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Shahini E, Maida M. Surveillance strategies for precancerous gastric conditions after Helicobacter pylori eradication: There is still need for a tailored approach. World J Gastroenterol 2021; 27:8033-8039. [PMID: 35046629 PMCID: PMC8678819 DOI: 10.3748/wjg.v27.i46.8033] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/04/2021] [Revised: 10/03/2021] [Accepted: 11/25/2021] [Indexed: 02/06/2023] Open
Abstract
Prevailing evidence declares that Helicobacter pylori (H. pylori) eradication therapy could shift precancerous gastric conditions (PGC) and positively confines gastric cancer (GC) risk during long-term endoscopic follow-up. Nonetheless, there is a yet unsolved controversy regarding the best-individualized surveillance strategies following H. pylori eradication, based on malignant risk stratification. This last dispute is due to the uncertainty of contemporary evidence and the role of H. pylori inflammatory changes in underestimating PGC at the index endoscopy. However, the current state of the art suggests that it is reasonable that high-quality endoscopy with histological assessment for the most accurate diagnosis of PGC may be delayed in selected high-risk patients without alarm signs for malignancy, following the eradication of H. pylori. Notwithstanding, these aspects need to be further examined in the next future to establish and optimize the most beneficial and cost-effective strategies for recognizing and managing H. pylori-positive patients with PGC in the short- and long-term follow-up. Accordingly, additional studies are yet required to sharpen the hazard stratification of patients with the greatest chance of GC evolution, also recognizing the evolving racial, ethnic, immigration factors and the necessity of novel biomarkers to limit GC development or accomplish a diagnosis of malignancy at an early stage.
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Affiliation(s)
- Endrit Shahini
- Division of Gastroenterology, National Institute of Research "Saverio De Bellis", Castellana Grotte (Bari) 70013, Italy
| | - Marcello Maida
- Section of Gastroenterology, S.Elia - Raimondi Hospital, Caltanissetta 93017, Italy
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Waldum HL. Clinical consequences of controversies in gastric physiology. Scand J Gastroenterol 2020; 55:752-758. [PMID: 32515242 DOI: 10.1080/00365521.2020.1771758] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
Studies on the regulation of gastric acid secretion started more than 100 years ago at an early phase of experimental physiology. In nearly the whole last century there were disputes about the interpretation of the findings: the interaction between the three principle gastric acid secretagogues acetylcholine, gastrin and histamine, the cell producing the relevant histamine which turned out to be the ECL cell, the ability of the ECL cell to divide and thus develop into tumours, the classification of gastric carcinomas and the mechanism for Helicobacter pylori carcinogenesis. The elucidation of the central role of the ECL cell and thus its main regulator, gastrin, solve all these controversies, and gives a solid base for handling upper gastrointestinal diseases.
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Affiliation(s)
- Helge L Waldum
- Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway
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Abstract
Introduction: Atrophic gastritis (AG) is a complex syndrome which arises as a consequence of H. pylori infection or in the context of gastric autoimmunity. It often deserves a benign course but may lead to potentially life-threatening complications: cancer and anemia. This review aims to address traditional and innovative knowledge on this often under-diagnosed disorder.Areas covered: This review covers clinical presentation, risk factors, diagnosis, and management of AG and provides an updated resource for clinicians to get insight into this challenging disorder. Updated literature was searched in PubMed. Manual search from reference lists of publications was performed.Expert opinion: A case-finding strategy may be beneficial in individuals with anemia, dyspepsia, autoimmune thyropaties and type 1 diabetes, and family history of gastric cancer. AG is linked to gastric cancer risk and endoscopic surveillance is indicated according to topography of gastric atrophy and risk factors. The direction for future research in AG is summarized.
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Affiliation(s)
- Bruno Annibale
- Department of Medical-Surgical Sciences and Translational Medicine, Sant'Andrea Hospital, Sapienza University of Rome, Roma, Italy
| | - Gianluca Esposito
- Department of Medical-Surgical Sciences and Translational Medicine, Sant'Andrea Hospital, Sapienza University of Rome, Roma, Italy
| | - Edith Lahner
- Department of Medical-Surgical Sciences and Translational Medicine, Sant'Andrea Hospital, Sapienza University of Rome, Roma, Italy
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Lahner E, Zagari RM, Zullo A, Di Sabatino A, Meggio A, Cesaro P, Lenti MV, Annibale B, Corazza GR. Chronic atrophic gastritis: Natural history, diagnosis and therapeutic management. A position paper by the Italian Society of Hospital Gastroenterologists and Digestive Endoscopists [AIGO], the Italian Society of Digestive Endoscopy [SIED], the Italian Society of Gastroenterology [SIGE], and the Italian Society of Internal Medicine [SIMI]. Dig Liver Dis 2019; 51:1621-1632. [PMID: 31635944 DOI: 10.1016/j.dld.2019.09.016] [Citation(s) in RCA: 99] [Impact Index Per Article: 16.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/29/2019] [Revised: 09/03/2019] [Accepted: 09/23/2019] [Indexed: 02/08/2023]
Abstract
Chronic atrophic gastritis (CAG) is an underdiagnosed condition characterised by translational features going beyond the strict field of gastroenterology as it may manifest itself by a variable spectrum of gastric and extra-gastric symptoms and signs. It is relatively common among older adults in different parts of the world, but large variations exist. Helicobacter pylori-related CAG [multifocal] and autoimmune CAG (corpus-restricted) are apparently two different diseases, but they display overlapping features. Patients with cobalamin and/or iron deficiency anaemia or autoimmune disorders, including autoimmune thyroiditis and type 1 diabetes mellitus, should be offered screening for CAG. Pepsinogens, gastrin-17, and anti-H. pylori antibodies serum assays seem to be reliable non-invasive screening tools for the presence of CAG, helpful to identify individuals to refer to gastroscopy with five standard gastric biopsies in order to obtain histological confirmation of diagnosis. Patients with CAG are at increased risk of developing gastric cancer, and they should be estimated with histological staging systems (OLGA or OLGIM). H. pylori eradication may be beneficial by modifying the natural history of atrophy, but not that of intestinal metaplasia. Patients with advanced stages of CAG (Stage III/IV OLGA or OLGIM) should undergo endoscopic surveillance every three years, those with autoimmune CAG every three-five years. In patients with CAG, a screening for autoimmune thyroid disease and micronutrient deficiencies, including iron and vitamin B12, should be performed. The optimal treatment for dyspeptic symptoms in patients with CAG remains to be defined. Proton pump inhibitors are not indicated in hypochlorhydric CAG patients.
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Affiliation(s)
- Edith Lahner
- Department of Surgical-Medical Sciences and Translational Medicine, Digestive and Liver Disease Unit, Sant'Andrea Hospital, Sapienza University of Rome, Rome, Italy.
| | | | - Angelo Zullo
- Gastroenterology and Digestive Endoscopy, 'Nuovo Regina Margherita' Hospital, Rome, Italy
| | - Antonio Di Sabatino
- First Department of Internal Medicine, IRCCS San Matteo Hospital Foundation, University of Pavia, Pavia, Italy
| | - Alberto Meggio
- Department of Gastroenterology, Trento and Rovereto Hospital, Trento, Italy
| | - Paola Cesaro
- Digestive Endoscopy Unit and Gastroenterology, Fondazione Poliambulanza, Brescia, Italy
| | - Marco Vincenzo Lenti
- First Department of Internal Medicine, IRCCS San Matteo Hospital Foundation, University of Pavia, Pavia, Italy
| | - Bruno Annibale
- Department of Surgical-Medical Sciences and Translational Medicine, Digestive and Liver Disease Unit, Sant'Andrea Hospital, Sapienza University of Rome, Rome, Italy
| | - Gino Roberto Corazza
- First Department of Internal Medicine, IRCCS San Matteo Hospital Foundation, University of Pavia, Pavia, Italy
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Wang D, Guo Q, Yuan Y, Gong Y. The antibiotic resistance of Helicobacter pylori to five antibiotics and influencing factors in an area of China with a high risk of gastric cancer. BMC Microbiol 2019; 19:152. [PMID: 31272365 PMCID: PMC6611032 DOI: 10.1186/s12866-019-1517-4] [Citation(s) in RCA: 55] [Impact Index Per Article: 9.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/09/2018] [Accepted: 06/17/2019] [Indexed: 12/18/2022] Open
Abstract
Background H. pylori exhibits antibiotic resistance with regional differences. In this paper, we explored antibiotic resistance of H. pylori to five antibiotics in an area with a high risk of gastric cancer. Results H. pylori resistance rates to metronidazole, levofloxacin, clarithromycin, amoxicillin, and tetracycline were 78.0, 56.0, 31.0, 9.0, and 15.0%, respectively. Double, triple, quadruple, and quintuple resistance rates were 23, 20, 6, and 4%, respectively. The clarithromycin and multidrug resistance rates were significantly higher in males than females (clarithromycin: 44.4% vs 15.2%, respectively, P = 0.002; multidrug: 75.5% vs 37.2%, respectively; P < 0.001). During the three periods of 1998–1999, 2002–2004 and 2016–2017, the resistance rates to levofloxacin and amoxicillin were increasing (OR: 2.089, 95%CI: 1.142–3.821, P = 0.017; and OR: 5.035, 95%CI: 1.327–19.105, P = 0.018, respectively). The antibiotic resistance rates were unassociated with the host disease state. Metronidazole resistance was lower in the vacAs1m1/m2 group than the vacAs1m1m2 group (65% vs 85.7%, respectively; P = 0.026). As for levofloxacin resistance, it was higher with cagA+ than cagA− (60.9% vs 23.1%, respectively; P = 0.020) but lower with slyD+ than slyD− (41.4% vs 68.5%, respectively; P = 0.009). Clarithromycin had a lower resistance rate with iceA++ than iceA−+ (19.7% vs 52.4%, respectively; P = 0.017). For amoxicillin, the iceA++ group had a lower resistance rate than the iceA−− group (1.6% vs 27.8%, respectively; P = 0.009). Conclusions The total resistance rates of H. pylori to metronidazole, levofloxacin, clarithromycin, amoxicillin, and tetracycline were high in Zhuanghe. The resistanc rates to levofloxacin and amoxicillin increased over time. Clarithromycin resistance was associated with male and iceA. The resistance of metronidazole was related to vacA. Levofloxacin resistance was concerned with cagA and slyD and amoxicillin resistance was concerned with iceA. While, the antibiotic resistance of H. pylori had nothing to do with the status of gastric disease.
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Affiliation(s)
- Dan Wang
- Tumor Etiology and Screening Department of Cancer Institute and General Surger, the First Hospital of China Medical University, Shenyang, 110001, China.,Key Laboratory of Cancer Etiology and Prevention in Liaoning Education Department, the First Hospital of China Medical University, Shenyang, 110001, China.,Key Laboratory of GI Cancer Etiology and Prevention in Liaoning Province, the First Hospital of China Medical University, Shenyang, 110001, China
| | - Qianqian Guo
- Tumor Etiology and Screening Department of Cancer Institute and General Surger, the First Hospital of China Medical University, Shenyang, 110001, China.,Key Laboratory of Cancer Etiology and Prevention in Liaoning Education Department, the First Hospital of China Medical University, Shenyang, 110001, China.,Key Laboratory of GI Cancer Etiology and Prevention in Liaoning Province, the First Hospital of China Medical University, Shenyang, 110001, China
| | - Yuan Yuan
- Tumor Etiology and Screening Department of Cancer Institute and General Surger, the First Hospital of China Medical University, Shenyang, 110001, China. .,Key Laboratory of Cancer Etiology and Prevention in Liaoning Education Department, the First Hospital of China Medical University, Shenyang, 110001, China. .,Key Laboratory of GI Cancer Etiology and Prevention in Liaoning Province, the First Hospital of China Medical University, Shenyang, 110001, China.
| | - Yuehua Gong
- Tumor Etiology and Screening Department of Cancer Institute and General Surger, the First Hospital of China Medical University, Shenyang, 110001, China. .,Key Laboratory of Cancer Etiology and Prevention in Liaoning Education Department, the First Hospital of China Medical University, Shenyang, 110001, China. .,Key Laboratory of GI Cancer Etiology and Prevention in Liaoning Province, the First Hospital of China Medical University, Shenyang, 110001, China.
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6
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Chen F, Liu Y, Tsay A, McAllister BP, Karamchandani DM. Hit or a miss: Concordance between histopathologic-endoscopic findings in gastric mucosal biopsies. Ann Diagn Pathol 2019; 38:106-114. [DOI: 10.1016/j.anndiagpath.2018.12.002] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/15/2018] [Revised: 11/30/2018] [Accepted: 12/13/2018] [Indexed: 12/21/2022]
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Wang D, Li Q, Gong Y, Yuan Y. The association between vacA or cagA status and eradication outcome of Helicobacter pylori infection: A meta-analysis. PLoS One 2017; 12:e0177455. [PMID: 28493953 PMCID: PMC5426689 DOI: 10.1371/journal.pone.0177455] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/15/2016] [Accepted: 04/27/2017] [Indexed: 12/14/2022] Open
Abstract
Background H. pylori virulence factors, especially vacA and cagA are important in gastroduodenal disease pathogenesis and affect cure rates. This meta-analysis aimed to clarify the association between vacA or cagA status and eradication outcome of H. pylori infection. Methods A literature search was performed using electronic databases to identify studies. Twenty-six prospective studies were determined eligible. Meta-analytical techniques were conducted to calculate eradication rates and pooled relative ratios (RR). Results The eradication rate was greater approximately 10% in vacA s1 compared with vacA s2 infected patients, and the pooled RR was 1.164 (95%CI: 1.040–1.303, P = 0.008). A significant association existed between vacA s1 and higher eradication rates in Europe (RR: 1.203, 95%CI: 1.003–1.442, P = 0.046) and Asia (RR: 1.187, 95%CI: 1.028–1.371, P = 0.020), in triple therapy patients (RR: 1.175, 95%CI: 1.012–1.365, P = 0.035). Eradication rates were similar for vacA m1 and m2 genotypes (RR: 0.981, 95%CI: 0.891–1.080, P = 0.690), whereas they were higher by approximately 8% in cagA-positive compared with cagA-negative infected patients, with a pooled RR of 1.094 (95%CI: 1.025–1.168, P = 0.007). A significant association existed between cagA-positive and increased eradication rates in Europe (RR: 1.138, 95%CI: 1.000–1.295, P = 0.049) and Asia (RR: 1.118, 95%CI: 1.051–1.190, P<0.001), in using PCR (RR: 1.232, 95%CI: 1.142–1.329, P<0.001) and protein chips (RR: 1.200, 95%CI: 1.060–1.359, P = 0.004), in triple therapy patients (RR: 1.090, 95%CI: 1.006–1.181, P = 0.034). Conclusions Evidence indicates that infection with vacA s1, cagA-positive strains, but not vacA s2, cagA-negative, is more conducive to H. pylori eradication.
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Affiliation(s)
- Dan Wang
- Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department, Shenyang, China
| | - Qiuping Li
- Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department, Shenyang, China
| | - Yuehua Gong
- Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department, Shenyang, China
- * E-mail: (GY); (YY)
| | - Yuan Yuan
- Tumor Etiology and Screening Department of Cancer Institute and General Surgery, the First Affiliated Hospital of China Medical University, and Key Laboratory of Cancer Etiology and Prevention (China Medical University), Liaoning Provincial Education Department, Shenyang, China
- * E-mail: (GY); (YY)
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Malfertheiner P, Megraud F, O'Morain CA, Gisbert JP, Kuipers EJ, Axon AT, Bazzoli F, Gasbarrini A, Atherton J, Graham DY, Hunt R, Moayyedi P, Rokkas T, Rugge M, Selgrad M, Suerbaum S, Sugano K, El-Omar EM. Management of Helicobacter pylori infection-the Maastricht V/Florence Consensus Report. Gut 2017; 66:6-30. [PMID: 27707777 DOI: 10.1136/gutjnl-2016-312288] [Citation(s) in RCA: 1934] [Impact Index Per Article: 241.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/19/2016] [Accepted: 08/09/2016] [Indexed: 02/06/2023]
Abstract
Important progress has been made in the management of Helicobacter pylori infection and in this fifth edition of the Maastricht Consensus Report, key aspects related to the clinical role of H. pylori were re-evaluated in 2015. In the Maastricht V/Florence Consensus Conference, 43 experts from 24 countries examined new data related to H. pylori in five subdivided workshops: (1) Indications/Associations, (2) Diagnosis, (3) Treatment, (4) Prevention/Public Health, (5) H. pylori and the Gastric Microbiota. The results of the individual workshops were presented to a final consensus voting that included all participants. Recommendations are provided on the basis of the best available evidence and relevance to the management of H. pylori infection in the various clinical scenarios.
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Affiliation(s)
- P Malfertheiner
- Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University Magdeburg, Magdeburg, Germany
| | - F Megraud
- Laboratoire de Bactériologie, Inserm U853, Université de Bordeaux, Bordeaux, France
| | - C A O'Morain
- Faculty of Health Sciences, Trinity College, Dublin, Ireland
| | - J P Gisbert
- Department of Gastroenterology, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa (IP), Madrid, Spain.,Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Madrid, Spain
| | - E J Kuipers
- Erasmus University Medical Center, Rotterdam, The Netherlands
| | | | - F Bazzoli
- Internal Medicine and Gastroenterology, University of Bologna Italy, Bologna, Italy
| | - A Gasbarrini
- Gastroenterology, and Liver Unit, Internal Medicine, Roma, Italy
| | | | - D Y Graham
- Department of Medicine (111D), Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas, USA
| | - R Hunt
- Department of Medicine, McMaster University, Hamilton, Canada.,Hillcroft, Beaconsfield, Buckinghamshire, UK
| | - P Moayyedi
- Department of Gastroenterology, McMaster University, Hamilton, Canada
| | - T Rokkas
- Department of Gastroenterology, Henry Dunant Hospital, Athens, Greece
| | - M Rugge
- Department of Diagnostic Sciences, University of Padova, Padova, Italy
| | | | - S Suerbaum
- Medizinische Hochschule Hannover, Institut für Medizinische Mikrobiologie, Hannover, Germany
| | - K Sugano
- Department of Medicine, Jichi Medical School, Tochigi, Japan
| | - E M El-Omar
- St George and Sutherland Clinical School, University of New South Wales, Sydney, Australia
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Miftahussurur M, Yamaoka Y. Population-Based Strategies for Helicobacter pylori-Associated Disease Management: Asian Perspective. HELICOBACTER PYLORI RESEARCH 2016:519-542. [DOI: 10.1007/978-4-431-55936-8_23] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/06/2025]
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Mansour-Ghanaei F, Joukar F, Mojtahedi K, Sokhanvar H, Askari K, Shafaeizadeh A. Does treatment of Helicobacter pylori infection reduce gastric precancerous lesions? Asian Pac J Cancer Prev 2015; 16:1571-4. [PMID: 25743833 DOI: 10.7314/apjcp.2015.16.4.1571] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/10/2022] Open
Abstract
BACKGROUND Treatment of Helicobacter pylori (H. pylori) decreases the prevalence of gastric cancer, and may inhibit gastric precancerous lesions progression into gastric cancer. The aim of this study was to determine the effect of treatment on subsequent gastric precancerous lesion development. MATERIALS AND METHODS We prospectively studied 27 patients who had low grade dysplasia at the time of enrollment, in addition to dysplasia atrophic gastritis and intestinal metaplasia observed in all patients. All were prescribed quadruple therapy to treat H. Pylori infection for 10 days. Patients underwent endoscopy with biopsy at enrollment and then at follow up two years later. Biopsy samples included five biopsies from the antrum of lesser curvature, antrum of greater curvature, angularis, body of stomach and fundus. RESULTS of these biopsies were compared before and after treatment. RESULTS Overall, the successful eradication rate after two years was 15/27 (55.6%). After antibiotic therapy, the number of patients with low grade dysplasia decreased significantly (p=0.03), also with reduction of the atrophic lesions (p=0.01), but not metaplasia. CONCLUSIONS Treatment of H. pylori likely is an effective therapy in preventing the development of subsequent gastric premalignant lesions.
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Affiliation(s)
- Fariborz Mansour-Ghanaei
- Gastrointestinal and Liver Diseases Research Center, Guilan University of Medical Sciences (GUMS), Rasht, Iran E-mail : ,
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Oh S, Kim N, Yoon H, Choi YJ, Lee JY, Park KJ, Kim HJ, Kang KK, Oh DH, Seo AY, Lee JW, Shin CM, Park YS, Oh JC, Lee DH, Jung HC. Risk factors of atrophic gastritis and intestinal metaplasia in first-degree relatives of gastric cancer patients compared with age-sex matched controls. J Cancer Prev 2014; 18:149-60. [PMID: 25337541 PMCID: PMC4189453 DOI: 10.15430/jcp.2013.18.2.149] [Citation(s) in RCA: 31] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/16/2013] [Revised: 06/19/2013] [Accepted: 06/20/2013] [Indexed: 01/14/2023] Open
Abstract
Background: To identify whether first-degree relatives (FDRs) of gastric cancer (GC) patients have increased risk for atrophic gastritis (AG) and intestinal metaplasia (IM) in relation to other risk factors of GC. Methods: The study cohort consisted of 224 pairs of age-sex matched controls and FDRs. AG and IM in the gastric mucosa were scored histologically using the updated Sydney classification. Risk of having AG and IM was studied by comparing FDRs to controls. Impacts of age, H. pylori infection, smoking, dietary and socioeconomic factors on the presence of AG and IM were studied. Results: In multivariate regression analysis, FDRs had adjusted OR of 2.69 (95% CI 1.06–6.80, P=0.037) for antral IM in male population. Adjusted OR for antral AG and IM were 9.28 (95% CI 4.73–18.18, P<0.001) and 7.81 (95% CI 3.72–16.40, P<0.001) for the H. pylori infected subjects in total population. Getting old by 5 years increased the ORs of having AG and IM by approximately 1.25 fold (P<0.001). Spicy food increased the OR of antral IM by 2.28 fold (95% CI 1.36–3.84, P=0.002). Conclusions: Family history of GC was an independent risk factor for antral IM in male in our study, which could be one reason for the increase of gastric cancer in the family member of gastric cancer. It could be an evidence for the necessity of frequent endoscopy in the presence of family history of GC compared to general population in male.
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Affiliation(s)
- Sooyeon Oh
- Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul
| | - Nayoung Kim
- Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul ; Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - Hyuk Yoon
- Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - Yun Jin Choi
- Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - Ju Yup Lee
- Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - Kyoung Jun Park
- Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - Hee Jin Kim
- Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - Kyu Keun Kang
- Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - Dong Hyun Oh
- Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - A Young Seo
- Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - Jae Woo Lee
- Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul
| | - Cheol Min Shin
- Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - Young Soo Park
- Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | | | - Dong Ho Lee
- Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul ; Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea
| | - Hyun Chae Jung
- Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul
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Kong YJ, Yi HG, Dai JC, Wei MX. Histological changes of gastric mucosa after Helicobacter pylori eradication: a systematic review and meta-analysis. World J Gastroenterol 2014; 20:5903-11. [PMID: 24914352 PMCID: PMC4024801 DOI: 10.3748/wjg.v20.i19.5903] [Citation(s) in RCA: 84] [Impact Index Per Article: 7.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/03/2013] [Revised: 12/13/2013] [Accepted: 01/08/2014] [Indexed: 02/06/2023] Open
Abstract
AIM To systematically review pathological changes of gastric mucosa in gastric atrophy (GA) and intestinal metaplasia (IM) after Helicobacter pylori (H. pylori) eradication. METHODS A systematic search was made of PubMed, Web of Science, EMBASE, ClinicalTrials.gov, OVID and the Cochran Library databases for articles published before March 2013 pertaining to H. pylori and gastric premalignant lesions. Relevant outcomes from articles included in the meta-analysis were combined using Review Manager 5.2 software. A Begg's test was applied to test for publication bias using STATA 11 software. χ(2) and I(2) analyses were used to assess heterogeneity. Analysis of data with no heterogeneity (P > 0.1, I (2) < 25%) was carried out with a fixed effects model, otherwise the causes of heterogeneity were first analyzed and then a random effects model was applied. RESULTS The results of the meta-analysis showed that the pooled weighted mean difference (WMD) with 95%CI was 0.23 (0.18-0.29) between eradication and non-eradication of H. pylori infection in antral IM with a significant overall effect (Z = 8.19; P <0.00001) and no significant heterogeneity (χ(2) = 27.54, I(2) = 16%). The pooled WMD with 95%CI was -0.01 (-0.04-0.02) for IM in the corpus with no overall effect (Z = 0.66) or heterogeneity (χ(2) = 14.87, I(2) =0%) (fixed effects model). In antral GA, the pooled WMD with 95% CI was 0.25 (0.15-0.35) with a significant overall effect (Z = 4.78; P < 0.00001) and significant heterogeneity (χ(2) = 86.12, I(2) = 71%; P < 0.00001). The pooled WMD with 95% CI for GA of the corpus was 0.14 (0.04-0.24) with a significant overall effect (Z = 2.67; P = 0.008) and significant heterogeneity (χ(2) = 44.79, I(2) = 62%; P = 0.0003) (random effects model). CONCLUSION H. pylori eradication strongly correlates with improvement in IM in the antrum and GA in the corpus and antrum of the stomach.
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Murakami K, Kodama M, Nakagawa Y, Mizukami K, Okimoto T, Fujioka T. Long-term monitoring of gastric atrophy and intestinal metaplasia after Helicobacter pylori eradication. Clin J Gastroenterol 2012; 5:247-50. [DOI: 10.1007/s12328-012-0317-2] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/30/2012] [Accepted: 05/31/2012] [Indexed: 12/17/2022]
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14
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Shiota S, Nguyen LT, Murakami K, Kuroda A, Mizukami K, Okimoto T, Kodama M, Fujioka T, Yamaoka Y. Association of helicobacter pylori dupA with the failure of primary eradication. J Clin Gastroenterol 2012; 46:297-301. [PMID: 22298090 PMCID: PMC3296869 DOI: 10.1097/mcg.0b013e318243201c] [Citation(s) in RCA: 32] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
GOALS To determine whether the presence of dupA Helicobacter pylori (H. pylori) influences the cure rate of primary eradication therapy. BACKGROUND Several virulence factors of H. pylori have been reported to affect the efficacy of the eradication rate. However, no study has investigated whether the presence of dupA affects eradication failure. STUDY The presence of dupA was evaluated in 142 H. pylori strains isolated from 142 patients with gastrointestinal diseases. Of these patients, 104 received primary eradication therapy for 1 week. The risk factors for eradication failure were determined using univariate and multivariate analyses. RESULTS Among 142 strains, 44 (31.0%) were dupA positive. There was no association between dupA status and gastroduodenal diseases (P>0.05). The clarithromycin (CLR) resistance rate was generally lower in the dupA-positive than in the dupA-negative group (20.4% vs. 35.7%, P=0.06). However, dupA prevalence was higher in the eradication failure group than in the success group (36.3% vs. 21.9%). Among the CLR-resistant H. pylori infected group, the successful eradication rate was significantly lower in patients infected with dupA-positive H. pylori than dupA-negative H. pylori (P=0.04). In multivariate analysis adjusted for age, sex, and type of disease, not only CLR resistance but also dupA presence was independent risk factors for eradication failure (adjusted odds ratio=3.71; 95% confidence interval,1.07-12.83). CONCLUSIONS Although CLR resistant was more reliable predictor, the presence of dupA may also be an independent risk factor for eradication failure.
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Affiliation(s)
- Seiji Shiota
- Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, 1-1 Idaigaoka, Hasama-machi, Yufu-City, Oita 879-5593, Japan
- Department of General Medicine, Oita University Faculty of Medicine 1-1 Idaigaoka, Hasama-machi, Yufu-City, Oita 879-5593, Japan
| | - Lam Tung Nguyen
- Department of General Medicine, Oita University Faculty of Medicine 1-1 Idaigaoka, Hasama-machi, Yufu-City, Oita 879-5593, Japan
| | - Kazunari Murakami
- Department of General Medicine, Oita University Faculty of Medicine 1-1 Idaigaoka, Hasama-machi, Yufu-City, Oita 879-5593, Japan
| | - Akiko Kuroda
- Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, 1-1 Idaigaoka, Hasama-machi, Yufu-City, Oita 879-5593, Japan
| | - Kazuhiro Mizukami
- Department of General Medicine, Oita University Faculty of Medicine 1-1 Idaigaoka, Hasama-machi, Yufu-City, Oita 879-5593, Japan
| | - Tadayoshi Okimoto
- Department of General Medicine, Oita University Faculty of Medicine 1-1 Idaigaoka, Hasama-machi, Yufu-City, Oita 879-5593, Japan
| | - Masaaki Kodama
- Department of General Medicine, Oita University Faculty of Medicine 1-1 Idaigaoka, Hasama-machi, Yufu-City, Oita 879-5593, Japan
| | - Toshio Fujioka
- Department of General Medicine, Oita University Faculty of Medicine 1-1 Idaigaoka, Hasama-machi, Yufu-City, Oita 879-5593, Japan
| | - Yoshio Yamaoka
- Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, 1-1 Idaigaoka, Hasama-machi, Yufu-City, Oita 879-5593, Japan
- Department of Medicine-Gastroenterology, Baylor College of Medicine and Michael E. DeBakey Veterans Affairs Medical Center, 2002 Holcombe Blvd. Houston, Texas 77030, United States
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Kang JM, Kim N, Shin CM, Lee HS, Lee DH, Jung HC, Song IS. Predictive factors for improvement of atrophic gastritis and intestinal metaplasia after Helicobacter pylori eradication: a three-year follow-up study in Korea. Helicobacter 2012; 17:86-95. [PMID: 22404438 DOI: 10.1111/j.1523-5378.2011.00918.x] [Citation(s) in RCA: 43] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
BACKGROUND AND AIMS To date, data on the effects of anti-Helicobacter therapy on the improvement of atrophic gastritis (AG) and intestinal metaplasia (IM) have been conflicting. This study was performed to investigate whether eradication of H. pylori could lead to the improvement of AG and IM, and the prognostic factors associated with the improvement of AG and IM. METHODS Four hundred patients consisting of H. pylori-negative (n = 116) and H. pylori-positive (n = 284) groups were followed up 1 and 3 years after initial H. pylori tests. Serum levels of pepsinogen (PG), bacteria, environmental factors, and genetic polymorphisms were determined. RESULTS The grade of corpus atrophy decreased at 1 and 3 years after successful eradication (p < .001 and p = .033, respectively). However, there was no significant change in the IM in the antrum and in the corpus. Prediction factors for the improvement of corpus AG by H. pylori eradication were baseline low PG I/II ratio (≤3), high salt intake, and corpus-predominant gastritis. IM improvement was also associated with spicy food intake and high baseline grade of IM, in addition to these factors. In addition, IL-1B-511 C/T and IL-6-572 C/G alleles were found to inhibit IM improvement. However, H. pylori-negative and noneradicated group did not show any significant change in AG or IM. CONCLUSION Corpus AG was reversed by H. pylori eradication, and improvement of IM by H. pylori eradiation was more definite in patients with severe IM, low PG I/II ratio, and corpus-predominant gastritis, suggesting that H. pylori eradication is valuable even in severe cases.
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Affiliation(s)
- Jung Mook Kang
- Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, Korea
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16
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Lee SY. Future candidates for indications of Helicobacter pylori eradication: do the indications need to be revised? J Gastroenterol Hepatol 2012; 27:200-11. [PMID: 22098099 DOI: 10.1111/j.1440-1746.2011.06961.x] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
Since the discovery of Helicobacter pylori in 1982, the development of several treatment guidelines has allowed a consensus on the indications for H. pylori eradication. Beyond these currently accepted indications, including various upper gastrointestinal disorders and extragastric diseases, a significant amount of new information regarding H. pylori eradication is emerging. Certain types of acute gastritis, such as nodular gastritis, hypertrophic gastritis, Ménétrier's disease, hemorrhagic gastritis, and granulomatous gastritis are reversible after H. pylori eradication. Further, for chronic gastritis, closed-type atrophic gastritis and complete-type intestinal metaplasia appear to be more reversible after H. pylori eradication than open-type atrophic gastritis and incomplete-type intestinal metaplasia. Eradication can also be considered in subjects younger than 40 years who have a family history of gastric cancer and in subjects with long-term medications that might lead to bleeding (antiplatelet agents) or atrophy (proton pump inhibitors). Emerging evidence indicates that H. pylori eradication could be an effective treatment for some extragastric diseases that are unresponsive to conventional therapy. In such conditions, routine screening for eradication of H. pylori has not previously been recommended; a "test-and-treat" approach is suggested in the aforementioned situations. Given that H. pylori eradication is effective when the gastritis is reversible, future indications should be expanded to include acute gastric lesions that show marked improvement upon H. pylori eradication rather than just focusing on chronic gastric lesions. Future indications for H. pylori eradication should focus more on reversible lesions before preneoplastic conditions develop.
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Affiliation(s)
- Sun-Young Lee
- Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea.
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Vannella L, Lahner E, Bordi C, Pilozzi E, Di Giulio E, Corleto VD, Osborn J, Delle Fave G, Annibale B. Reversal of atrophic body gastritis after H. pylori eradication at long-term follow-up. Dig Liver Dis 2011; 43:295-9. [PMID: 21112822 DOI: 10.1016/j.dld.2010.10.012] [Citation(s) in RCA: 28] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/22/2010] [Revised: 09/20/2010] [Accepted: 10/21/2010] [Indexed: 02/08/2023]
Abstract
BACKGROUND The effect of Helicobacter pylori treatment on the potential reversal of atrophic body gastritis (ABG) is controversial. Body atrophy reversal was evaluated in a cohort of H. pylori-negative and treated H. pylori-positive ABG patients. METHODS Observational long-term follow-up cohort study including 300 ABG patients with at least one follow-up gastroscopy with three biopsies from the antrum and three from the body performed no earlier than 1 year after diagnosis was included. H. pylori was diagnosed by Giemsa-stain and serology. H. pylori-positive patients (n = 192) were treated with bismuth-based triple regimen. RESULTS After a mean follow-up of 5.2 years, body atrophy reversal was observed in 42/300 patients (14%). Body atrophy reversal occurred more frequently in patients treated for H. pylori than in H. pylori-negative ones (21.3% vs 0.9%, p < 0.00001) and was observed between 2 and 8 years after treatment in 52% of cases. Predictive factors for body atrophy reversal at Cox-regression analysis were mild atrophy (HR 2.14; 95% CI 1.12-4.1), moderate-severe inflammation (HR 5.3; 95% CI 1.64-17.3), and absence of intestinal metaplasia (HR 2.4; 95% CI 1.2-4.8). CONCLUSION Body atrophy reversal was observed in about 20% of ABG patients treated for H. pylori infection, and about 50% of reversals occurred during long-term follow-up.
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Affiliation(s)
- Lucy Vannella
- Department of Digestive and Liver Disease, Sant'Andrea Hospital, II School of Medicine University Sapienza of Rome, Italy
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Furukawa M, Fujita M, Takinishi A, Misaka R, Nagahara H. Low-dose aspirin delays gastric healing after Helicobacter pylori eradication. Intern Med 2011; 50:951-9. [PMID: 21532216 DOI: 10.2169/internalmedicine.50.4778] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/06/2022] Open
Abstract
BACKGROUND AND AIM Helicobacter pylori (H. pylori) and aspirin are the major causes of gastric injury, and eradication of H. pylori can restore mucosal injury such as gastric ulcer. The aim of the present study was to investigate the effects of low-dose aspirin on the healing process, determined by endoscopic features, after H. pylori eradication. METHODS From 2001 to 2008, 12,887 patients underwent endoscopic examination at our hospital. From these, 100 patients with and 100 patients without H. pylori infection were analyzed to identify the endoscopic features characteristic of H. pylori-infected stomach. Based on these characteristic features, we observed the healing process of 89 patients not taking low-dose aspirin and 12 patients taking low-dose aspirin for 6 months, 1 year, and 5 years, which was successful in eradicating H. pylori. RESULTS Diffuse redness (DR) of the fundic mucosa was the characteristic feature of H. pylori-infected stomach, whereas reddish streaks (RS) on the greater curvature of the antrum was the characteristic finding in non-infected stomach. In the no aspirin group, DR faded by 6 months and new expression of RS was observed 1 year after H. pylori eradication. In contrast, in the aspirin group, both fading of DR and the expression of RS were observed 5 years after eradication. CONCLUSION Low-dose aspirin delayed the early phase of the healing process in the gastric mucosa after H. pylori eradication.
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Affiliation(s)
- Maiko Furukawa
- Aoyama Hospital, Tokyo Women's Medical University, Japan
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Sun LM, Shang Y, Zeng YM, Deng YY, Cheng JF. HOGG1 polymorphism in atrophic gastritis and gastric cancer after Helicobacter pylori eradication. World J Gastroenterol 2010; 16:4476-82. [PMID: 20845517 PMCID: PMC2941073 DOI: 10.3748/wjg.v16.i35.4476] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.9] [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 association between Ser326Cys human oxoguanine glycosylase 1 (hOGG1) polymorphism and atrophic gastritis and gastric cancer after Helicobacter pylori (H. pylori) eradication.
METHODS: A total of 488 subjects (73 patients with gastric cancer, 160 with atrophic gastritis after H. pylori eradication and 255 controls) were prospectively collected. Polymerase chain reaction-restriction fragment length polymorphism analysis was performed to distinguish hOGG1 Ser326Cys polymorphism. Statistical analysis was conducted by two-sample t test for continuous variables and χ2 test for categorical variables. Logistic regression models were used to find the risk factors for gastric cancer and atrophic gastritis.
RESULTS: Neither the hOGG1 Ser/Cys nor the Cys/Cys genotype was associated with gastric cancer. Compared with the Ser/Ser genotype, odds ratio (OR) for Ser/Cys was 0.96, (95% CI: 0.51-1.84) and OR for Cys/Cys was 1.1 (95% CI: 0.48-2.1). No association was detected between hOGG1 polymorphism and Lauren type of gastric cancer (P = 0.61) either. However, Ser/Cys and Cys/Cys were significantly associated with atrophic gastritis with OR: 1.76 for Ser/Cys (95% CI: 1.03-3.0) and 2.38 for Cys/Cys (95% CI: 1.34-4.23). After controlling for age, gender, smoking and alcohol, there were still significant associations with OR: 2.05 for Ser/Cys (95% CI: 1.14-3.68) and 2.76 for Cys/Cys (95% CI: 1.47-5.18).
CONCLUSION: HOGG1 polymorphisms (Cys/Cys and Ser/Cys) are associated with atrophic gastritis. No significant association is detected between hOGG1 polymorphisms (Cys/Cys or Ser/Cys) and gastric cancer.
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20
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Alshenawy HA, Alshafey AM. Eradication of Helicobacter pylori decreases the expression of p53 and c-Myc oncogenes. Arab J Gastroenterol 2009. [DOI: 10.1016/j.ajg.2009.10.003] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/20/2022]
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Li XB, Chen HM, Lu H, Zheng Q, Chen XY, Peng YS, Ge ZZ, Liu WZ. Role of Helicobacter pylori infection on neuronal expression in the stomach and spinal cord of a murine model. J Dig Dis 2009; 10:286-92. [PMID: 19906107 DOI: 10.1111/j.1751-2980.2009.00397.x] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
OBJECTIVE To investigate the effect of Helicobacter pylori (H. pylori) infection on neuronal expressions in the stomach and spinal cord of mice so as to explain dyspepsia symptoms in H. pylori infected patients. METHODS C57BL/6 female mice were studied at 2 weeks (acute infection group) and 12 weeks (chronic infection group) after H. pylori inoculation. Histological analyses for gastric inflammation and bacterial colonization were assessed by HE staining and Warthin-Starry staining. Fos, vasoactive intestinal polypeptide (VIP) and calcitonin gene-related peptide expressions (CGRP) were studied by immunohistochemistry. RESULTS H. pylori colonization was present mainly in pyloric region, but bacterial density was similar in both infected groups. The intensity of mucosal inflammation and activity was significantly higher in two infected groups than in those in the control group. The degree of mononuclear and polymorphonuclear cell infiltration in proventricular-glandular region and gastric corpus at 12 weeks after H. pylori inoculation was higher than that at 2 weeks after inoculation. The neuronal expressions of fos, VIP, and CGRP in the stomach and spinal cord were significantly more marked in the infected groups than in the control group, but there was no significant difference between two infected groups. CONCLUSION H. pylori infection induced different degrees of gastric mucosal inflammation in the murine model. Both early and chronic infection groups of mice showed enhanced neuronal expressions of fos, VIP and CGRP of stomach and spinal cord and these could form a basis for appearance of functional dyspeptic symptoms in patients with H. pylori infection.
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Affiliation(s)
- Xiao Bo Li
- Department of Gastroenterology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai Institute of Digestive Disease, Shanghai, China
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22
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Sugimoto M, Furuta T, Yamaoka Y. Influence of inflammatory cytokine polymorphisms on eradication rates of Helicobacter pylori. J Gastroenterol Hepatol 2009; 24:1725-32. [PMID: 20136959 PMCID: PMC3128255 DOI: 10.1111/j.1440-1746.2009.06047.x] [Citation(s) in RCA: 35] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
Pro-inflammatory cytokines and anti-inflammatory cytokines are produced in gastric mucosa from inflammatory cells activated by Helicobacter pylori (H. pylori) infection. Of the inflammatory cytokines, interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha have a potent inhibitive effect on gastric acid production. Polymorphisms in these genes are associated with individual differences in cytokine messenger RNA levels, which result in different gastric mucosal inflammation, different acid inhibition and different gastroduodenal disease risks in response to H. pylori infection. The sustained higher intragastric pH during an eradication therapy is known to be one of the therapeutic determinants of the H. pylori eradication as well as antibiotics resistance and poor compliance. The IL-1B-511 polymorphism is related to eradication rate, and, in combined analysis of previous reports, the eradication rate in patients with the IL-1B-511 C/C genotype (77.4%, 209/270), low IL-1beta producer genotype, is lower than that of the IL-1B-511 C/T and T/T genotypes (87.2%, 631/724) (Odds ratio for eradication failure: 1.98, 95% confidence interval: 1.38-2.84, P = 0.0002). Moreover, the odds ratio of combined CYP2C19 rapid metabolizer-IL-1B-511 C/C type for eradication failure is 11.15 (5.23-23.78) times that of the CYP2C19 poor metabolizer-IL-1B-511 non-C/C type. However, there is no positive data indicating the role of other inflammatory cytokine polymorphisms (e.g. IL-1RN, TNF-A or IL-10) in eradication therapy. Nevertheless, the studies show that inflammatory cytokine polymorphisms, especially the IL-1B-511 T/T genotype, are the determinants of eradication by affecting gastric acid secretion and mucosal inflammation. Therefore, the tailored eradication therapy, considering inflammatory cytokine polymorphisms, may be effective for the higher eradication rates.
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Affiliation(s)
- Mitsushige Sugimoto
- Department of Medicine-Gastroenterology, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas, USA, Center for Clinical Research, Hamamatsu University School of Medicine, Shizuoka
| | - Takahisa Furuta
- Center for Clinical Research, Hamamatsu University School of Medicine, Shizuoka
| | - Yoshio Yamaoka
- Department of Medicine-Gastroenterology, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas, USA, Department of Environmental and Preventive Medicine, Faculty of Medicine, Oita University, Yufu, Japan
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Hung KH, Wu JJ, Yang HB, Su LJ, Sheu BS. Host Wnt/beta-catenin pathway triggered by Helicobacter pylori correlates with regression of gastric intestinal metaplasia after H. pylori eradication. J Med Microbiol 2009; 58:567-576. [PMID: 19369517 DOI: 10.1099/jmm.0.007310-0] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022] Open
Abstract
Helicobacter pylori eradication can reverse gastric intestinal metaplasia (IM) in some but not all patients. H. pylori induces high levels of nuclear beta-catenin staining in IM tissues, as well as overexpression of cyclooxygenase-2 (COX-2). This study investigated whether the Wnt/beta-catenin pathway plays a role in IM regression following H. pylori eradication. Sixty-five H. pylori-infected patients with IM who had achieved successful H. pylori eradication provided paired gastric samples before and after eradication to analyse the persistence of IM, and to assess COX-2 and nuclear beta-catenin expression. The host genotypes of single nucleotide polymorphisms (SNPs) of the COX-2, beta-catenin (CTNNB1) and adenomatous polyposis coli (APC) genes were analysed. In addition, expression of beta-catenin, E-cadherin and phosphorylated and unphosphorylated glycogen synthase kinase 3beta (GSK-3beta) in cell lines challenged with H. pylori isolates from patients with and without IM persistence was compared by immunoanalysis. After a mean 33.9-month follow-up after H. pylori eradication, 44 patients (67.7%) with IM persistence had a higher rate of high-level nuclear beta-catenin expression in IM tissue than those without IM persistence (P=0.008). The patients with IM persistence had a higher rate of AA, GG and AA APC SNP genotypes at positions 4479, 5268 and 5465, respectively, than the patients without IM persistence (P=0.022). The H. pylori isolates from the patients with IM regression after H. pylori eradication induced more phospho-GSK-3beta in AGS cells than isolates from patients with IM persistence (P=0.011). It is likely that interactions with H. pylori and the patient's Wnt/beta-catenin genetic predisposition determine the outcome of IM persistence following H. pylori eradication.
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Affiliation(s)
- Kuei-Hsiang Hung
- Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC
| | - Jiunn-Jong Wu
- Department of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.,Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC
| | - Hsiao-Bai Yang
- Department of Pathology, Ton-Yen General Hospital, Hsinchu, Taiwan, ROC.,Department of Pathology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC
| | - Li-Ju Su
- Institute of Clinical Pharmacy, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC
| | - Bor-Shyang Sheu
- Department of Internal Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.,Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.,Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC
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Virulence factor genotypes of Helicobacter pylori affect cure rates of eradication therapy. Arch Immunol Ther Exp (Warsz) 2009; 57:45-56. [PMID: 19219527 DOI: 10.1007/s00005-009-0007-z] [Citation(s) in RCA: 47] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/07/2008] [Accepted: 10/20/2008] [Indexed: 12/11/2022]
Abstract
The cure rates of Helicobacter pylori infection by using a combination of a proton pump inhibitor (PPI) and antimicrobial agents are mainly influenced by bacterial susceptibility to antimicrobial agents and the magnitude of acid inhibition during the treatment. Currently used empirical triple therapies do not reliably produce a > or =80% cure rate on an intention-to-treat basis. Therefore, tailored regimens based on relevant microbiological findings and pharmacogenomics are recommended for attaining an acceptable > or =95% cure rate. Recently, virulence factors of H. pylori, such as cagA and vacA, are reported to be major factors determining the cure rates. Individuals infected with strains with cagA-negative and vacA s2 genotypes have significantly increased risk of eradication failure of H. pylori infection. These virulence factors enhance gastric mucosal inflammation and are associated with the development of peptic ulcer and gastric cancer. H. pylori virulence factors induce proinflammatory cytokines, such as interleukin (IL)-1, IL-8, and tumor necrosis factor (TNF)- which influence mucosal inflammation and/or gastric acid secretion. When physicians select an H. pylori eradication regimen with an acceptable cure rate, they might need to consider H. pylori virulence factors, especially cagA and vacA.
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25
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De Leest HTJI, Steen KS, Bloemena E, Lems WF, Kuipers EJ, Van de Laar MAFJ, Bijlsma JWJ, Janssen M, Houben HHML, Kostense PJ, Boers M, Dijkmans BAC. Helicobacter pylori eradication in patients on long-term treatment with NSAIDs reduces the severity of gastritis: a randomized controlled trial. J Clin Gastroenterol 2009; 43:140-6. [PMID: 18797408 DOI: 10.1097/mcg.0b013e3181595b40] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
BACKGROUND Maintenance use of nonsteroidal anti-inflammatory drugs (NSAIDs) is often complicated by gastropathy. In non-NSAID users, eradication of Helicobacter pylori is associated with decreased mucosal inflammation, and may halt the progression to atrophy and intestinal metaplasia, but the continuous use of NSAIDs may interfere with these processes. GOAL To investigate the effect of H. pylori eradication on gastric mucosal histology during long-term NSAID use, with and without gastroprotective therapy. STUDY Patients were eligible for inclusion if they were on long-term NSAIDs and were H. pylori-positive on serologic testing. Patients were randomly assigned to either eradication or placebo. Gastritis was assessed according to the updated Sydney classification for activity, chronic inflammation, gastric glandular atrophy, intestinal metaplasia, and H. pylori density. RESULTS Biopsy specimens were available for histology of 305 patients. Of these, 48% were on chronic gastroprotective medication. Significant less active gastritis, inflammation, and H. pylori density was found in the eradication group compared with the placebo group in both corpus and antrum (P<0.001). In the corpus, less atrophy was found in the eradication group compared with the placebo group. CONCLUSIONS H. pylori eradication in patients on long-term NSAID therapy leads to healing of gastritis despite ongoing NSAID therapy.
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Affiliation(s)
- Helena T J I De Leest
- Department of Rheumatology, VU University Medical Center, Amsterdam, The Netherlands.
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Busuttil RA, Boussioutas A. Intestinal metaplasia: a premalignant lesion involved in gastric carcinogenesis. J Gastroenterol Hepatol 2009; 24:193-201. [PMID: 19215332 DOI: 10.1111/j.1440-1746.2008.05774.x] [Citation(s) in RCA: 68] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Despite a plateau in incidence, gastric cancer remains a significant problem globally. The majority of gastric cancer is associated with histologically recognizable premalignant stages as first described by Pelayo Correa in the mid-1970s. The mortality from gastric cancer remains high especially in Western countries where, arguably, the index of suspicion of gastric cancer in patients presenting with upper abdominal symptoms is lower than in high prevalence countries. What is the evidence that intestinal metaplasia (IM) is a premalignant condition? What should the clinician know about IM and the relative risks of progression to gastric cancer? Finally, what are the current and future strategies that may help stratify patients into high risk and low risk for the development of gastric cancer? This review focuses on gastric IM and outlines some of the literature that discusses it as a premalignant condition. It also reviews the issue of surveillance of patients with IM in order to attempt to reduce the significant mortality of gastric cancer by detection of earlier stages of disease which are eminently treatable.
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Affiliation(s)
- Rita A Busuttil
- Cancer Genomics and Predictive Medicine, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
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27
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Kim MN, Kim N, Lee SH, Park YS, Hwang JH, Kim JW, Jeong SH, Lee DH, Kim JS, Jung HC, Song IS. The effects of probiotics on PPI-triple therapy for Helicobacter pylori eradication. Helicobacter 2008; 13:261-8. [PMID: 18665934 DOI: 10.1111/j.1523-5378.2008.00601.x] [Citation(s) in RCA: 89] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]
Abstract
BACKGROUND This study was performed to evaluate whether the addition of probiotics to proton pump inhibitor (PPI)-based triple therapy increases the likelihood of successful Helicobacter pylori eradication. MATERIALS AND METHODS Three hundred and forty-seven H. pylori-infected patients were randomized into a triple-plus-yogurt group (yogurt group, n = 168) or a triple-only group (control group, n = 179). Triple therapy consisted of PPI b.i.d., clarithromycin 500 mg b.i.d., and amoxicillin 1 g b.i.d. for 7 days. Yogurt group received triple therapy for 1 week and one bottle of Will yogurt per day for at 3 weeks, starting on the first day of triple therapy. Will yogurt (a Korean brand) contains Lactobacillus acidophilus HY2177, Lactobacillus casei HY2743, Bifidobacterium longum HY8001, and Streptococcus thermophilus B-1. (13)C-urea breath test was performed at least 4 weeks after completion of triple therapy. Eradication rates, compliances, and adverse events were compared. RESULTS By intention-to treat analysis the H. pylori eradication rates in the yogurt group 79.2% (133 of 168) was similar to that in the control group 72.1% (129 of 179) (p = .124). However, by per-protocol (PP) analysis, the eradication rate in the yogurt group, 87.5% (133 of 152) was higher than that in the control group, 78.7% (129 of 164) (p = .037). Common adverse events were metallic taste (11.8%) and diarrhea (8.6%). The frequency of adverse effects in the yogurt group 41.1% (69/168) were higher than in the control group, 26.3% (47 of 179) (p = .003). However, most adverse events were mild to moderate in intensity, and the severities of adverse effects were similar in both groups (p = .401). CONCLUSIONS The addition of Will yogurt to triple therapy did not reduce the side-effects of triple therapy. But it increased the H. pylori eradication rate by PP analysis, encouraging more research in this field.
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Affiliation(s)
- Mi Na Kim
- Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, South Korea
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Watari J, Das KK, Amenta PS, Tanabe H, Tanaka A, Geng X, Lin JJC, Kohgo Y, Das KM. Effect of eradication of Helicobacter pylori on the histology and cellular phenotype of gastric intestinal metaplasia. Clin Gastroenterol Hepatol 2008; 6:409-17. [PMID: 18321787 DOI: 10.1016/j.cgh.2007.12.044] [Citation(s) in RCA: 27] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
BACKGROUND & AIMS Eradication of Helicobacter pylori appears to reduce gastric cancer incidence. We examined the effect of successful H pylori therapy on histology, phenotype of gastric intestinal metaplasia (GIM) (complete vs incomplete), and expression of several biomarkers related to carcinogenesis. METHODS Ninety-six H pylori-positive patients from Japan were treated successfully and followed up prospectively over 4 years with yearly endoscopy and were classified into 3 groups: group CG, chronic gastritis without GIM (n = 36); group IM, chronic gastritis with GIM (n = 33); group DYS, and GIM with dysplasia/cancer in a different location of the stomach (n = 27). A total of 288 endoscopic procedures were performed. Histology, mucin-histochemistry, and immunoperoxidase assays using monoclonal antibodies (mAbs) for cell phenotype (monoclonal antibody Das-1/colonic) and for neoplasia (TC22 and p53) were performed. RESULTS The GIM histologic score was higher in group DYS than in group IM (P < .05) and group CG (P < .0001). The GIM scores did not change in groups IM and DYS over 4 years. mAb Das-1 reactivity was higher in group DYS (63%) than in group IM (39%) and group GC (0%). After eradication of H pylori, mAb Das-1 reactivity disappeared in 40% of patients (P < .0001) despite the unchanged GIM scores, and regression of TC22-4 was noted in the same patients. CONCLUSIONS H pylori eradication does not reduce the histologic GIM score, but changes the cellular phenotype of GIM. This change of phenotype may be an important factor in the reduction of cancer incidence after eradication of H pylori.
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Affiliation(s)
- Jiro Watari
- Division of Gastroenterology and Hematology/Oncology, Department of Medicine, Asahikawa Medical College, Asahikawa, Japan
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Abstract
Gastric cancer is the second commonest fatal malignancy in the world with a high incidence in China. Helicobacter pylori infection is an important factor in the pathogenesis of gastric cancer. Epidemiological studies have shown a strong causal relationship between H. pylori infection and gastric cancer. Animal studies also show that eradication of H. pylori infection, especially at the early stage, is effective in preventing H. pylori-related gastric carcinogenesis. H. pylori eradication leads to regression and prevents the progression of gastric precancerous lesions, but only in a minority of cases. H. pylori eradication appears to be the most promising approach in gastric cancer prevention. The current available data in human studies showed that H. pylori eradication can reduce the risk of developing gastric cancer and this strategy is more useful in patients without atrophic gastritis or intestinal metaplasia. A longer follow-up and additional studies are needed for better understanding this issue.
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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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31
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Rokkas T, Pistiolas D, Sechopoulos P, Robotis I, Margantinis G. The long-term impact of Helicobacter pylori eradication on gastric histology: a systematic review and meta-analysis. Helicobacter 2007; 12 Suppl 2:32-8. [PMID: 17991174 DOI: 10.1111/j.1523-5378.2007.00563.x] [Citation(s) in RCA: 165] [Impact Index Per Article: 9.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
BACKGROUND Helicobacter pylori infection is a crucial factor in the multistep carcinogenic process of gastric cancer. In this process the gastric mucosa evolves through the stages of acute gastritis, chronic gastritis, gastric atrophy (GA), and intestinal metaplasia (IM) before developing gastric adenocarcinoma. AIMS The main aim of this study was to systematically review the long-term effects of H. pylori eradication on gastric histology (i.e. effects on GA and IM for both antrum and corpus) by meta-analyzing all relevant studies. METHODS Extensive English-language medical literature searches for human studies were performed through October 2006, using suitable key words. Pooled estimates [odds ratio (OR) with 95% confidence intervals (CI)] were obtained using random-effects model. RESULTS For antrum GA the pooled OR with 95% CI was 0.554 (0.372-0.825), p=0.004. For corpus GA the pooled OR was 0.209 (0.081-0.538), p<0.001. For antrum IM the pooled OR was 0.795 (0.587-1.078), p=0.14. For corpus IM the pooled OR was 0.891 (0.663-1.253), p=0.506. CONCLUSION The results showed significant improvement of GA, whereas improvement was not shown for IM.
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32
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Dinis-Ribeiro M, da Costa-Pereira A, Lopes C, Moreira-Dias L. Feasibility and cost-effectiveness of using magnification chromoendoscopy and pepsinogen serum levels for the follow-up of patients with atrophic chronic gastritis and intestinal metaplasia. J Gastroenterol Hepatol 2007; 22:1594-604. [PMID: 17845687 DOI: 10.1111/j.1440-1746.2007.04863.x] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
BACKGROUND The follow-up of patients with atrophic chronic gastritis or intestinal metaplasia may lead to early diagnosis of gastric cancer. However, to-date no cost-effective model has been proposed. Improved endoscopic examination using magnification chromoendoscopy together with non-invasive functional assessment with pepsinogen serum levels are accurate in the diagnosis of intestinal metaplasia (extension) and minute dysplastic lesions. The aim of this study was to assess the feasibility and cost-effectiveness of a follow-up model for patients with atrophic chronic gastritis and intestinal metaplasia based on gastric mucosal status using magnification chromoendoscopy and pepsinogen. METHODS A cohort of patients with lesions as severe as atrophic chronic gastritis were followed-up according to a standardized protocol using magnification chromoendoscopy with methylene blue and measurement of serum pepsinogen I and II levels. A single node decision tree and Markov chain modeling were used to define cost-effectiveness of this follow-up model versus its absence. Transition rates were considered time-independent and calculated using primary data following cohort data analysis. Costs, quality of life and survival were estimated based on published data and extensive sensitivity analysis was performed. RESULTS A total of 100 patients were successfully followed-up over 3 years. Seven cases of dysplasia were diagnosed during follow-up, all among patients with incomplete intestinal metaplasia at baseline, six of whom had extensive (pepsinogen I to II ratio <3) incomplete intestinal metaplasia. For those individuals with atrophic chronic gastritis or complete intestinal metaplasia, a yearly measurement of pepsinogen levels or an endoscopic examination on a 3-yearly basis would cost 455 euros per quality-adjusted life year (QALY) gain. Endoscopic examination and pepsinogen serum level measurement on a yearly basis would cost 1868 euros per QALY for patients with extensive intestinal metaplasia. CONCLUSIONS The follow-up of patients with atrophic chronic gastritis or intestinal metaplasia is both feasible and cost-effective if improved accurate endoscopic examination of gastric mucosa together with non-invasive assessment of gastric mucosal status are used to identify individuals at high-risk for development of gastric cancer.
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Affiliation(s)
- Mário Dinis-Ribeiro
- Department of Gastroenterology, Portuguese Oncology Institute, Porto, Portugal.
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Lv B. Is the eradication of Helicobacter pylori a way to prevent gastric cancer? Shijie Huaren Xiaohua Zazhi 2007; 15:2669-2671. [DOI: 10.11569/wcjd.v15.i25.2669] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [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
Helicobacter pylori is a major pathogen of chronic gastritis and peptic ulcers, as well as type I carcinogenesis. Inflammation of gastric mucosa is improved after eradication of H. pylori. However, does eradication of H. pylori reverse atrophic gastritis and intestinal metaplasia, and therefore may it be a way to prevent gastric cancer? This paper reviews studies of the relationship between H. pylori and gastric cancer. It was concluded that eradication of H. pylori is a potential method to prevent gastric cancer, and that H. pylori should especially be tested for and treated in high-risk populations.
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Singh S, Bansal A, Puli S, Wani S, Mathur S, Rastogi A, Sharma P. Effect of proton pump inhibitor therapy on inflammatory changes in the gastric cardia (carditis). Dig Dis Sci 2007; 52:2178-82. [PMID: 17436103 DOI: 10.1007/s10620-006-9688-x] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/27/2006] [Accepted: 11/26/2006] [Indexed: 12/20/2022]
Abstract
The etiology of inflammation of the gastric cardia (carditis) is controversial, and gastroesophageal reflux disease (GERD) and H. pylori infection have been proposed as etiological factors. This study aimed to investigate the effect of acid suppression on histological changes in the gastric cardia. Gastric cardia biopsies of reflux patients were evaluated at baseline and after proton pump inhibitor (PPI) therapy. The updated Sydney classification was used to score the biopsies, and carditis scores (pre- and post-PPI therapy) were compared. A total of 31 patients were included, of which 5 patients were excluded, as cardiac mucosa was not documented in either pre- or post-PPI biopsies. The mean duration of PPI therapy was 30 months (SE, 3.04 months). There was no significant change in carditis scores post-PPI therapy. The mean mononuclear and neutrophil scores were 1.23 and 0.35 pre-PPI therapy and 1.73 and 0.62 post-PPI therapy, respectively. No change in mean intestinal metaplasia and atrophy scores was identified. In conclusion, acid suppressive therapy with PPI did not lead to a significant reduction in carditis scores. These results suggest that GERD probably does not play a major role in the pathogenesis of inflammation in the gastric cardia.
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Affiliation(s)
- Shailender Singh
- University of Kansas School of Medicine and Veterans Affairs Medical Center, Kansas City, Kansas, Missouri 64128, USA
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35
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Watari J, Tanaka A, Tanabe H, Sato R, Moriichi K, Zaky A, Okamoto K, Maemoto A, Fujiya M, Ashida T, Das KM, Kohgo Y. K-ras mutations and cell kinetics in Helicobacter pylori associated gastric intestinal metaplasia: a comparison before and after eradication in patients with chronic gastritis and gastric cancer. J Clin Pathol 2007; 60:921-6. [PMID: 16997920 PMCID: PMC1994498 DOI: 10.1136/jcp.2006.041939] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 08/14/2006] [Indexed: 01/10/2023]
Abstract
BACKGROUND Helicobacter pylori related gastric intestinal metaplasia (IM) is considered to be a precancerous lesion. AIMS To identify the effects of H pylori eradication on K-ras mutations, cell kinetics in IM and histological changes in patients with and without gastric cancers in a one-year prospective study. METHODS Patients included group A (n = 39), chronic gastritis, and group B (n = 53), intestinal-type early gastric cancer patients who had all undergone endoscopic mucosal resection (n = 25) or surgical resection (n = 28). K-ras codon 12 mutations in IM were examined, followed by DNA sequencing analysis. Proliferating and apoptotic cells were detected with anti-Ki-67 antibody and using the TUNEL method, respectively. RESULTS The incidence of K-ras mutations in the cancer was only 3.8%. The mutant K-ras in IM was observed more frequently in group A (46.2%) than in group B patients (1.9%) (p<0.005). After eradication, the K-ras mutations significantly declined to 12.8% in group A (p<0.005). The mutation pattern of K-ras codon 12 before eradication was that GGT was mainly changed to AGT (50%) in group A. AGT transformation was not affected by treatment. Apoptosis in IM showed an increase after H pylori eradication in both groups (p<0.05 in group A) although no histological improvement in IM was observed. The monocyte score was significantly higher in group A than in group B (p<0.05); the score improved significantly after eradication. CONCLUSIONS K-ras mutations in IM do not always play a role in gastric carcinogenesis but cell kinetics, especially apoptosis, in IM may contribute to it. There are early events in K-ras mutations which are influenced by H pylori infection; some mutations may also be selected by eradication. These unstable K-ras mutations in IM may be related to lymphocyte infiltration caused by H pylori infection.
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Affiliation(s)
- J Watari
- Division of Gastroenterology and Hepatology, Department of Medicine, Asahikawa Medical College, Asahikawa, Japan.
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Fuccio L, Zagari RM, Minardi ME, Bazzoli F. Systematic review: Helicobacter pylori eradication for the prevention of gastric cancer. Aliment Pharmacol Ther 2007; 25:133-41. [PMID: 17229238 DOI: 10.1111/j.1365-2036.2006.03183.x] [Citation(s) in RCA: 69] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
BACKGROUND Helicobacter pylori is recognized as one of the most significant risk factors for gastric cancer, and H. pylori eradication has been proposed as a possible primary chemo-preventive strategy to reduce gastric cancer incidence. AIM To evaluate the available evidence on the efficacy of H. pylori eradication in the prevention of gastric cancer. METHODS Epidemiological, observational and interventional studies, as well as decisional models, were taken into account in this review. RESULTS Large-scale epidemiological studies clearly link H. pylori infection with non-cardia gastric cancer. Current evidence suggests that, in a subpopulation of treated subjects, H. pylori eradication prevents the progression of preneoplastic lesions. Studies that have attempted to evaluate the effect of H. pylori eradication on the incidence of gastric cancer have not provided definitive answers. H. pylori eradication seems to reduce the incidence of gastric cancer in patients without baseline precancerous gastric lesions. Decisional models suggest that H. pylori screening could be cost-effective, but there is not yet sufficient evidence to support the setting up of a general screening programme. CONCLUSION Helicobacter pylori eradication is a plausible intervention for gastric cancer prevention; however, it seems to be relevant in only a subset of subjects.
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Affiliation(s)
- L Fuccio
- Department of Internal Medicine and Gastroenterology, University of Bologna, Bologna, Italy
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37
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Abstract
Gastric cancer is the second most common fatal malignancy in the world. Its incidence is high in East Asia. Helicobacter pylori infection is an important factor in the pathogenesis of gastric cancer. Epidemiological studies have established a strong causal relationship between H. pylori infection and gastric cancer. H. pylori eradication is therefore likely to be one of the most promising approaches to gastric cancer prevention. Animal studies have shown that eradication of H. pylori infection, especially at the early stage, is effective in preventing H. pylori-related gastric carcinogenesis. However, the available data from human studies show that H. pylori eradication does not completely prevent gastric cancer and that it might be useful only in patients without atrophic gastritis or intestinal metaplasia at baseline. Longer follow-up and additional studies are needed to clarify this issue.
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Affiliation(s)
- Ting Kin Cheung
- Department of Medicine, University of Hong Kong, Queen Mary Hospital, Pokfulam Road, Hong Kong, China
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38
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Take S, Mizuno M, Ishiki K, Nagahara Y, Yoshida T, Yokota K, Oguma K. Baseline gastric mucosal atrophy is a risk factor associated with the development of gastric cancer after Helicobacter pylori eradication therapy in patients with peptic ulcer diseases. J Gastroenterol 2007; 42 Suppl 17:21-7. [PMID: 17238021 DOI: 10.1007/s00535-006-1924-9] [Citation(s) in RCA: 93] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
BACKGROUND We previously reported that eradication of Helicobacter pylori could reduce the risk of developing gastric cancer in patients with peptic ulcer diseases. In the present study, we further followed up our patient groups to identify factors associated with the development of gastric cancer. METHODS Prospective posteradication evaluations were conducted in 1342 consecutive patients (1191 men and 151 women; mean age, 50 years) with peptic ulcer disease who had received H. pylori eradication therapy. The patients had undergone endoscopic examination before eradication therapy to evaluate peptic ulcers, background gastric mucosa, and H. pylori infection. After confirmation of eradication, follow-up endoscopy was performed yearly. RESULTS A total of 1131 patients were followed for up to 9.5 years (mean, 3.9 years). Gastric cancer developed in 9 of 953 patients cured of infection and in 4 of 178 who had persistent infection (P=0.04). The risk of developing gastric cancer after receiving H. pylori eradication therapy was increased according to the grade of baseline gastric mucosal atrophy (P=0.01). In patients with peptic ulcer diseases, persistent infection of H. pylori (hazard ratio, 3.9; P=0.03), the grade of baseline gastric mucosal atrophy (3.3, P=0.01) and age (2.0, P=0.04) were identified as significant risk factors for developing gastric cancer. CONCLUSIONS The grade of gastric atrophy was closely related to the development of gastric cancer after receiving H. pylori eradication therapy. Thus, eradication of H. pylori before the significant expansion of atrophy is most beneficial to prevent gastric cancer.
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Affiliation(s)
- Susumu Take
- Fukuwatari Municipal Hospital, Okayama, Japan
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Roberts D, Hopkins M, Miller S, Schafer W. Gastric MALT lymphoma in the absence of Helicobacter pylori infection presenting as an upper gastrointestinal hemorrhage. South Med J 2006; 99:1134-6. [PMID: 17100037 DOI: 10.1097/01.smj.0000215746.17667.b1] [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: 11/26/2022]
Abstract
Gastric MALT lymphoma is almost exclusively a sequelae of Helicobacter pylori infection and rarely presents with profuse bleeding. Gastric mucosa is not normally thought to contain lymphoid tissue, yet in the presence of H pylori reactive lymphoid follicles form which are possibly throught to predispose the patient to developing lymphoma. GI bleeding from these tumors is common during treatment as a consequence of tumor regression or necrosis. We present the case of a MALT Lymphoma in a 59 year-old woman manifesting as a brisk upper GI bleed without serologic or microbiologic evidence of an H pylori infection.
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Affiliation(s)
- Dustin Roberts
- Department of Internal Medicine, Naval Medical Center, Portsmouth, VA 23708, USA
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40
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Eisig JN, Zaterka S, Silva FM, Malfertheiner P, Mattar R, Rodriguez TN, Hashimoto CL, Iriya K, Laudanna AA, Moraes-Filho JPP. Helicobacter pylori recurrence in patients with duodenal ulcer: Clinical, endoscopic, histologic, and genotypic aspects. A 10-year Brazilian series. Helicobacter 2006; 11:431-5. [PMID: 16961804 DOI: 10.1111/j.1523-5378.2006.00434.x] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/06/2023]
Abstract
BACKGROUND Recurrence infection following successful eradication of Helicobacter pylori is usually low, except for countries with high prevalence of H. pylori. The aim of this study was to verify H. pylori recurrence rate in patients with duodenal ulcer after eradication and the possible relationship with environmental factors, histologic pattern of the mucosa and bacterial genotype. MATERIALS AND METHODS One-hundred and ninety-four patients with an active duodenal ulcer and who were successfully treated for H. pylori infection from 1990 to 1999 were studied. A questionnaire was answered about their living conditions, and a 14C-urea breath test was performed. Patients with a positive breath test underwent an upper endoscopy to investigate for possible ulcer recurrence; gastric biopsy samples were than collected for rapid urease test and for histologic assessment. H. pylori vacA and cagA genotype was determined by polymerase chain reaction in those samples with positive urease test. RESULTS H. pylori infection was detected in 11 patients (recurrence rate of 5.7%) that were not associated with the type of bacterial virulence. In 10 patients the ulcer was healed and all of them were clinically asymptomatic. In eight, histology showed an intensification of gastritis. All 11 patients had adequate housing and sanitary conditions and no other risk for H. pylori recurrence was identified. CONCLUSIONS The recurrence rate of H. pylori in Brazil was higher than that reported in developed countries, but lower than usually reported in developing ones. Ulcer relapse rarely occurs even in long-term follow up.
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Affiliation(s)
- Jaime N Eisig
- Department of Gastroenterology, University of São Paulo School of Medicine, São Paulo, Brazil.
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Abstract
The prognosis of gastric cancer is closely related to the stage of disease at diagnosis. Early gastric cancer, whereby disease is limited to mucosa and submucosa, confers a survival rate of greater than 90% in 5 years in many centres. Gastric cancer is still a major cause of cancer mortality worldwide. In high incidence areas such as Japan, screening of asymptomatic population has been advocated. However, in Western countries, mass screening is not cost-effective. Hence, strategy has been directed to screen symptomatic individuals who are at higher risk of gastric cancer. Most patients with early gastric cancer present with symptoms indistinguishable from benign peptic ulcer disease. Screening for this group of patients improves detection rate of early gastric cancer and therefore its prognosis. Endoscopy for surveillance of premalignant lesions has been explored with this objective in mind. Serology testing for biomarkers such as pepsinogen, anti-Helicobacter pylori antibody and gastrin has been studied as an alternative to endoscopy. There is compelling evidence for the role of H. pylori in the initiation of Correa's cascade (stepwise progression from chronic active gastritis, atrophic gastritis, intestinal metaplasia, dysplasia and finally adenocarcinoma). Regression of premalignant lesions has been demonstrated with H. pylori eradication. However, it is not known whether this might effectively prevent gastric cancer in either low or high-risk population.
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Affiliation(s)
- Yih K Tan
- Department of Surgery, Queen Elizabeth Hospital, Edgbaston, Birmingham, UK
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Murakami K, Kodama M, Sato R, Okimoto T, Watanabe K, Fujioka T. Helicobacter pylori eradication and associated changes in the gastric mucosa. Expert Rev Anti Infect Ther 2006; 3:757-64. [PMID: 16207167 DOI: 10.1586/14787210.3.5.757] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
Persistent Helicobacter pylori infection contributes towards the development of chronic gastritis. To clarify the changes in chronic gastritis as a precursor of gastric cancer secondary to H. pylori eradication is an important issue, as it has significant implications for reducing the risk of gastric cancer. Studies published to date, however, are far from consistent with regard to the morphologic changes reported following H. pylori eradication. Of these, some papers reported improvement in gastric atrophy or intestinal metaplasia, versus others reporting no improvement, with the majority of papers published after 2000 reporting improvement in these end points. The inconsistent results concerning the impact of H. pylori eradication on gastric atrophy could be due to the inconsistency of the diagnostic criteria employed for evaluation of the morphology, confounded by the difficulties involved in evaluating atrophic changes in the gastric mucosa. While adherence to the Updated Sydney System available for evaluation of gastritis is primarily required worldwide to ensure consistency in evaluating gastritis, long-term research into the morphologic changes associated with H. pylori eradication is also required to explore strategies for the prevention of gastric cancer with H. pylori eradication.
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Affiliation(s)
- Kazunari Murakami
- Department of Gastroenterology, Oita University, Faculty of Medicine, 1-1 Hasama, Oita 879-5593, Japan.
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Suzuki T, Matsuo K, Sawaki A, Ito H, Hirose K, Wakai K, Sato S, Nakamura T, Yamao K, Ueda R, Tajima K. Systematic review and meta-analysis: importance of CagA status for successful eradication of Helicobacter pylori infection. Aliment Pharmacol Ther 2006; 24:273-80. [PMID: 16842453 DOI: 10.1111/j.1365-2036.2006.02994.x] [Citation(s) in RCA: 34] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
BACKGROUND Some, but not all studies have provided evidence that the CagA status of Helicobacter pylori strains is a predictive factor for the outcome of eradication therapy. AIM To clarify the association between CagA status and eradication outcome. METHODS We included studies reporting the numbers of successful and failed cases in H. pylori-eradication therapy according to the CagA status. Fourteen studies (1529 patients) were included of 325 articles identified in the search. The pooled risk ratio for H. pylori-eradication failure in CagA-negative relative to CagA-positive strains and the pooled risk difference in eradication success between the two groups were used as summary statistics. Meta-regression was used for examining the source of heterogeneity. RESULTS The summary risk ratio for eradication failure in CagA-negative relative to CagA-positive was 2.0 (95% CI: 1.6-2.4, P < 0.001), corresponding with the summary risk difference for eradication success between the groups of 11% (95% CI: 3-19%, P = 0.011). Meta-regression analysis demonstrated that usage of polymerase chain reaction examination for CagA status and a high proportion of non-ulcer dyspepsia patients were factors for heterogeneity among studies. CONCLUSIONS Our meta-analysis confirmed the importance of the presence of CagA as a predictor for successful eradication of H. pylori.
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Affiliation(s)
- T Suzuki
- Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya, Japan
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Arkkila PET, Seppälä K, Färkkilä MA, Veijola L, Sipponen P. Helicobacter pylori eradication in the healing of atrophic gastritis: a one-year prospective study. Scand J Gastroenterol 2006; 41:782-90. [PMID: 16785190 DOI: 10.1080/00365520500463175] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
OBJECTIVE Whether gastric atrophy or intestinal metaplasia heals after successful treatment of Helicobacter pylori (H. pylori) infection is still a matter of controversy. The aim of this article was to clarify whether, after one year, H. pylori eradication is associated with healing in glandular atrophy and intestinal metaplasia in the corpus and antrum. MATERIAL AND METHODS Ninety-two H. pylori-positive peptic ulcer patients with atrophic gastritis (panatrophy, antral or corpus predominant) participated in the baseline study, 1-year prospective follow-up data being available from 76 patients. Mean age was 58+/-12.6 years (mean+/-SD) and the male/female ratio 2/1. The patients participated in an H. pylori eradication study in which they randomly received active eradication therapy. Endoscopy was performed before H. pylori eradication therapy and after 8 and 52 weeks, with specimens examined according to the Sydney system. RESULTS Of the 92 patients, 8 (9%) had panatrophy, 58 (63%) had antral- and 26 (28%) had corpus-predominant atrophic gastritis. After H. pylori eradication, the mean atrophy score declined in patients with antral-predominant atrophy from 1.5 (mean) to 0.7 (p<0.05), in corpus-predominant atrophy from 1.7 to 0.2 (p=NS) and in patients with panatrophy from 1.2 to 0.8 (p=NS). Atrophy healing was seen in 55% of antral-predominant atrophy patients who had successful H. pylori eradication. The mean antral atrophic score in one year declined in patients with duodenal ulcer (from 1.0 mean to 0.4) whereas it remained the same (1.3) in those with gastric ulcer (p<0.05). CONCLUSIONS Atrophy can diminish or even disappear, especially in the antrum, during a 1-year follow-up after eradication of infection. Atrophy progression seems milder in patients with duodenal ulcer than in patients with gastric ulcer.
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Affiliation(s)
- Perttu E T Arkkila
- Department of Medicine, Division of Gastroenterology, Helsinki University Central Hospital, FI-00290 Helsinki, Finland.
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Lu B, Chen MT, Fan YH, Liu Y, Meng LN. Effects of Helicobacter pylori eradication on atrophic gastritis and intestinal metaplasia: A 3-year follow-up study. World J Gastroenterol 2005; 11:6518-20. [PMID: 16425426 PMCID: PMC4355796 DOI: 10.3748/wjg.v11.i41.6518] [Citation(s) in RCA: 39] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate the effect of H pylori eradication on atrophic gastritis and intestinal metaplasia (IM).
METHODS: Two hundred and fifty-nine patients with atrophic gastritis in the antrum were included in the study, 154 patients were selected for H pylori eradication therapy and the remaining 105 patients served as untreated group. Gastroscopy and biopsies were performed both at the beginning and at the end of a 3-year follow-up study. Gastritis was graded according to the updated Sydney system.
RESULTS: One hundred and seventy-nine patients completed the follow-up, 92 of them received H pylori eradication therapy and the remaining 87 H pylori-infected patients were in the untreated group. Chronic gastritis, active gastritis and the grade of atrophy significantly decreased in H pylori eradication group (P<0.01). However, the grade of IM increased in H pylori -infected group (P<0.05).
CONCLUSION: H pylori eradication may improve gastric mucosal inflammation, atrophy and prevent the progression of IM.
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Affiliation(s)
- Bin Lu
- Department of Gastroenterology, Affiliated Hospital of Zhejiang Traditional Chinese Medicine College, Hangzhou 310006, Zhejiang Province China.
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Di Mario F, Moussa AM, Dal Bò N, Caruana P, Pilotto A, Cavallaro LG, Cavestro GM, Iori V, Merli R, Franzé A, Rugge M. Recovery of gastric function after Helicobacter pylori eradication in subjects with body atrophic gastritis: prospective 4-year study. J Gastroenterol Hepatol 2005; 20:1661-6. [PMID: 16246182 DOI: 10.1111/j.1440-1746.2005.04051.x] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
BACKGROUND The relationship between Helicobacter pylori (H. pylori) eradication and atrophic changes in the gastric mucosa has not yet been fully defined. Although studies report a partial restoration of serum pepsinogen I (sPGI) levels after eradication, it is not clear if this finding reflects gastric mucosal healing on a morphological level. AIM To assess alterations in gastric function after H. pylori eradication on moderate/severe body atrophic gastritis by determination of sPGI levels. METHODS Twenty-three dyspeptic patients, selected from 284 consecutive H. pylori positive patients, with histological features of moderate/severe body atrophic gastritis and sPGI < 25 microg/L (11 men, mean age: 51.8 years, range: 29-79 years), underwent an upper gastrointestinal endoscopy with gastric biopsies and sPGI determination at baseline. All patients underwent eradication therapy. Serum pepsinogen I was measured again after 6 months, and at 1, 2, 3 and 4 years after eradication therapy. RESULTS Mean sPGI levels prior to eradication were 11.9 microg/L (range: 4-23 microg/L). Six months after eradication therapy, mean sPGI levels significantly increased to 17.4 microg/L (P = 0.04). At the completion of the study, 4 years after eradication, sPGI levels increased from 17.4 to 32.7 microg/L (P = 0.01). A significant progressive increase in sPGI levels was observed from 6 months to 1 year (17.4 to 23.9 microg/L) and from 1 to 2 years (23.9 to 26.0 microg/L, P = 0.01). Serum pepsinogen I levels higher than the cut-off value of 25 microg/L were observed at various time-points: 6.3% of patients at 6 months (1/16), 33.3% (5/15) at 1 year, 50% (7/14) at 24 months, 66.7% (6/9) at 36 months and 87.5% (7/8) at 4 years. CONCLUSION After H. pylori eradication, subjects with body atrophic gastritis showed long-term improvement of physiological gastric function, reflected by significantly and continually increasing sPGI levels over a 4-year period.
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Malfertheiner P, Sipponen P, Naumann M, Moayyedi P, Mégraud F, Xiao SD, Sugano K, Nyrén O. Helicobacter pylori eradication has the potential to prevent gastric cancer: a state-of-the-art critique. Am J Gastroenterol 2005; 100:2100-15. [PMID: 16128957 DOI: 10.1111/j.1572-0241.2005.41688.x] [Citation(s) in RCA: 146] [Impact Index Per Article: 7.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
Helicobacter pylori infection continues to play a key role in gastric diseases. Colonization of the gastric mucosa with the bacterium invariably results in the development of chronic gastritis and subsets of patients have a progression of the chronic gastritis to either ulcer or cancer. Epidemiological evidence indicates that the proportion of all gastric cancers attributable to H. pylori infection, and hence potentially preventable upon elimination of this risk factor, is somewhere in the range of 60% to 90%. This portends significant benefit in terms of morbidity and mortality, not least in populations with high prevalence of H. pylori infection coupled with high incidence of gastric cancer. The effect of prophylactic H. pylori eradication on gastric cancer incidence in humans remains unknown, however. Results from randomized trials are eagerly awaited, but availability of strong conclusive results may take many years. A growing number of studies show considerable variation in risk for gastric cancer development, depending on H. pylori strain type and the genetic predisposition of the host. There is also a remote possibility that elimination of the infection may have adverse health implications (e.g., antibiotic resistance), and therefore "simple" risk stratification and targeted chemoprevention is required. Based on "in depth" evidence presented at this workshop, the majority of the scientific task force favored a search-and-treat strategy in first-degree relatives of gastric cancer patients and an overwhelming majority felt that a more general screen-and-treat strategy should be focused in the first instance on a population with a high incidence of H. pylori-associated diseases.
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Affiliation(s)
- Peter Malfertheiner
- Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University, Magdeburg, Germany
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Lam S. Eradication of Helicobacter pylori and gastric cancer: Experience in Fujian Province of China. ACTA ACUST UNITED AC 2005; 6:116-8. [PMID: 16045600 DOI: 10.1111/j.1443-9573.2005.00209.x] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Affiliation(s)
- Sk Lam
- Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong
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Salih BA, Abasiyanik MF, Saribasak H, Huten O, Sander E. A follow-up study on the effect of Helicobacter pylori eradication on the severity of gastric histology. Dig Dis Sci 2005; 50:1517-22. [PMID: 16110845 DOI: 10.1007/s10620-005-2871-7] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
Helicobacter pylori genetic diversity and geographic distribution affect the severity of gastric histology; while eradication heals gastritis, the improvement of atrophy and intestinal metaplasia (IM) is still controversial. We investigated whether H. pylori infection and genotypes (cagA-vacA) influence the histological changes and whether eradication resolves these changes. Twenty-one patients (11 duodenal ulcer, 2 gastric ulcer, 8 gastritis) received treatment. Biopsies for CLO, PCR, histology, and culture were collected before and at 1 and 12 months after treatment, and serum samples at 0, 1, 2, 6, and 12 months. H. pylori eradication was achieved in 71% of the patients. Histological scores for H. pylori densities were significantly higher in the antrum and incisura angularis. Scores for mononuclear cell and neutrophil infiltration were significantly higher in regions with a high H. pylori density and improved progressively after eradication. Eight patients with atrophy including five with IM showed no significant changes 12 months after eradication. The cagA gene, detected in 13 (62%), the vacA-sla gene, in 20 (95%), and the vacA-m1 gene, in 12 (57%) of 21 patients were significantly associated with duodenal ulcer. A gradual decline in antibody titer reached an average of 67% 12 months after eradication. H. pylori infection and the associated genotypes (cagA of Western type) affect the severity of the gastric histology (mild forms of atrophy and IM) and the disease outcome. Eradication of H. pylori resulted in healing of gastritis, but with no significant improvement in atrophy or IM.
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Affiliation(s)
- Barik A Salih
- Fatih University, Faculty of Science, Department of Biology, Microbiology Unit, B. Cekmece, Istanbul, Turkey.
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Tatsuguchi A, Miyake K, Gudis K, Futagami S, Tsukui T, Wada K, Kishida T, Fukuda Y, Sugisaki Y, Sakamoto C. Effect of Helicobacter pylori infection on ghrelin expression in human gastric mucosa. Am J Gastroenterol 2004; 99:2121-7. [PMID: 15554990 DOI: 10.1111/j.1572-0241.2004.30291.x] [Citation(s) in RCA: 78] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
OBJECTIVES One of the counter-effects of Helicobacter pylori eradication therapy is subsequent obesity. Ghrelin is a recently discovered growth hormone releasing peptide. This endogenous secretagogue increases appetite and facilitates fat storage. The majority of circulating ghrelin is produced in the gastric mucosa. Therefore, we aimed at investigating changes in ghrelin immunoreactivity in gastric mucosa tissues of patients infected with H. pylori. METHODS Sixty-one patients with H. pylori infection (25 cases each of duodenal and gastric ulcer, and 11 cases of gastritis) and 22 healthy controls without H. pylori infection were included in the study. H. pylori-infected patients received standard proton pump-based triple therapy followed by histological examination and (13)C-urea breath test to confirm H. pylori eradication. H. pylori was eradicated in 50 out of 61 patients. Biopsy specimens were obtained from antrum and corpus before and 3 months following eradication. Ghrelin expression was evaluated immunohistochemically with an anti-ghrelin antibody, and the number of ghrelin-positive cells determined per 1 mm(2) of the lamina propria mucosa. RESULTS There was no relationship between ghrelin immunoreactivity and body weight or body mass index for healthy controls. The number of ghrelin-positive cells was significantly lower for H. pylori-infected patients than for healthy controls. However, the ghrelin-positive cell number increased significantly following H. pylori eradication without significant change in severity of atrophy. CONCLUSIONS These data indicated that H. pylori infection affected ghrelin expression. After H. pylori eradication, gastric tissue ghrelin concentration increased significantly. This could lead to the increased appetite and weight gain seen following H. pylori eradication.
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Affiliation(s)
- Atsushi Tatsuguchi
- Third Department of Internal Medicine, Division of Surgical Pathology, Nippon Medical School Hospital, Tokyo, Japan
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