bengal, India
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Yeh JM, Hur C, Ward Z, Schrag D, Goldie SJ. Gastric adenocarcinoma screening and prevention in the era of new biomarker and endoscopic technologies: a cost-effectiveness analysis. Gut 2016; 65:563-74. [PMID: 25779597 PMCID: PMC4573370 DOI: 10.1136/gutjnl-2014-308588] [Citation(s) in RCA: 70] [Impact Index Per Article: 7.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/07/2014] [Accepted: 02/21/2015] [Indexed: 12/12/2022]
Abstract
OBJECTIVE To estimate the cost-effectiveness of noncardia gastric adenocarcinoma (NCGA) screening strategies based on new biomarker and endoscopic technologies. DESIGN Using an intestinal-type NCGA microsimulation model, we evaluated the following one-time screening strategies for US men: (1) serum pepsinogen to detect gastric atrophy (with endoscopic follow-up of positive screen results), (2) endoscopic screening to detect dysplasia and asymptomatic cancer (with endoscopic mucosal resection (EMR) treatment for detected lesions) and (3) Helicobacter pylori screening and treatment. Screening performance, treatment effectiveness, cancer and cost data were based on published literature and databases. Subgroups included current, former and never smokers. Outcomes included lifetime cancer risk and incremental cost-effectiveness ratios (ICERs), expressed as cost per quality-adjusted-life-year (QALY) gained. RESULTS Screening the general population at age 50 years reduced the lifetime intestinal-type NCGA risk (0.24%) by 26.4% with serum pepsinogen screening, 21.2% with endoscopy and EMR and 0.2% with H. pylori screening/treatment. Targeting current smokers reduced the lifetime risk (0.35%) by 30.8%, 25.5%, and 0.1%, respectively. For all subgroups, serum pepsinogen screening was more effective and more cost-effective than all other strategies, although its ICER varied from $76,000/QALY (current smokers) to $105,400/QALY (general population). Results were sensitive to H. pylori prevalence, screen age and serum pepsinogen test sensitivity. Probabilistic sensitivity analysis found that at a $100,000/QALY willingness-to-pay threshold, the probability that serum pepsinogen screening was preferred was 0.97 for current smokers. CONCLUSIONS Although not warranted for the general population, targeting high-risk smokers for serum pepsinogen screening may be a cost-effective strategy to reduce intestinal-type NCGA mortality.
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Affiliation(s)
- Jennifer M. Yeh
- Center for Health Decision Science, Harvard School of Public Health, Boston, MA, USA
| | - Chin Hur
- Massachusetts General Hospital Institute for Technology Assessment, Boston, MA, USA
| | - Zachary Ward
- Center for Health Decision Science, Harvard School of Public Health, Boston, MA, USA
| | - Deborah Schrag
- Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA
| | - Sue J. Goldie
- Center for Health Decision Science, Harvard School of Public Health, Boston, MA, USA
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Santibáñez M, Aguirre E, Belda S, Aragones N, Saez J, Rodríguez JC, Galiana A, Sola-Vera J, Ruiz-García M, Paz-Zulueta M, Sarabia-Lavín R, Brotons A, López-Girona E, Pérez E, Sillero C, Royo G. Relationship between tobacco, cagA and vacA i1 virulence factors and bacterial load in patients infected by Helicobacter pylori. PLoS One 2015; 10:e0120444. [PMID: 25794002 PMCID: PMC4368826 DOI: 10.1371/journal.pone.0120444] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/09/2014] [Accepted: 01/22/2015] [Indexed: 12/19/2022] Open
Abstract
Background and Aim Several biological and epidemiological studies support a relationship between smoking and Helicobacter pylori (H. pylori) to increase the risk of pathology. However, there have been few studies on the potential synergistic association between specific cagA and vacA virulence factors and smoking in patients infected by Helicobacter pylori. We studied the relationship between smoking and cagA, vacA i1 virulence factors and bacterial load in H. pylori infected patients. Methods Biopsies of the gastric corpus and antrum from 155 consecutive patients in whom there was clinical suspicion of infection by H. pylori were processed. In 106 patients H. pylori infection was detected. Molecular methods were used to quantify the number of microorganisms and presence of cagA and vacA i1 genes. A standardized questionnaire was used to obtain patients’ clinical data and lifestyle variables, including tobacco and alcohol consumption. Adjusted Odds Ratios (ORadjusted) were estimated by unconditional logistic regression. Results cagA was significantly associated with active-smoking at endoscope: ORadjusted 4.52. Evidence of association was found for vacA i1 (ORadjusted 3.15). Bacterial load was higher in active-smokers, although these differences did not yield statistical significance (median of 262.2 versus 79.4 copies of H. pylori per cell). Conclusions The association between smoking and a higher risk of being infected by a virulent bacterial population and with higher bacterial load, support a complex interaction between H. pylori infection and environmental factors.
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Affiliation(s)
- Miguel Santibáñez
- Departamento de Salud Pública, Universidad de Cantabria, Santander, Spain
- IDIVAL-Instituto de Investigación Marqués de Valdecilla, Santander, Spain
- * E-mail:
| | - Estefanía Aguirre
- Microbiology S. Elche University General Hospital, Elche (Alicante), Spain
| | - Sofía Belda
- Microbiology S. Elche University General Hospital, Elche (Alicante), Spain
| | - Nuria Aragones
- CIBER in Epidemiology and Public Health (CIBERESP), Madrid, Spain
- Environmental and Cancer Epidemiology Unit, National Center of Epidemiology, ISCIII, Madrid, Spain
| | - Jesús Saez
- Digestive Medicine S. Elche University General Hospital, Elche (Alicante), Spain
| | - Juan Carlos Rodríguez
- Microbiology S. Alicante University General Hospital, Alicante, Spain
- Miguel Hernández University, Elche, Spain
| | - Antonio Galiana
- Microbiology S. Elche University General Hospital, Elche (Alicante), Spain
| | - Javier Sola-Vera
- Digestive Medicine S. Elche University General Hospital, Elche (Alicante), Spain
| | | | - María Paz-Zulueta
- Departamento de Enfermería, Universidad de Cantabria, Santander, Spain
| | | | - Alicia Brotons
- Digestive Medicine S. Elche University General Hospital, Elche (Alicante), Spain
| | - Elena López-Girona
- Microbiology S. Elche University General Hospital, Elche (Alicante), Spain
| | - Estefanía Pérez
- Digestive Medicine S. Elche University General Hospital, Elche (Alicante), Spain
| | - Carlos Sillero
- Digestive Medicine S. Elche University General Hospital, Elche (Alicante), Spain
| | - Gloria Royo
- Microbiology S. Elche University General Hospital, Elche (Alicante), Spain
- Miguel Hernández University, Elche, Spain
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17
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Malakar M, Devi KR, Phukan RK, Kaur T, Deka M, Puia L, Sailo L, Lalhmangaihi T, Barua D, Rajguru SK, Mahanta J, Narain K. p53 codon 72 polymorphism interactions with dietary and tobacco related habits and risk of stomach cancer in Mizoram, India. Asian Pac J Cancer Prev 2014; 15:717-23. [PMID: 24568485 DOI: 10.7314/apjcp.2014.15.2.717] [Citation(s) in RCA: 24] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/10/2022] Open
Abstract
BACKGROUND This study was carried out to investigate the interaction of p53 codon 72 polymorphism, dietary and tobacco habits with reference to risk of stomach cancer in Mizoram, India. A total of 105 histologically confirmed stomach cancer cases and 210 age, sex and ethnicity matched healthy population controls were included in this study. MATERIALS AND METHODS The p53 codon 72 polymorphism was detected by PCR-RFLP and sequencing. H. pylori infection status was determined by ELISA. Information on various dietary and tobacco related habits was recorded with a standard questionnaire. RESULTS This study revealed that overall, the Pro/ Pro genotype was significantly associated with a higher risk of stomach cancer (OR, 2.54; 95%CI, 1.01-6.40) as compared to the Arg/Arg genotype. In gender stratified analysis, the Pro/Pro genotype showed higher risk (OR, 7.50; 95%CI, 1.20-47.0) than the Arg/Arg genotype among females. Similarly, the Pro/Pro genotype demonstrated higher risk of stomach cancer (OR, 6.30; 95%CI, 1.41-28.2) among older people (>60 years). However, no such associations were observed in males and in individuals <60 years of age. Smoke dried fish and preserved meat (smoke dried/sun dried) consumers were at increased risk of stomach cancer (OR, 4.85; 95%CI, 1.91-12.3 and OR, 4.22; 95%CI, 1.46-12.2 respectively) as compared to non-consumers. Significant gene-environment interactions exist in terms of p53 codon 72 polymorphism and stomach cancer in Mizoram. Tobacco smokers with Pro/Pro and Arg/Pro genotypes were at higher risk of stomach cancer (OR, 16.2; 95%CI, 1.72-153.4 and OR, 9.45; 95%CI, 1.09-81.7 respectively) than the non-smokers Arg/Arg genotype carriers. The combination of tuibur user and Arg/Pro genotype also demonstrated an elevated risk association (OR, 4.76; 95%CI, 1.40-16.21). CONCLUSIONS In conclusion, this study revealed that p53 codon 72 polymorphism and dietary and tobacco habit interactions influence stomach cancer development in Mizoram, India.
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Affiliation(s)
- Mridul Malakar
- Regional Medical Research Centre, NE Region (Indian Council of Medical Research), Dibrugarh, India E-mail :
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Morais S, Rodrigues S, Amorim L, Peleteiro B, Lunet N. Tobacco smoking and intestinal metaplasia: Systematic review and meta-analysis. Dig Liver Dis 2014; 46:1031-7. [PMID: 25195087 DOI: 10.1016/j.dld.2014.08.034] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/27/2014] [Revised: 07/30/2014] [Accepted: 08/02/2014] [Indexed: 12/11/2022]
Abstract
BACKGROUND The evaluation of specific risk factors for early endpoints in the gastric carcinogenesis pathway may further contribute to the understanding of gastric cancer aetiology. AIMS To quantify the relation between smoking and intestinal metaplasia through systematic review and meta-analysis. METHODS Articles providing data on the association between smoking and intestinal metaplasia were identified in PubMed(®), Scopus(®) and Web of Science™, searched until April 2014, and through backward citation tracking. Summary odds ratio estimates and 95% confidence intervals were computed using the DerSimonian and Laird method. Heterogeneity was quantitatively assessed using the I(2) statistic. RESULTS A total of 32 articles were included in this systematic review and 19 provided data for meta-analysis. Smoking was defined as ever vs. never (crude estimates, six studies, summary odds ratio=1.54, 95% confidence interval: 1.12-2.12, I(2)=67.4%; adjusted estimates, seven studies, summary odds ratio=1.26, 95% confidence interval: 0.98-1.61, I(2)=65.0%) and current vs. non-smokers (crude estimates, seven studies, summary odds ratio=1.27, 95% confidence interval: 0.88-1.84, I(2)=73.4%; adjusted estimates, two studies, summary odds ratio 1.49, 95% confidence interval: 0.99-2.25, I(2)=0.0%). CONCLUSION The weak and non-statistically significant association found through meta-analysis of the available evidence does not confirm smoking as an independent risk factor for intestinal metaplasia.
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Affiliation(s)
- Samantha Morais
- EPIUnit - Institute of Public Health, University of Porto, Porto, Portugal
| | - Sandra Rodrigues
- EPIUnit - Institute of Public Health, University of Porto, Porto, Portugal
| | - Liliana Amorim
- EPIUnit - Institute of Public Health, University of Porto, Porto, Portugal
| | - Bárbara Peleteiro
- EPIUnit - Institute of Public Health, University of Porto, Porto, Portugal; Department of Clinical Epidemiology, Predictive Medicine and Public Health of the University of Porto Medical School, Porto, Portugal
| | - Nuno Lunet
- EPIUnit - Institute of Public Health, University of Porto, Porto, Portugal; Department of Clinical Epidemiology, Predictive Medicine and Public Health of the University of Porto Medical School, Porto, Portugal.
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Bharath TS, Reddy MS, Dhanapal R, Raj Kumar NG, Neeladri Raju P, Saraswathi T. Molecular detection and corelation of Helicobacter pylori in dental plaque and gastric biopsies of dyspeptic patients. J Oral Maxillofac Pathol 2014; 18:19-24. [PMID: 24959032 PMCID: PMC4065441 DOI: 10.4103/0973-029x.131885] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022] Open
Abstract
UNLABELLED Helicobacter pylori is a microaerophilic organism, which colonizes in the gastric mucosa. Its role in etiology and development of acute and chronic gastritis and peptic ulcer diseases is scientifically proved. Oral cavity especially supragingival, subgingival plaque and so forth simulate the same microaerophilic environment favorable for the growth of this bacterium. AIM Detection of H. pylori simultaneously in the oral cavity and gastric mucosa of patients suffering from gastric pathologies. OBJECTIVES To detect H. pylori in the oral cavity and gastric mucosa using endoscopy, urease test and real-time polymerase chain reaction (PCR) (urease A gene). Determining its association and corelation with patient demographics, oral hygiene maintenance and periodontal disease status. MATERIALS AND METHODS Endoscopic examination, oral findings oral hygiene index-simplified (OHI-S) and community periodontal index and treatment needs (CPITN) indices were recorded. Antral biopsies and supragingival plaque samples were taken from 56 dyspeptic adult patients. The collected samples were subjected to histological examination, urease broth test and urease A gene amplification using real-time PCR. RESULT H. pylori was detected in the supragingival plaque of individuals with H. pylori-induced gastric diseases using rapid urease test and real-time PCR analysis. Occurrence of same strain of H. pylori simultaneously in plaque and gastric mucosa was observed. Positive correlation was obtained between the collected indices and quantity of H. pylori colonization.
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Affiliation(s)
- T Sreenivasa Bharath
- Department of Oral Pathology, Vishnu Dental College, Bhimavaram, Andhra Pradesh, India
| | - M Sesha Reddy
- Department of Periodontics, Vishnu Dental College, Bhimavaram, Andhra Pradesh, India
| | - Raghu Dhanapal
- Department of Oral Pathology, Institute of Technology and Science Dental College, Ghaziabad, Uttar Pradesh, India
| | - N Govind Raj Kumar
- Department of Oral Pathology, Vishnu Dental College, Bhimavaram, Andhra Pradesh, India
| | - Pv Neeladri Raju
- Gastroenterologist, Neeladri Institute of Gastroenterology, Bhimavaram, Andhra Pradesh, India
| | - Tr Saraswathi
- Department of Oral Pathology, Vishnu Dental College, Bhimavaram, Andhra Pradesh, India
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20
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Sadjadi A, Derakhshan MH, Yazdanbod A, Boreiri M, Parsaeian M, Babaei M, Alimohammadian M, Samadi F, Etemadi A, Pourfarzi F, Ahmadi E, Delavari A, Islami F, Farzadfar F, Sotoudeh M, Nikmanesh A, Alizadeh BZ, de Bock GH, Malekzadeh R. Neglected role of hookah and opium in gastric carcinogenesis: a cohort study on risk factors and attributable fractions. Int J Cancer 2014; 134:181-188. [PMID: 23797606 PMCID: PMC5821120 DOI: 10.1002/ijc.28344] [Citation(s) in RCA: 72] [Impact Index Per Article: 6.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/12/2013] [Revised: 05/30/2013] [Accepted: 06/03/2013] [Indexed: 01/01/2023]
Abstract
A recent study showed an association between hookah/opium use and gastric cancer but no study has investigated the relationship with gastric precancerous lesions. We examined the association between hookah/opium and gastric precancerous lesions and subsequent gastric cancer. In a population-based cohort study, 928 randomly selected, healthy, Helicobacter pylori-infected subjects in Ardabil Province, Iran, were followed for 10 years. The association between baseline precancerous lesions and lifestyle risk factors (including hookah/opium) was analyzed using logistic regression and presented as odds ratios (ORs) and 95% confidence intervals (CIs). We also calculated hazard ratios (HRs) and 95% CIs for the associations of lifestyle risk factors and endoscopic and histological parameters with incident gastric cancers using Cox regression models. Additionally, the proportion of cancers attributable to modifiable risk factors was calculated. During 9,096 person-years of follow-up, 36 new cases of gastric cancer were observed (incidence rate: 3.96/1,000 persons-years). Opium consumption was strongly associated with baseline antral (OR: 3.2; 95% CI: 1.2-9.1) and body intestinal metaplasia (OR: 7.3; 95% CI: 2.5-21.5). Opium (HR: 3.2; 95% CI: 1.4-7.7), hookah (HR: 3.4; 95% CI: 1.7-7.1) and cigarette use (HR: 3.2; 95% CI: 1.4-7.5), as well as high salt intake, family history of gastric cancer, gastric ulcer and histological atrophic gastritis and intestinal metaplasia of body were associated with higher risk of gastric cancer. The fraction of cancers attributable jointly to high salt, low fruit intake, smoking (including hookah) and opium was 93% (95% CI: 83-98). Hookah and opium use are risk factors for gastric cancer as well as for precancerous lesions. Hookah, opium, cigarette and high salt intake are important modifiable risk factors in this high-incidence gastric cancer area.
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Affiliation(s)
- Alireza Sadjadi
- Digestive Disease Research Center, Tehran University of Medical Sciences, Tehran, Iran; Department of Epidemiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
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21
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Malakar M, Devi KR, Phukan RK, Kaur T, Deka M, Puia L, Baruah D, Mahanta J, Narain K. CYP2E1 genetic polymorphism with dietary, tobacco, alcohol habits, H. pylori infection status and susceptibility to stomach cancer in Mizoram, India. Asian Pac J Cancer Prev 2014; 15:8815-22. [PMID: 25374213 DOI: 10.7314/apjcp.2014.15.20.8815] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2023] Open
Abstract
BACKGROUND The incidence of stomach cancer in India is highest in the state of Mizoram. In this population based matched case-control study, we evaluated the relationship between CYP450 2E1 RsaI polymorphism and risk of stomach cancer taking into considering various important dietary habits along with tobacco, alcohol consumption and H. pylori infection status. MATERIALS AND METHODS A total of 105 histologically confirmed stomach cancer cases and 210 matched healthy population controls were recruited. CYP2E1 RsaI genotypes were determined by PCR-RFLP and H. pylori infection status by ELISA. Information on various dietary, tobacco and alcohol habits was recorded in a standard questionnaire. RESULTS Our study revealed no significant association between the CYP2E1 RsaI polymorphism and overall risk of stomach cancer in Mizoram. However, we observed a non-significant protective effect of the variant allele (A) of CYP2E1 against stomach cancer. Tobacco smokers carrying C/C genotype have three times more risk of stomach cancer, as compared to non-smokers carrying C/C genotype. Both Meiziol and cigarette current and past smokers who smoked for more than 10 times per day and carrying the (C/C) genotype are more prone to develop stomach cancer. Smoke dried fish and preserved meat (smoked/sun dried) consumers carrying C/C genotype possesses higher risk of stomach cancer. No significant association between H. pylori infection and CYP2E1 RsaI polymorphism in terms of stomach cancer was observed. CONCLUSIONS Although no direct association between the CYP2E1 RsaI polymorphism and stomach cancer was observed, relations with different tobacco and dietary risk habits in terms of developing stomach cancer exist in this high risk population of north-eastern part of India. Further in-depth study recruiting larger population is required to shed more light on this important problem.
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Affiliation(s)
- Mridul Malakar
- Regional Medical Research Centre, NE Region (Indian Council of Medical Research), Dibrugarh, Assam, India E-mail :
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Malakar M, Devi KR, Phukan RK, Kaur T, Deka M, Puia L, Barua D, Mahanta J, Narain K. Genetic polymorphism of glutathione S-transferases M1 and T1, tobacco habits and risk of stomach cancer in Mizoram, India. Asian Pac J Cancer Prev 2013; 13:4725-32. [PMID: 23167410 DOI: 10.7314/apjcp.2012.13.9.4725] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open
Abstract
AIM The incidence of stomach cancer in Mizoram is highest in India. We have conducted a population based matched case-control study to identify environmental and genetic risk factors in this geographical area. METHODS A total of 102 histologically confirmed stomach cancer cases and 204 matched healthy population controls were recruited. GSTM1 and GSTT1 genotypes were determined by PCR and H. pylori infections were determined by ELISA. RESULTS Tobacco-smoking was found to be an important risk factor for high incidence of stomach cancer in Mizoram. Meiziol (local cigarette) smoking was a more important risk factor than other tobacco related habits. Cigarette, tuibur (tobacco smoke infused water) and betel nut consumption synergistically increased the risk of stomach cancer. Polymorphisms of GSTM1 and GSTT1 genes were not found to be directly associated with stomach cancer in Mizoram. However, they appeared to be effect modifiers. Persons habituated with tobacco smoking and/or tuibur habit had increased risk of stomach cancer if they carried the GSTM1 null genotype and GSTT1 non-null genotype. CONCLUSION Tobacco smoking, especially meiziol is the important risk factor for stomach cancer in Mizoram. GSTM1 and GSTT1 genes modify the effect of tobacco habits. This study is a first step in understanding the epidemiology of stomach cancer in Mizoram, India.
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Affiliation(s)
- Mridul Malakar
- Regional Medical Research Centre, NE Region (Indian Council of Medical Research), Assam, India
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Yeh JM, Hur C, Schrag D, Kuntz KM, Ezzati M, Stout N, Ward Z, Goldie SJ. Contribution of H. pylori and smoking trends to US incidence of intestinal-type noncardia gastric adenocarcinoma: a microsimulation model. PLoS Med 2013; 10:e1001451. [PMID: 23700390 PMCID: PMC3660292 DOI: 10.1371/journal.pmed.1001451] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/16/2012] [Accepted: 04/05/2013] [Indexed: 02/07/2023] Open
Abstract
BACKGROUND Although gastric cancer has declined dramatically in the US, the disease remains the second leading cause of cancer mortality worldwide. A better understanding of reasons for the decline can provide important insights into effective preventive strategies. We sought to estimate the contribution of risk factor trends on past and future intestinal-type noncardia gastric adenocarcinoma (NCGA) incidence. METHODS AND FINDINGS We developed a population-based microsimulation model of intestinal-type NCGA and calibrated it to US epidemiologic data on precancerous lesions and cancer. The model explicitly incorporated the impact of Helicobacter pylori and smoking on disease natural history, for which birth cohort-specific trends were derived from the National Health and Nutrition Examination Survey (NHANES) and National Health Interview Survey (NHIS). Between 1978 and 2008, the model estimated that intestinal-type NCGA incidence declined 60% from 11.0 to 4.4 per 100,000 men, <3% discrepancy from national statistics. H. pylori and smoking trends combined accounted for 47% (range = 30%-58%) of the observed decline. With no tobacco control, incidence would have declined only 56%, suggesting that lower smoking initiation and higher cessation rates observed after the 1960s accelerated the relative decline in cancer incidence by 7% (range = 0%-21%). With continued risk factor trends, incidence is projected to decline an additional 47% between 2008 and 2040, the majority of which will be attributable to H. pylori and smoking (81%; range = 61%-100%). Limitations include assuming all other risk factors influenced gastric carcinogenesis as one factor and restricting the analysis to men. CONCLUSIONS Trends in modifiable risk factors explain a significant proportion of the decline of intestinal-type NCGA incidence in the US, and are projected to continue. Although past tobacco control efforts have hastened the decline, full benefits will take decades to be realized, and further discouragement of smoking and reduction of H. pylori should be priorities for gastric cancer control efforts.
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Affiliation(s)
- Jennifer M Yeh
- Center for Health Decision Science, Harvard School of Public Health, Boston, Massachusetts, United States of America.
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Zullo A, Hassan C, Romiti A, Giusto M, Guerriero C, Lorenzetti R, Campo SM, Tomao S. Follow-up of intestinal metaplasia in the stomach: When, how and why. World J Gastrointest Oncol 2012; 4:30-6. [PMID: 22468181 PMCID: PMC3312926 DOI: 10.4251/wjgo.v4.i3.30] [Citation(s) in RCA: 69] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/22/2011] [Revised: 10/14/2011] [Accepted: 10/21/2011] [Indexed: 02/05/2023] Open
Abstract
Gastric cancer remains the second most frequent cause of cancer-related mortality in the world. Screening programs in some Asian countries are impractical in the majority of other countries worldwide. Therefore, follow-up of precancerous lesions is advisable for secondary gastric cancer prevention. Intestinal metaplasia (IM) is recognized as a precancerous lesion for gastric cancer, increasing the risk by 6-fold. IM is highly prevalent in the general population, being detected in nearly 1 of every 4 patients undergoing upper endoscopy. The IM prevalence rate is significantly higher in patients with Helicobacter pylori (H. pylori) infection, in first-degree relatives of gastric cancer patients, in smokers and it increases with patient age. IM is the “breaking point” in the gastric carcinogenesis cascade and does not appear to regress following H. pylori eradication, although the cure of infection may slow its progression. Gastric cancer risk is higher in patients with incomplete-type IM, in those with both antral and gastric body involvement, and the risk significantly increases with IM extension over 20% of the gastric mucosa. Scheduled endoscopic control could be cost-effective in IM patients, depending on the yearly incidence of gastric cancer in IM patients, the stage of gastric cancer at diagnosis discovered at surveillance, and the cost of endoscopy. As a pragmatic behavior, yearly endoscopic control would appear justified in all IM patients with at least one of these conditions: (1) IM extension > 20%; (2) the presence of incomplete type IM; (3) first-degree relative of gastric cancer patients; and (4) smokers. In the remaining IM patients, a less intensive (2-3 years) could be proposed.
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Affiliation(s)
- Angelo Zullo
- Angelo Zullo, Cesare Hassan, Michela Giusto, Carmine Guerriero, Roberto Lorenzetti, Salvatore MA Campo, Gastroenterology and Digestive Endoscopy, Nuovo Regina Margherita Hospital, 00153 Rome, Italy
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Sakitani K, Hirata Y, Watabe H, Yamada A, Sugimoto T, Yamaji Y, Yoshida H, Maeda S, Omata M, Koike K. Gastric cancer risk according to the distribution of intestinal metaplasia and neutrophil infiltration. J Gastroenterol Hepatol 2011; 26:1570-5. [PMID: 21575058 DOI: 10.1111/j.1440-1746.2011.06767.x] [Citation(s) in RCA: 48] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
BACKGROUND AND AIM Gastritis and intestinal metaplasia (IM) have long been known to be risk factors for and precursors of gastric cancer. We aimed to elucidate the association between gastric cancer risk and the distribution of precancerous lesions in the stomach by histological analyses. METHODS We analyzed patients from whom two biopsy specimens (one from the antrum and one from the corpus) were obtained by upper gastrointestinal endoscopy. Specimens were assessed for Helicobacter pylori, IM, and neutrophil infiltration (NI). Patients were classified into three groups based on the presence of IM. Patients were also classified into four groups based on the presence of NI. The prevalence of gastric cancer was compared between groups. RESULTS A total of 1395 patients were analyzed. Of these, 54 had gastric cancer (34 intestinal and 20 diffuse type). A multivariate analysis showed that male sex and the distribution of IM were independent risk factors for intestinal-type cancer. Compared with patients without IM (n = 1005), the odds ratio (OR) for patients with IM in the antrum only (n = 240) was 2.34 (95% confidence interval: 1.08-4.96), and that for patients with IM in the corpus (n = 150) was 5.84 (2.92-11.8). However, NI was related to diffuse-type cancer. Compared with patients without NI (n = 899), the OR for patients with NI in the corpus only (n = 122) was 3.66 (1.02-12.2). CONCLUSIONS The histological pattern and distribution of gastric mucosal change assessed by two biopsy specimens were related to gastric cancer.
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Affiliation(s)
- Kosuke Sakitani
- Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
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Wang XQ, Yan H, Terry PD, Wang JS, Cheng L, Wu WA, Hu SK. Interactions between CagA and smoking in gastric cancer. World J Gastroenterol 2011; 17:3330-4. [PMID: 21876621 PMCID: PMC3160537 DOI: 10.3748/wjg.v17.i28.3330] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/28/2010] [Revised: 02/15/2011] [Accepted: 02/22/2011] [Indexed: 02/06/2023] Open
Abstract
AIM: To examine the interactions between cytotoxin-associated gene (CagA) positive Helicobacter pylori infection and smoking in non-cardiac gastric cancer.
METHODS: A case-control study (257 cases and 514 frequency-matched controls) was conducted from September 2008 to July 2010 in Xi’an, China. Cases were newly diagnosed, histologically confirmed non-cardiac cancer. Controls were randomly selected from similar communities to the cases and were further matched by sex and age (± 5 years). A face-to-face interview was performed by the investigators for each participant. Data were obtained using a standardized questionnaire that included questions regarding known or suspected lifestyle and environmental risk factors of gastric cancer. A 5 mL sample of fasting venous blood was taken. CagA infection was serologically detected by enzyme-linked immunosorbent assays.
RESULTS: Smoking and CagA infection were statistically significant risk factors of non-cardiac cancer. CagA was categorized in tertiles, and the odds ratio (OR) was 12.4 (95% CI: 6.1-20.3, P = 0.003) for CagA after being adjusted for confounding factors when the high-exposure category was compared with the low-exposure category. Smokers had an OR of 5.4 compared with subjects who never smoked (95% CI: 2.3-9.0, P = 0.002). The OR of non-cardiac cancer was 3.5 (95% CI: 1.8-5.3) for non-smokers with CagA infection, 3.5 (95% CI: 1.9-5.1) for smokers without CagA infection, and 8.7 (95% CI: 5.1-11.9) for smokers with CagA infection compared with subjects without these risk factors. After adjusting for confounding factors, the corresponding ORs of non-cardiac cancer were 3.2 (95% CI: 1.5-6.8), 2.7 (95% CI: 1.3-4.9) and 19.5 (95% CI: 10.3-42.2), respectively. There was a multiplicative interaction between smoking and CagA, with a synergistic factor of 2.257 (Z = 2.315, P = 0.021).
CONCLUSION: These findings support a meaningful interaction between CagA and smoking for the risk of gastric cancer which may have implications for its early detection.
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Pintalhao M, Dias-Neto M, Peleteiro B, Lopes C, Figueiredo C, David L, Lunet N. Salt intake and type of intestinal metaplasia in Helicobacter pylori-infected Portuguese men. Nutr Cancer 2010; 62:1153-60. [PMID: 21058204 DOI: 10.1080/01635581.2010.513799] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/18/2022]
Abstract
The relation between salt intake and intestinal metaplasia (IM) types and the potential interaction with H. pylori virulence are poorly understood and may contribute to further understand gastric carcinogenesis. We quantified the association between dietary salt exposure and complete, incomplete, and mixed IM, taking into account the potential effect modification according to the virulence of H. pylori infecting strains. H. pylori-infected male volunteers (n = 233) underwent an upper digestive endoscopy and completed questionnaires comprising different measures of salt exposure (main food items/groups contributing to dietary salt intake, estimated dietary sodium intake, visual analogical scale for salt intake, preference for salty/salted foods). A histological diagnosis was assigned based on the most severe lesion observed. H. pylori virulence was assessed by characterizing vacA and cagA genes. Odds ratios were estimated through age- and education-adjusted logistic regression models. The risk of IM was not significantly increased in H. pylori infected subjects with higher levels of salt consumption. The lack of association was consistent across measures of salt exposure, categories of H. pylori virulence, and types of IM. In conclusion, in this H. pylori positive population, salt intake did not increase the risk of any IM type, regardless of the virulence of the infecting strains.
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Affiliation(s)
- Mariana Pintalhao
- Department of Hygiene and Epidemiology, Medical Faculty and Institute of Public Health, University of Porto, Porto, Portugal
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González CA, Pardo ML, Liso JMR, Alonso P, Bonet C, Garcia RM, Sala N, Capella G, Sanz-Anquela JM. Gastric cancer occurrence in preneoplastic lesions: a long-term follow-up in a high-risk area in Spain. Int J Cancer 2010; 127:2654-60. [PMID: 20178099 DOI: 10.1002/ijc.25273] [Citation(s) in RCA: 63] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
There are no established criteria to classify patients into high or low risk of progressing to gastric cancer (GC). The aim of the study was to identify predictors of GC occurrence among patients with gastric preneoplastic lesions. A prospective and retrospective follow-up study was carried out in a province in Spain with one of the highest risk of GC. The study included 478 patients who underwent gastric biopsy in 1988-1994 with diagnoses of normal mucosa, nonatrophic gastritis (NAG), non-metaplastic multifocal atrophic gastritis (MAG) and complete or incomplete intestinal metaplasia (IM) and who accepted to undergo a new biopsy during 2005-2007 or had an event during follow up. Inter- and intra-observer variability of histological diagnosis was assessed. Analysis was done using Cox proportional hazards risk (HR) models. The mean age of the patients was 50 years, 47% were males and the mean follow-up time was 12.8 years. During follow-up, 23 GC (4.8%) were diagnosed (21 adenocarcinomas and 2 lymphomas) with an incidence of 3.77 per 1,000 person per year. The incidence rate of GC for those with incomplete IM was 16.5 per 1,000 person years. Out the 21 adenocarcinomas, 16 had an incomplete IM in the baseline diagnosis. Incomplete IM (HR 11.3; 95% CI 3.8-33.9) and a family history of GC (HR 6.1; 95% CI 1.7-22.4) were the strongest risk factors for gastric adenocarcinoma. Subtyping of IM and family history of GC may be useful for the identification of high-risk patients who need more intensive surveillance.
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Affiliation(s)
- Carlos A González
- Unit of Nutrition, Environment and Cancer, Catalan Institute of Oncology (IDIBELL-ICO), Barcelona, Spain.
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Ren HT, Xu XW, Li AH. Diagnostic value of gene chip test for detection of H.pylori infection and relationship between H.pylori virulence factors and the severity of gastroduodenal lesions. Shijie Huaren Xiaohua Zazhi 2010; 18:2826-2830. [DOI: 10.11569/wcjd.v18.i26.2826] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate the diagnostic value of gene chip test for detection of Helicobacter pylori (H.pylori) infection in children, and to assess the relationship between H.pylori virulence factors and the severity of gastroduodenal lesions.
METHODS: A total of 30 children with symptoms of the digestive system, such as abdominal pain, vomiting, melena and hematemesis, underwent the 13C breath test at Beijing Children's Hospital from October 2007 to April 2008. A gene chip test was then performed for positive cases. The sensitivity and specificity of the gene chip test were analyzed. Gastroscopy was performed in patients diagnosed with H.pylori infection by both of the above methods. The pathological changes in gastroduodenal lesions were examined by gastroscopy to assess the relationship between H.pylori virulence factors and the severity of H.pylori. The results were analyzed by the Kappa test.
RESULTS: The gene chip test has a sensitivity of 93.7%, a specificity of 60%, and a rate of missed diagnosis of 6.3%. The coincidence rate between the 13C breath test and gene chip test is 89.1%, showing a good consistency. H.pylori CagA antibody was detected in 96.6% (29/30) of the patients, while the detection rate of VacA antibody is 3.3%. H.pylori carrying CagA may have a stronger pathogenicity. The presence of CagA antibody was often related with gastritis, peptic ulcer and Henoch-Schonlein syndrome (abdominal type), while the presence of VacA antibody predicted more severe pathological manifestations.
CONCLUSION: The gene chip test has a high specificity and sensitivity in detection of H.pylori infection, and is useful for finding the relationship between H.pylori virulence factors and the severity of disease.
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Dias-Neto M, Pintalhao M, Ferreira M, Lunet N. Salt intake and risk of gastric intestinal metaplasia: systematic review and meta-analysis. Nutr Cancer 2010; 62:133-47. [PMID: 20099187 DOI: 10.1080/01635580903305391] [Citation(s) in RCA: 31] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
The understanding of the association between salt intake and precancerous lesions may contribute to clarify the causal relation with gastric cancer. We systematically reviewed 17 articles addressing the association between dietary salt exposure and gastric intestinal metaplasia and conducted meta-analyses for quantitative synthesis (random effects model). Salt exposure was estimated assessing salted/salty food consumption, preference for salted/salty foods, use of table salt, or sodium urinary excretion. Heterogeneity was also large regarding food items evaluated, consumption categories, and data analysis. The combined odds ratio (OR) was 1.68 (95% confidence interval (CI) = 0.98-2.90; I(2) = 55.4%) for the association between salted/salty meat and intestinal metaplasia (4 studies) and the OR was 1.53 (95% CI = 0.72-3.24; I(2) = 76.8%) for salt preference. There was a positive, nonstatistically significant association between intestinal metaplasia and urinary sodium excretion. The heterogeneity of methodological options and results preclude quantitative synthesis or its proper interpretation, even if the available evidence may suggest a positive association between salt and intestinal metaplasia.
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Affiliation(s)
- Marina Dias-Neto
- Porto University Medical School and Institute of Public Health-University of Porto (ISPUP), 4200-319 Porto, Portugal
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Mansour KB, Keita A, Zribi M, Masmoudi A, Zarrouk S, Labbene M, Kallel L, Karoui S, Fekih M, Matri S, Boubaker J, Cheikh I, Chouaib S, Filali A, Mami NB, Najjar T, Fendri C. Seroprevalence of Helicobacter pylori among Tunisian blood donors (outpatients), symptomatic patients and control subjects. ACTA ACUST UNITED AC 2009; 34:75-82. [PMID: 19879082 DOI: 10.1016/j.gcb.2009.06.015] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/21/2009] [Revised: 06/23/2009] [Accepted: 06/25/2009] [Indexed: 12/18/2022]
Abstract
OBJECTIVES Helicobacter pylori is a worldwide infection, although little data are available in the Tunisian population. The aims of our study were to detect the prevalence of H. pylori in a blood-donor population (n=250) and in another population of hospital-consulting patients comprising 87 symptomatic patients and 59 controls, and to determine the factors that influence the prevalence. MATERIALS AND METHODS Study subjects answered a standardized questionnaire, and IgG anti-H. pylori and anti-cag were detected by ELISA. In the second population, culture and cagA polymerase chain reaction were performed. RESULTS The seroprevalence of H. pylori in blood donors was 64%, and 11% had anti-cag. All patients positive for anti-cag were also positive for anti-H. pylori antibodies. The seroprevalence of H. pylori was 99.3% in the hospital-consulting patients, of whom 55.5% were positive for anti-cag. The difference between the anti-cag and symptomatic patients (66.7%) and controls (39%) was significant. Symptomatic patients had a higher rate of anti-cag (66.7%) compared with the controls (39%) and blood donors (11%). CONCLUSION H. pylori seroprevalence in blood donors is low (64%) compared with symptomatic patients (99.3%), and anti-cag was statistically associated with symptomatic patients and pathology. Also, some environmental factors were correlated with H. pylori seroprevalence.
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Affiliation(s)
- K B Mansour
- Laboratoire de microbiologie, UR04SP08, CHU Rabta, 1007 El Jebbari, Tunis, Tunisia. khansa
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de Vries AC, Capelle LG, Looman CWN, van Blankenstein M, van Grieken NCT, Casparie MK, Meijer GA, Kuipers EJ. Increased risk of esophageal squamous cell carcinoma in patients with gastric atrophy: independent of the severity of atrophic changes. Int J Cancer 2009; 124:2135-8. [PMID: 19107937 DOI: 10.1002/ijc.23955] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/14/2023]
Abstract
An association between gastric atrophy and esophageal squamous cell carcinomas (ESCC) has been described. However, the mechanism of this association is unknown. In this study, we aimed to examine this relationship in a cohort of patients with varying grades of gastric atrophy to increase the understanding about the causality of the association. Patients diagnosed with gastric atrophy between 1991 and 2005 were identified in the Dutch nationwide histopathology registry (PALGA). The incidence of ESCC and, presumably unrelated, small cell lung carcinomas (SCLC) observed in these patients was compared with that in the general Dutch population. Relative risks (RRs) and 95% confidence intervals were calculated by a Poisson model. At baseline histological examination, 97,728 patients were diagnosed with gastric atrophy, of whom 23,278 with atrophic gastritis, 65,934 with intestinal metaplasia and 8,516 with dysplasia. During follow-up, 126 patients were diagnosed with ESCC and 263 with SCLC (overall rates 0.19, respectively 0.39/1,000 person-years at risk). Compared with the general Dutch population, patients with gastric atrophy ran a RR of developing ESCC of 2.2 [95% CI 1.8-2.6] and of SCLC of 1.8 [95% CI 1.6-2.1]. The risk of ESCC did not increase with increasing severity of gastric atrophy (p = 0.90). In conclusion, this study found an association between gastric atrophy and both ESCC and SCLC, but the risk of ESCC did not increase with the severity of gastric atrophy. Therefore, a causal relationship seems unlikely. Confounding factors, such as smoking, may explain both associations.
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Affiliation(s)
- Annemarie C de Vries
- Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands.
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Peleteiro B, Bastos J, Barros H, Lunet N. Systematic review of the prevalence of gastric intestinal metaplasia and its area-level association with smoking. GACETA SANITARIA 2008; 22:236-247. [PMID: 18579050 DOI: 10.1157/13123970] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2025]
Abstract
OBJECTIVES We aimed to show an area-level association between the frequency of intestinal metaplasia (IM) in Helicobacter pylori-infected patients and tobacco consumption. METHODS We systematically reviewed the literature to retrieve data on the prevalence of IM in different countries and performed an ecological analysis to quantify the association between the prevalence of IM among infected subjects and smoking, using data on national tobacco availability. Articles evaluating IM in the general population or in dyspeptic patients were identified by a MEDLINE search. We selected one study per country, giving preference to those for which the study design/populations evaluated provided the highest external validity and inter-study comparability of methodology. RESULTS This systematic review of published data retrieved information for 29 countries from 5 continents depicting a wide variation in the prevalence of IM among H. pylori-infected subjects in different regions, ranging from 3% in Argentina to 55% in New Zealand. In countries exhibiting a simultaneously high prevalence of infection and low incidence of gastric cancer, IM was also relatively infrequent (Thailand, 6%; India, 8.2%; Nigeria, 11.1%; Gambia, 11.8%; Saudi Arabia, 15.5%; Iran, 15.6%; Egypt, 24.4%). A significant correlation was observed between IM prevalence in infected subjects and tobacco availability (r = 0.45; p = 0.02). CONCLUSIONS Our results show that the concept of the African and Asian "enigmas" may be extended to precancerous lesions. Tobacco availability was positively associated with the prevalence of IM among H. pylori-infected subjects at an area level.
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Affiliation(s)
- Bárbara Peleteiro
- Department of Hygiene and Epidemiology, University of Porto Medical School, Porto, Portugal
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Kim HJ, Choi BY, Byun TJ, Eun CS, Song KS, Kim YS, Han DS. The Prevalence of Atrophic Gastritis and Intestinal Metaplasia according to Gender, Age and Helicobacter Pylori Infection in a Rural Population. J Prev Med Public Health 2008; 41:373-9. [PMID: 19037166 DOI: 10.3961/jpmph.2008.41.6.373] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/10/2023] Open
Affiliation(s)
- Hyun Ja Kim
- Department of Preventive Medicine, Hanyang University College of Medicine, Korea
| | - Bo Youl Choi
- Department of Preventive Medicine, Hanyang University College of Medicine, Korea
| | - Tae Joon Byun
- Department of Internal Medicine, Hanyang University College of Medicine, Korea
| | - Chang Soo Eun
- Department of Internal Medicine, Hanyang University College of Medicine, Korea
| | - Kyu Sang Song
- Department of Pathology, Chungnam National University College of Medicine, Korea
| | | | - Dong Soo Han
- Department of Internal Medicine, Hanyang University College of Medicine, Korea
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de Vries AC, Kuipers EJ. Epidemiology of premalignant gastric lesions: implications for the development of screening and surveillance strategies. Helicobacter 2007; 12 Suppl 2:22-31. [PMID: 17991173 DOI: 10.1111/j.1523-5378.2007.00562.x] [Citation(s) in RCA: 54] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Gastric cancer is one of the most common cancers worldwide; however, gastric cancer incidence varies greatly between different geographic areas. As gastric cancer is usually diagnosed at an advanced stage, the disease causes considerable morbidity and mortality. To detect gastric carcinomas at an early and curable stage, screening and surveillance seem necessary. Premalignant gastric lesions are well known risk factors for the development of intestinal type gastric adenocarcinomas. In a multistep cascade, chronic Helicobacter pylori-induced gastritis progresses through premalignant stages of atrophic gastritis, intestinal metaplasia and dysplasia, to eventually gastric cancer. Therefore, this cascade may provide a basis for early detection and treatment of gastric cancer. Epidemiology of gastric cancer and premalignant gastric lesions should guide the development of screening and surveillance strategies, as distinct approaches are required in countries with low and high gastric cancer incidences.
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Affiliation(s)
- Annemarie C de Vries
- Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands.
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Peleteiro B, Lunet N, Figueiredo C, Carneiro F, David L, Barros H. Smoking, Helicobacter pylori virulence, and type of intestinal metaplasia in Portuguese males. Cancer Epidemiol Biomarkers Prev 2007; 16:322-6. [PMID: 17301266 DOI: 10.1158/1055-9965.epi-06-0885] [Citation(s) in RCA: 44] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022] Open
Abstract
High-virulence Helicobacter pylori strains and smoking increase the risk of gastric precancerous lesions. However, its association with specific types of intestinal metaplasia has been poorly studied. We aimed to quantify the association between different types of intestinal metaplasia (complete, incomplete, and mixed) and these two risk factors. Male volunteers (n = 227) underwent an upper digestive endoscopy and completed symptoms and lifestyle questionnaires. A histologic diagnosis was assigned based on the lesions found in any of the biopsy specimens (antrum, body, or incisura). H. pylori vacA and cagA were directly genotyped by multiplex PCR and reverse hybridization. Each participant's smoking status at the time of endoscopy was assessed. Logistic and multinomial logistic regression models were fitted (including H. pylori virulence, smoking, age, and education as independent variables) using normal/chronic nonatrophic gastritis as the reference category. Compared with never smokers infected with low-virulence strains, the risk of intestinal metaplasia was increased in subjects infected with high-virulence strains [odds ratio (OR), 5.74; 95% confidence interval (95% CI), 1.68-19.63] and in ever smokers (OR, 3.54; 95% CI, 1.30-9.61). In ever smokers infected with high-virulence H. pylori strains, the risk of intestinal metaplasia was further increased (OR, 8.61; 95% CI, 3.07-24.17). Infection with high-virulence strains significantly increased the risk of incomplete (OR, 9.81; 95% CI, 2.39-40.31) and mixed (OR, 3.28; 95% CI, 1.51-7.14) intestinal metaplasia. Complete (OR, 2.82; 95% CI, 1.01-7.88) and mixed (OR, 2.97; 95% CI, 1.12-7.84) intestinal metaplasia were more frequent among ever smokers. High-virulence H. pylori strains and smoking are differentially associated with the complete and incomplete types of intestinal metaplasia, suggesting divergent pathways in gastric carcinogenesis.
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Affiliation(s)
- Bárbara Peleteiro
- Department of Hygiene and Epidemiology, Medical Faculty of the University of Porto, Portugal.
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Ito LS, Oba-Shinjo SM, Shinjo SK, Uno M, Marie SKN, Hamajima N. Community-based familial study of Helicobacter pylori infection among healthy Japanese Brazilians. Gastric Cancer 2007; 9:208-16. [PMID: 16952040 DOI: 10.1007/s10120-006-0384-5] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/07/2005] [Accepted: 05/14/2006] [Indexed: 02/06/2023]
Abstract
BACKGROUND The present study of Helicobacter pylori infection was conducted in family units of Japanese Brazilians living in São Paulo city. The authors attempted to determine the seroprevalence of H. pylori infection within family units of Japanese Brazilians and to identify risk factors associated with intrafamilial transmission. METHODS The seroprevalence was determined in 1037 healthy and asymptomatic volunteer subjects aged 0-69 years (530 adults and 507 children) of 265 families. Demographic data and details of living conditions were obtained from each family. RESULTS H. pylori seropositive infection was found in 39.2% of the parents and 9.3% of the children. A reduced risk of H. pylori infection was found for girls (odds ratio [OR] 0.45; 95% confidence interval [CI], 0.23-0.86). The prevalence of infection was 3.5% for children with uninfected parents; 9.9% (OR, 2.51; 95% CI, 0.95-6.61) for those with a seronegative mother and a seropositive father; 14.9% (OR, 4.93; 95% CI, 1.86-13.06) for those with a seropositive mother and a seronegative father; and 16.0% (OR, 5.29; 95% CI, 1.98-14.14) for those with seropositive parents. On multivariate analysis, the use of a pacifier, and mother's symptoms of nausea and vomiting were significantly associated with the risk of H. pylori infection for children, and the child having her/his own room was significantly associated with a reduced risk. Income was not associated with H. pylori infection in children and was inversely associated in parents. CONCLUSION The prevalence of H. pylori infection in family units of Japanese Brazilians supports the hypothesis of a predominant role for mother-child transmission of H. pylori infection, mainly through contact with regurgitated gastric juice in the mother's mouth.
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Affiliation(s)
- Lucy S Ito
- Japanese Brazilian Health Professional Volunteer Group, São Paulo, Brazil
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Lunet N, Lacerda-Vieira A, Barros H. Fruit and vegetables consumption and gastric cancer: a systematic review and meta-analysis of cohort studies. Nutr Cancer 2006; 53:1-10. [PMID: 16351501 DOI: 10.1207/s15327914nc5301_1] [Citation(s) in RCA: 113] [Impact Index Per Article: 5.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Fruit and vegetable intake is widely recognized as protective for gastric cancer occurrence but prospective research challenged this belief. To evaluate the influence of design options in such results we did a meta-analysis of relevant published cohort studies identified from inception to 2004 in PubMed, EMBASE, and LILACS. Random-effects meta-analysis, stratification, and meta-regression were used to pool effects and to analyze the association with type of outcome event and length of follow-up independent of other study characteristics. An inverse association was observed between fruit intake and gastric cancer incidence (relative risk, RR = 0.82; 95% confidence interval, CI = 0.73-0.93) and stronger for follow-up periods of > or = 10 yr (RR = 0.66; 95% CI = 0.52-0.83) but not when the study outcome was death (RR = 1.08; 95% CI = 0.86-1.35). For vegetables, the RR was 0.88 (95% CI = 0.69-1.13) using all incidence studies and 0.71 (95% CI = 0.53-0.94) when considering only those with the longer follow-up. The association observed between vegetable intake and gastric cancer mortality was 1.05 (95% CI = 0.89-1.25). Other study characteristics assessed added no significant contribution to explain heterogeneity. This meta-analysis showed that design options might play a key role in the observed magnitude or the direction of the association between fruit and vegetable intake and gastric cancer.
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Affiliation(s)
- Nuno Lunet
- Department of Hygiene and Epidemiology, University of Porto Medical School, Portugal.
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Bleich A, Mahler M. Environment as a Critical Factor for the Pathogenesis and Outcome of Gastrointestinal Disease: Experimental and Human Inflammatory Bowel Disease and Helicobacter-Induced Gastritis. Pathobiology 2006; 72:293-307. [PMID: 16582581 DOI: 10.1159/000091327] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/11/2005] [Accepted: 10/18/2005] [Indexed: 12/20/2022] Open
Abstract
Environmental factors play an important role in the manifestation, course, and prognosis of diseases of the gastrointestinal tract such as inflammatory bowel disease (IBD) and Helicobacter pylori-induced gastritis. These two disease complexes were chosen for a discussion of the contribution of environmental factors to the disease outcome in humans and animal models. Dissecting complex diseases like IBD and Helicobacter-induced gastritis has shown that the outcome of disease depends on the allelic constellation of a host and the microbial and physical environments. Host alleles predisposing to a disease in one genomic and/or environmental milieu may not be deleterious in other constellations; on the other hand, microbes can have different effects in different hosts and under different environmental conditions. The impact of the complex interaction between host genetics and environmental factors, particularly microflora, also underlines the importance of a defined genetic background and defined environments in animal studies and is indicative of the difficulties in analyzing complex diseases in humans.
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Affiliation(s)
- A Bleich
- Institute for Laboratory Animal Science and Central Animal Facility, Hannover Medical School, Hannover, Germany.
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Environmental Factors in Helicobacter pylori-Related Gastric Precancerous Lesions in Venezuela. Cancer Epidemiol Biomarkers Prev 2004. [DOI: 10.1158/1055-9965.468.13.3] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
Abstract
Abstract
Although Helicobacter pylori (HP) infection has been acknowledged to play an etiological role in gastric carcinogenesis, its relatively weak association particularly in developing countries suggests critical roles of cofactors. Among a population with an extremely high prevalence of HP infection (≈95%) in Venezuela, we examined the relationship of household characteristics, smoking, alcohol drinking, dietary consumption, and plasma nutrient levels with the prevalence of three different stages of gastric precancerous lesions, chronic atrophic gastritis (AG; n = 337), intestinal metaplasia (IM; n = 551), and dysplasia (n = 157), in comparison with those without any of these lesions (n = 1154). Length of refrigerator use was marginally inversely associated with the prevalence of the precursor lesions studied. The association was most pronounced for AG followed by dysplasia. On the other hand, smoking status was a significant predictor for IM and dysplasia. Those smoking ≥10 cigarettes/day had 1.8-fold risk of IM and 3.6-fold risk of dysplasia compared with never smokers. There were no associations with alcohol consumption. When six food groups known to be associated with stomach cancer risk in Venezuela were tested, the prevalence of these lesions progressively increased with increasing starchy vegetable consumption and decreasing fresh fruit/fruit juice consumption. The association with fruits was more evident for dysplasia and AG and that with starchy vegetables for IM and AG. However, there were no inverse associations with plasma antioxidant vitamins. These findings offer important public health implications in preventing progression of HP-associated gastric precancerous lesions in high-risk populations.
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Gumurdulu Y, Serin E, Ozer B, Kayaselcuk F, Ozsahin K, Cosar AM, Gursoy M, Gur G, Yilmaz U, Boyacioglu S. Low eradication rate of Helicobacter pylori with triple 7-14 days and quadriple therapy in Turkey. World J Gastroenterol 2004; 10:668-71. [PMID: 14991935 PMCID: PMC4716906 DOI: 10.3748/wjg.v10.i5.668] [Citation(s) in RCA: 83] [Impact Index Per Article: 4.0] [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: The eradication rate of Helicobacter pylori (H pylori) shows variation among countries and regimens of treatment. We aimed to study the eradication rates of different regimens in our region and some factors affecting the rate of eradication.
METHODS: One hundred and sixty-four H pylori positive patients (68 males, 96 females; mean age: 48 ± 12 years) with duodenal or gastric ulcer without a smoking history were included in the study. The patients were divided into three groups according to the treatment regimens. Omeprazole 20 mg, clarithromycin 500 mg, amoxicillin 1 g were given twice daily for 1 week (Group I) and 2 weeks (Group II). Patients in Group III received bismuth subsitrate 300 mg, tetracyline 500 mg and metronidazole 500 mg four times daily in addition to Omeprazole 20 mg twice daily. Two biopsies each before and after treatment were obtained from antrum and corpus, and histopathologically evaluated. Eradication was assumed to be successful if no H pylorus was detected from four biopsy specimens taken after treatment. The effects of factors like age, sex, H pylori density on antrum and corpus before treatment, the total H pylori density, and the inflammation scores on the rate of H pylori eradication were evaluated.
RESULTS: The overall eradication rate was 42%. The rates in groups II and III were statistically higher than that in group I (P < 0.05). The rates of eradication were 24.5%, 40.7% and 61.5% in groups I, II and III, respectively. The eradication rate was negatively related to either corpus H pylori density or total H pylori density (P < 0.05). The median age was older in the group in which the eradication failed in comparison to that with successful eradication (55 yr vs 39 yr, P < 0.001). No correlation between sex and H pylori eradication was found.
CONCLUSION: Our rates of eradication were significantly lower when compared to those reported in literature. We believe that advanced age and high H pylori density are negative predictive factors for the rate of H pylori eradication.
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Affiliation(s)
- Yuksel Gumurdulu
- Baskent Universitesi Tip Fakultesi, Adana Uygulama ve Arastirma Merkezi, Dadaloğlu Mahallesi, 39 Sokak, No: 6, 01250 Adana, Turkey.
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Chen SY, Liu TY, Shun CT, Wu MS, Lu TH, Lin JT, Sheu JC, Santella RM, Chen CJ. Modification effects of GSTM1, GSTT1 and CYP2E1 polymorphisms on associations between raw salted food and incomplete intestinal metaplasia in a high-risk area of stomach cancer. Int J Cancer 2004; 108:606-12. [PMID: 14696128 DOI: 10.1002/ijc.11535] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
Incomplete intestinal metaplasia (IM) is a precursor of stomach cancer. To identify risk factors of incomplete IM, a 2-stage survey was carried out in 1995 among 1,485 residents in Matzu, an area with highest mortality from stomach cancer in Taiwan. There were 312 study subjects including 174 men and 138 women sampled for the gastroendoscopic examination of IM. Information on personal and familial history of stomach cancer, cigarette smoking, alcohol consumption and intake frequency of various salted food items were obtained by personal interview based on a structured questionnaire. Blood samples were collected from each participant. Four biopsies per subject were taken from all subjects at gastroendoscopic examination to diagnose the status of IM pathologically. The Helicobacter pylori in biopsies was detected by the histomorphological or immunochemistry method, and antibodies against H. pylori in serum by the enzyme-linked immunosorbent assay. Plasma level of selenium was determined by atomic absorption spectrometry, plasma level of retinol, alpha-tocopherol, alpha-carotene, and beta-carotene by high performance liquid chromatography, genotypes of glutathione S-transferase (GST) M1 and T1 and cytochrome P450 (CYP) 2E1 by polymerase chain reaction. The significant association between history of stomach cancer among first-degree relatives and incomplete IM was found (odds ratio [OR] = 2.50; 95% confidence interval [CI] = 1.15-5.43). There was no association between H. pylori infection and incomplete IM. Alcohol drinkers for >20 years had an elevated risk compared to non-drinkers (OR = 3.34; 95% CI = 1.19-9.39). No associations between incomplete IM and plasma levels of selenium, retinol, alpha-tocopherol, alpha-carotene and beta-carotene were found. Salted food including salted meat, dehydrated salted vegetables and raw salted seafood consumed at ages of </=15 and 16-30 years old was associated with an increased IM risk with OR ranging from 2-3. More striking associations between incomplete IM and salted food intake were observed among subjects with genotypes of GSTM1 null, GSTT1 non-null and CYP2E1 c1/c1. Our study suggests the importance of gene-environment interaction on the development of incomplete IM.
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Affiliation(s)
- Shu-Yuan Chen
- Division of Biostatistics and Bioinformatics, National Health Research Institutes, Taipei, Taiwan
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Russo A, Maconi G, Lombardo C, Settesoldi D, Ferrari D, Ravagnani F, Andreola S, Pizzetti P, Spinelli P, Bertario L. Human leukocyte antigen class II genes and Helicobacter pylori infection: does genotype overwhelm environmental exposure? Nutrition 2003; 19:708-15. [PMID: 12921878 DOI: 10.1016/s0899-9007(02)01034-1] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
OBJECTIVE We investigated associations between human leukocyte antigen class II genes, environmental exposures, and Helicobacter pylori infection. METHODS Sixty-eight subjects with histologically confirmed H. pylori and intestinal metaplasia (cases) and 70 healthy subjects without H. pylori (controls) matched for age, sex, and year of birth were included in this study. All patients answered a detailed questionnaire designed to collect sociodemographic characteristics, smoking, alcohol drinking, and dietary habits. Human leukocyte antigen class II genes were typed with genomic DNA. The cytotoxins CagA and VacA were investigated with serology. Odds ratios and corresponding 95% confidence intervals were estimated from multivariate conditional logistic regression. Multiple correspondence analysis was used to represent the interrelationships of a multiple contingency table. RESULTS Human leukocyte antigen DRB1, DQA1, and DQB1 genotypes were not significantly associated with H. pylori infection and intestinal metaplasia. No significant association with blood group or Lewis antigen system was found. However, multiple correspondence analysis clearly associated H. pylori with environmental exposure: the control group largely consumed olive oil, fresh fruits, and vegetables and histories of never or formerly smoking and the case group (those positive for H. pylori and metaplasia) largely consumed eggs, meat and butter and had histories of smoking cigarettes. CONCLUSIONS These findings suggested that H. pylori infection is not influenced by a genetic compound and confirmed the relevance of environmental exposure.
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Affiliation(s)
- Antonio Russo
- Epidemiology Unit, Local Health Authority of Milan, Milan, Italy
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Chao A, Thun MJ, Henley SJ, Jacobs EJ, McCullough ML, Calle EE. Cigarette smoking, use of other tobacco products and stomach cancer mortality in US adults: The Cancer Prevention Study II. Int J Cancer 2002; 101:380-9. [PMID: 12209964 DOI: 10.1002/ijc.10614] [Citation(s) in RCA: 107] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
Cigarette smoking is associated with increased risk of stomach cancer in many studies but there are limited data on this relationship in women and on risk associated with use of tobacco products other than cigarettes. We examined stomach cancer death rates in relation to cigarette smoking in women and use of cigarette, cigar, pipe, or smokeless tobacco in men in a nationwide prospective mortality study in the United States (US). Cohort follow-up from 1982-96 identified 996 and 509 stomach cancer deaths among 467,788 men and 588,053 women, respectively. Cox proportional hazards models were fitted to estimate rate ratios (RR) and 95% confidence intervals (CI) using non-users of tobacco as the referent group. Multivariate-adjusted RRs were the highest for men who currently smoked cigars (RR = 2.29, 95% CI = 1.49-3.51) or cigarettes (RR = 2.16, 95% CI = 1.75-2.67) and both increased with smoking duration. Women who currently (RR = 1.49, 95% CI = 1.18-1.88) or formerly (RR = 1.36, 95% CI = 1.08-1.71) smoked cigarettes were at significantly increased risk, as were men who formerly smoked cigarettes (RR = 1.55, 95% CI = 1.28-1.88), or currently (RR = 1.81, 95% CI = 1.40-2.35) or formerly (RR: 1.57, 95% CI = 1.22-2.03) used more than one type of tobacco. Men who reported a history of chronic indigestion or gastroduodenal ulcer had substantially higher mortality rates associated with current cigarette (RR = 3.45, 95% CI = 2.05-5.80) or cigar (RR = 8.93, 95% CI = 4.02-19.90) smoking, as did men who were current aspirin users. If causal, the estimated proportion of stomach cancer deaths attributable to tobacco use would be 28% in US men and 14% in women. We conclude that prolonged use of tobacco products is associated with increased stomach cancer mortality in men and women. The accumulated evidence from this and other studies support reconsidering stomach cancer as a tobacco-related cancer.
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Affiliation(s)
- Ann Chao
- Epidemiology and Surveillance Research, American Cancer Society, Atlanta, GA 30329-4251, USA.
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