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Zhang F, Zhang H, Liu YM, Tang FS. Helicobacter pylori, esophageal precancerous lesions, and proton pump inhibitor overuse. World J Gastroenterol 2024; 30:4591-4596. [PMID: 39563751 PMCID: PMC11572623 DOI: 10.3748/wjg.v30.i42.4591] [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: 08/21/2024] [Revised: 09/20/2024] [Accepted: 10/08/2024] [Indexed: 10/31/2024] Open
Abstract
This article reviews the cohort study published in the World Journal of Gastroenterology, which reported low rates of Helicobacter pylori (H. pylori) infection among esophageal cancer (EC) patients, coupled with proton pump inhibitor (PPI) overuse. These findings suggest a potential protective role of H. pylori against EC and indicate a possible association between PPI use and increased cancer risk. In light of these findings, our article examines the complex relationship between H. pylori and esophageal precancerous lesions, exploring the potential underlying mechanisms. We also address growing concerns regarding PPI overuse, including its potential effects on cancer therapy efficacy and the risk of drug interactions. Ultimately, this article highlights the urgent need for further research to evaluate the safety and efficacy of PPIs in cancer patients and to better understand their broader implications.
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Affiliation(s)
- Feng Zhang
- Department of Clinical Pharmacy, Key Laboratory of Basic Pharmacology of Guizhou Province and School of Pharmacy, Zunyi Medical University, Zunyi 563006, Guizhou Province, China
- Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi 563006, Guizhou Province, China
| | - Hang Zhang
- Department of Clinical Pharmacy, Key Laboratory of Basic Pharmacology of Guizhou Province and School of Pharmacy, Zunyi Medical University, Zunyi 563006, Guizhou Province, China
- Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi 563006, Guizhou Province, China
| | - Yan-Miao Liu
- The First Clinical Institute, Zunyi Medical University, Zunyi 563006, Guizhou Province, China
| | - Fu-Shan Tang
- Department of Clinical Pharmacy, Key Laboratory of Basic Pharmacology of Guizhou Province and School of Pharmacy, Zunyi Medical University, Zunyi 563006, Guizhou Province, China
- Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi 563006, Guizhou Province, China
- Key Laboratory of Clinical Pharmacy in Zunyi City, Zunyi Medical University, Zunyi 563006, Guizhou Province, China
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Chen L, Cao R, Han J, Yu H, Li Y, Wang X, Chen J, Qi X. Association of Helicobacter pylori infection with colorectal polyps/adenomas: A single-center cross-sectional study. Cancer Epidemiol 2024; 92:102626. [PMID: 39079227 DOI: 10.1016/j.canep.2024.102626] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/07/2024] [Revised: 07/01/2024] [Accepted: 07/18/2024] [Indexed: 09/17/2024]
Abstract
BACKGROUND Helicobacter pylori (H. pylori) infection may be associated with colorectal polyps/adenomas, but the current evidence remains controversial. METHODS We retrospectively screened the medical records of 655 participants who underwent both colonoscopy and H. pylori test from June 15, 2020 to April 30, 2023. The number, size, location, and pathological type of colorectal polyps/adenomas were compared between H. pylori positive and negative groups. Adjusting for age, gender, smoking, drinking, hypertension, diabetes, fatty liver, body mass index, and inflammatory and metabolic indicators, multivariate logistic regression analyses were performed to evaluate the association of H. pylori infection with the number, size, location, and pathological type of colorectal polyps/adenomas, where no polyp/adenoma was used as reference. RESULTS Overall, 508 participants were included, of whom 154 and 354 were divided into H. pylori positive and negative groups, respectively. H. pylori positive group had significantly higher colorectal polyps/adenomas (74.7 % vs. 65.8 %, P=0.048), low-grade adenomas (55.7 % vs. 47.6 %, P=0.026), advanced adenomas (22.6 % vs. 13.3 %, P=0.008), and colorectal polyps/adenomas with sizes of ≥6 mm (61.7 % vs. 48.5 %, P=0.002) and ≥10 mm (25.2 % vs. 14.6 %, P=0.004) than H. pylori negative group. In multivariate logistic regression analyses, H. pylori infection was independently associated with low-grade adenomas (OR=2.677, 95 %CI=1.283-5.587, P=0.009), advanced adenomas (OR=3.017, 95 %CI=1.007-9.036, P=0.049), right-side colon polyps/adenomas (OR=5.553, 95 %CI=1.679-18.360, P=0.005), and colorectal polyps/adenomas with sizes of ≥10 mm (OR=4.436, 95 %CI=1.478-13.310, P=0.008), but not number of colorectal polyps/adenomas. CONCLUSION H. pylori infection is associated with increased risk of colorectal polyps/adenomas, especially low-grade adenomas, advanced adenomas, right-side colon polyps/adenomas, and large colorectal polyps/adenomas.
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Affiliation(s)
- Lan Chen
- Department of Gastroenterology, General Hospital of Northern Theater Command, Shenyang, China; Postgraduate College, Jinzhou Medical University, Jinzhou, China
| | - Rongrong Cao
- Department of Gastroenterology, General Hospital of Northern Theater Command, Shenyang, China
| | - Jie Han
- Department of Gastroenterology, General Hospital of Northern Theater Command, Shenyang, China
| | - Honglu Yu
- Department of Gastroenterology, General Hospital of Northern Theater Command, Shenyang, China
| | - Yingchao Li
- Department of Gastroenterology, General Hospital of Northern Theater Command, Shenyang, China
| | - Xiaomin Wang
- Department of Gastroenterology, General Hospital of Northern Theater Command, Shenyang, China
| | - Jiang Chen
- Department of Gastroenterology, General Hospital of Northern Theater Command, Shenyang, China.
| | - Xingshun Qi
- Department of Gastroenterology, General Hospital of Northern Theater Command, Shenyang, China.
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Ma S, Guo X, Wang C, Yin Y, Xu G, Chen H, Qi X. Association of Barrett's esophagus with Helicobacter pylori infection: a meta-analysis. Ther Adv Chronic Dis 2022; 13:20406223221117971. [PMID: 36034104 PMCID: PMC9403448 DOI: 10.1177/20406223221117971] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/24/2022] [Accepted: 07/19/2022] [Indexed: 11/25/2022] Open
Abstract
Background and Aims: Barrett’s esophagus (BE) is the only recognized precursor for esophageal
adenocarcinoma. Helicobacter pylori (H.
pylori) infection is a major contributing factor towards upper
gastrointestinal diseases, but its relationship with BE remains
controversial. Some previous studies suggested that H.
pylori infection negatively correlated with BE, while others
did not. This may be attributed to the difference in the selection of
control groups among studies. The present meta-analysis aims to clarify
their association by combining all available data from well-designed
studies. Methods: The PubMed, EMBASE, and Cochrane
Library databases were searched. Odds ratios (ORs) with 95%
confidence intervals (CIs) were pooled by a random-effects model.
Heterogeneity was evaluated using the Cochran’s Q test and
I2 statistics. Meta-regression, subgroup,
and leave-one-out sensitivity analyses were employed to explore the sources
of heterogeneity. Results: Twenty-four studies with 1,354,369 participants were included. Meta-analysis
found that patients with BE had a significantly lower prevalence of
H. pylori infection than those without (OR = 0.53, 95%
CI = 0.45–0.64; p < 0.001). The heterogeneity was
statistically significant (I² = 79%;
p < 0.001). Meta-regression, subgroup, and leave-one-out
sensitivity analyses did not find any source of heterogeneity. Meta-analysis
of 7 studies demonstrated that CagA-positive H. pylori
infection inversely correlated with BE (OR = 0.25, 95% CI = 0.15–0.44;
p = 0.000), but not CagA-negative H.
pylori infection (OR = 1.22, 95% CI = 0.90–1.67;
p = 0.206). Meta-analysis of 4 studies also
demonstrated that H. pylori infection inversely correlated
with LSBE (OR = 0.39, 95% CI = 0.18–0.86; p = 0.019), but
not SSBE (OR = 0.73, 95% CI = 0.30–1.77; p = 0.484). Conclusion: H. pylori infection negatively correlates with BE. More
experimental studies should be necessary to elucidate the potential
mechanisms in future.
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Affiliation(s)
| | | | | | | | - Guangqin Xu
- Department of Gastroenterology, General
Hospital of Northern Theater Command, Shenyang, China
- Graduate School, Dalian Medical University,
Dalian, China
| | - Hongxin Chen
- Department of Gastroenterology, General
Hospital of Northern Theater Command, Shenyang, China
- Graduate School, Liaoning University of
Traditional Chinese Medicine, Shenyang, China
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Engevik AC, Kaji I, Goldenring JR. The Physiology of the Gastric Parietal Cell. Physiol Rev 2020; 100:573-602. [PMID: 31670611 PMCID: PMC7327232 DOI: 10.1152/physrev.00016.2019] [Citation(s) in RCA: 128] [Impact Index Per Article: 25.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/18/2019] [Revised: 10/10/2019] [Accepted: 10/13/2019] [Indexed: 12/11/2022] Open
Abstract
Parietal cells are responsible for gastric acid secretion, which aids in the digestion of food, absorption of minerals, and control of harmful bacteria. However, a fine balance of activators and inhibitors of parietal cell-mediated acid secretion is required to ensure proper digestion of food, while preventing damage to the gastric and duodenal mucosa. As a result, parietal cell secretion is highly regulated through numerous mechanisms including the vagus nerve, gastrin, histamine, ghrelin, somatostatin, glucagon-like peptide 1, and other agonists and antagonists. The tight regulation of parietal cells ensures the proper secretion of HCl. The H+-K+-ATPase enzyme expressed in parietal cells regulates the exchange of cytoplasmic H+ for extracellular K+. The H+ secreted into the gastric lumen by the H+-K+-ATPase combines with luminal Cl- to form gastric acid, HCl. Inhibition of the H+-K+-ATPase is the most efficacious method of preventing harmful gastric acid secretion. Proton pump inhibitors and potassium competitive acid blockers are widely used therapeutically to inhibit acid secretion. Stimulated delivery of the H+-K+-ATPase to the parietal cell apical surface requires the fusion of intracellular tubulovesicles with the overlying secretory canaliculus, a process that represents the most prominent example of apical membrane recycling. In addition to their unique ability to secrete gastric acid, parietal cells also play an important role in gastric mucosal homeostasis through the secretion of multiple growth factor molecules. The gastric parietal cell therefore plays multiple roles in gastric secretion and protection as well as coordination of physiological repair.
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Affiliation(s)
- Amy C Engevik
- Departments of Surgery and of Cell and Developmental Biology and the Epithelial Biology Center, Vanderbilt University School of Medicine, Vanderbilt University Medical Center and the Nashville VA Medical Center, Nashville, Tennessee
| | - Izumi Kaji
- Departments of Surgery and of Cell and Developmental Biology and the Epithelial Biology Center, Vanderbilt University School of Medicine, Vanderbilt University Medical Center and the Nashville VA Medical Center, Nashville, Tennessee
| | - James R Goldenring
- Departments of Surgery and of Cell and Developmental Biology and the Epithelial Biology Center, Vanderbilt University School of Medicine, Vanderbilt University Medical Center and the Nashville VA Medical Center, Nashville, Tennessee
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5
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Yao X, Smolka AJ. Gastric Parietal Cell Physiology and Helicobacter pylori-Induced Disease. Gastroenterology 2019; 156:2158-2173. [PMID: 30831083 PMCID: PMC6715393 DOI: 10.1053/j.gastro.2019.02.036] [Citation(s) in RCA: 69] [Impact Index Per Article: 11.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/22/2018] [Revised: 02/12/2019] [Accepted: 02/14/2019] [Indexed: 12/13/2022]
Abstract
Acidification of the gastric lumen poses a barrier to transit of potentially pathogenic bacteria and enables activation of pepsin to complement nutrient proteolysis initiated by salivary proteases. Histamine-induced activation of the PKA signaling pathway in gastric corpus parietal cells causes insertion of proton pumps into their apical plasma membranes. Parietal cell secretion and homeostasis are regulated by signaling pathways that control cytoskeletal changes required for apical membrane remodeling and organelle and proton pump activities. Helicobacter pylori colonization of human gastric mucosa affects gastric epithelial cell plasticity and homeostasis, promoting epithelial progression to neoplasia. By intervening in proton pump expression, H pylori regulates the abundance and diversity of microbiota that populate the intestinal lumen. We review stimulation-secretion coupling and renewal mechanisms in parietal cells and the mechanisms by which H pylori toxins and effectors alter cell secretory pathways (constitutive and regulated) and organelles to establish and maintain their inter- and intracellular niches. Studies of bacterial toxins and their effector proteins have provided insights into parietal cell physiology and the mechanisms by which pathogens gain control of cell activities, increasing our understanding of gastrointestinal physiology, microbial infectious disease, and immunology.
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Affiliation(s)
- Xuebiao Yao
- MOE Key Laboratory of Cellular Dynamics, CAS Center for Excellence in Molecular Cell Science, University of Science and Technology of China, Hefei, China; Keck Center for Cellular Dynamics and Organoids Plasticity, Morehouse School of Medicine, Atlanta, Georgia.
| | - Adam J. Smolka
- Gastroenterology and Hepatology Division, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina
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6
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Waldum HL, Kleveland PM, Sørdal ØF. Helicobacter pylori and gastric acid: an intimate and reciprocal relationship. Therap Adv Gastroenterol 2016; 9:836-844. [PMID: 27803738 PMCID: PMC5076771 DOI: 10.1177/1756283x16663395] [Citation(s) in RCA: 54] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023] Open
Abstract
Helicobacter pylori (Hp) is the main cause of gastritis, peptic ulcer disease and gastric cancer. There are still unanswered questions related to the interaction between Hp and man, like what determines the susceptibility for the initial infection and the mechanisms for the carcinogenic effect. The initial infection seems to require a temporal gastric hypoacidity. For Hp to survive in the gastric mucous layer, some acidity is necessary. Hp itself is probably not directly carcinogenic. Only when inducing oxyntic mucosal inflammation and atrophy with hypoacidity, Hp predisposes for gastric cancer. Gastrin most likely plays a central role in the Hp pathogenesis of duodenal ulcer and gastric cancer.
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Affiliation(s)
- Helge L. Waldum
- Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway
| | - Per M. Kleveland
- Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway
| | - Øystein F. Sørdal
- Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway
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Oyola SO, Evans KJ, Smith TK, Smith BA, Hilley JD, Mottram JC, Kaye PM, Smith DF. Functional analysis of Leishmania cyclopropane fatty acid synthetase. PLoS One 2012; 7:e51300. [PMID: 23251490 PMCID: PMC3519623 DOI: 10.1371/journal.pone.0051300] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/04/2012] [Accepted: 10/31/2012] [Indexed: 01/14/2023] Open
Abstract
The single gene encoding cyclopropane fatty acid synthetase (CFAS) is present in Leishmania infantum, L. mexicana and L. braziliensis but absent from L. major, a causative agent of cutaneous leishmaniasis. In L. infantum, usually causative agent of visceral leishmaniasis, the CFAS gene is transcribed in both insect (extracellular) and host (intracellular) stages of the parasite life cycle. Tagged CFAS protein is stably detected in intracellular L. infantum but only during the early log phase of extracellular growth, when it shows partial localisation to the endoplasmic reticulum. Lipid analyses of L. infantum wild type, CFAS null and complemented parasites detect a low abundance CFAS-dependent C19Δ fatty acid, characteristic of a cyclopropanated species, in wild type and add-back cells. Sub-cellular fractionation studies locate the C19Δ fatty acid to both ER and plasma membrane-enriched fractions. This fatty acid is not detectable in wild type L. major, although expression of the L. infantum CFAS gene in L. major generates cyclopropanated fatty acids, indicating that the substrate for this modification is present in L. major, despite the absence of the modifying enzyme. Loss of the L. infantum CFAS gene does not affect extracellular parasite growth, phagocytosis or early survival in macrophages. However, while endocytosis is also unaffected in the extracellular CFAS nulls, membrane transporter activity is defective and the null parasites are more resistant to oxidative stress. Following infection in vivo, L. infantum CFAS nulls exhibit lower parasite burdens in both the liver and spleen of susceptible hosts but it has not been possible to complement this phenotype, suggesting that loss of C19Δ fatty acid may lead to irreversible changes in cell physiology that cannot be rescued by re-expression. Aberrant cyclopropanation in L. major decreases parasite virulence but does not influence parasite tissue tropism.
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Affiliation(s)
- Samuel O Oyola
- Centre for Immunology and Infection, Department of Biology/Hull York Medical School, University of York, York, United Kingdom
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8
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Choi KD, Kim N, Jang IJ, Park YS, Cho JY, Kim JR, Shin JM, Jung HC, Song IS. Optimal dose of intravenous pantoprazole in patients with peptic ulcer bleeding requiring endoscopic hemostasis in Korea. J Gastroenterol Hepatol 2009; 24:1617-24. [PMID: 19686407 DOI: 10.1111/j.1440-1746.2009.05939.x] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
BACKGROUND AND AIM The lowest effective dose of proton pump inhibitors (PPI) for prevention of peptic ulcer rebleeding remains unclear. The objective of the present study was to evaluate whether low-dose PPI has a similar efficacy to high-dose i.v. administration for maintaining intragastric pH above 6. METHODS Sixty-one patients with bleeding ulcers were randomized into one of three groups after endoscopic hemostasis: pantoprazole 80 mg bolus followed by 8 mg/h; 40 mg, 4 mg/h infusion; and bolus injection of 40 mg every 24 h. Intragastric pH values and rebleeding rates were measured. In addition, pharmacokinetic parameters and association with CYP2C19 polymorphisms and H. pylori infection were assessed. RESULTS Mean percentage of time with intragastric pH > 6, and the proportion of patients with pH > 6 for more than 60% of the time were significantly higher in the 40 mg, 4 mg/h infusion group compared to the 40 mg bolus injection. There was no significant difference between the 80 mg, 8 mg/h and the 40 mg, 4 mg/h groups. In the H. pylori (-) group, only 40% of patients that received continuous infusion reached the target pH > 6 for more than 60% of the time; this was significantly lower than the H. pylori (+) group, 87.5% (P = 0.026). CONCLUSIONS A continuous infusion, regardless of high or low dose, was more effective for acid suppression than a 40 mg bolus PPI injection in Korea. H. pylori infection was an important factor for the maintenance of an intragastric pH > 6.
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Affiliation(s)
- Kee Don Choi
- Department of Internal Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea
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9
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Nouraie M, Radmard AR, Zaer-Rezaii H, Razjouyan H, Nasseri-Moghaddam S, Malekzadeh R. Hygiene could affect GERD prevalence independently: a population-based study in Tehran. Am J Gastroenterol 2007; 102:1353-60. [PMID: 17437507 DOI: 10.1111/j.1572-0241.2007.01208.x] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
OBJECTIVE Population-based data on gastroesophageal reflux disease (GERD) in Iran are limited. Current study is going to determine the prevalence of GERD in Tehran, Iran, and its association with potential risk factors. METHODS In this cross-sectional study, a random clustered sample of Tehran province permanent households was selected from the latest postcodes. Data were collected by direct interview for each person aged 18-65 yr. GERD was defined as the existence of at least weekly episodes of heartburn and/or acid regurgitation during the last 6 months. All participants were asked about past and recent sanitary conditions, oral hygiene, and smoking. Odds ratios and 95% confidence intervals (CI) were calculated using multivariable analysis. RESULTS Interview was performed with 2,561 eligible subjects (42.3% men). Response rate was 84.8%. The prevalence of GERD was 21.2% (95% CI 18.7-23.7). According to multivariable logistic regression analyses, individuals whose drinking water was obtained from well or tank during childhood were more prone to experience GERD symptoms (OR 1.54, 95% CI 1.03-1.77 and OR 2.46, 95% CI 1.53-3.96, respectively). We also detected significant associations with increasing number of missing teeth (P value for linear trend = 0.02) and history of unpurified water consumption during past 10 yr (P < 0.001). Current smokers had a higher prevalence of reflux (OR 1.82, 95% CI 1.32-2.51). CONCLUSION The prevalence of GERD in our Iranian population was considerably higher than that reported from other Asian studies approaching western figures. GERD prevalence was significantly associated with the history of unpurified water consumption, poor sanitary conditions of childhood, number of missing teeth, and smoking in this population.
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Affiliation(s)
- Mehdi Nouraie
- Digestive Disease Research Center, Shariati Hospital, Medical Sciences/University of Tehran, Tehran, Iran
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10
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Scarpignato C. Antisecretory drugs, Helicobacter pylori infection and symptom relief in GORD: still an unexplored triangle. Dig Liver Dis 2005; 37:468-74. [PMID: 15893968 DOI: 10.1016/j.dld.2005.03.002] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Affiliation(s)
- C Scarpignato
- Laboratory of Clinical Pharmacology, School of Medicine and Dentistry, University of Parma, Italy.
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11
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Gisbert JP, Piqué JM. Indicaciones y consecuencias de la erradicación de Helicobacter pylori en la enfermedad por reflujo gastroesofágico. Med Clin (Barc) 2005; 124:697-709. [PMID: 15899166 DOI: 10.1157/13075094] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
Several epidemiological data indicate that H. pylori infection prevalence in patients with gastroesophageal reflux disease (GERD) is lower than that reported in respective controls, which would suggest that the organism plays a protective role against this disease. On the other hand, most studies demonstrate that the presence of the infection in patients with GERD does not negatively affect the therapeutic efficacy of proton pump inhibitors (PPIs), and, in case of negatively influencing it, the effects are not clinically relevant and are easily controllable with standard antisecretory treatment. Therefore, the decision to administer H. pylori eradication treatment to a patient should not be influenced by the concomitant presence of GERD. In most cases, H. pylori eradication does not seem to induce GERD development, and it does not seem to worsen GERD when it was already present. Nevertheless, when the gastritis pattern is unknown before the antibiotic administration, the effect of H. pylori eradication on gastric acid secretion and the incidence of GERD is unpredictable. In the exceptional cases in which H. pylori eradication could have negative effects on GERD, its clinical relevance will be limited, and reflux symptoms or endoscopic esophagitis will favourably respond to the standard PPI antisecretory treatment. Therefore, again, when H. pylori eradication is indicated in a particular patient, the concomitant diagnosis of GERD should not change our attitude. Finally, is has recently been recommended to eradicate H. pylori infection in those patients with GERD needing long-term treatment with PPI, as some studies have reported that these drugs induce, in presence of the organism, an atrophic gastritis, with the consequent risk of gastric cancer. However, most of these studies have important methodological defects, and several authors have reported contrary results. In any case, the appearance in the gastric mucosa of clinically relevant lesions, such as intestinal metaplasia, dysplasia or adenocarcinoma, in patients treated with PPI for several years, has not yet been demonstrated, although this could simply be a problem of time. This question seems to be too controversial to be answered with the available data, and we should wait until new studies clarify this topic. In the meantime, as it occurs with any controversial indication, the decision of the doctor facing a patient infected by H. pylori and needing maintenance therapy with PPIs should be assessed on a case by case basis.
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Affiliation(s)
- Javier P Gisbert
- Servicio de Aparato Digestivo, Hospital Universitario de La Princesa, Madrid, España.
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12
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Gööz M, Shaker M, Gööz P, Smolka AJ. Interleukin 1beta induces gastric epithelial cell matrix metalloproteinase secretion and activation during Helicobacter pylori infection. Gut 2003; 52:1250-6. [PMID: 12912854 PMCID: PMC1773796 DOI: 10.1136/gut.52.9.1250] [Citation(s) in RCA: 37] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 04/30/2003] [Indexed: 01/06/2023]
Abstract
BACKGROUND and aims: Matrix metalloproteinases (MMPs) are endopeptidases with roles in extracellular matrix remodelling, cell proliferation, and inflammatory processes. We showed previously that Helicobacter pylori infection of human gastric adenocarcinoma (AGS) cells increased epithelial secretion of epithelial MMP-1 and MMP-3 and bacterial secretion of MMP-3-like activity. In the present study, we sought to characterise the role of interleukin (IL)-1beta in H pylori induced secretion of epithelial MMPs. METHODS AND RESULTS AGS cells were treated with H pylori and/or IL-1beta. Comparable IL-8 secretory responses (approximately 1700 ng/ml) measured by ELISA were induced by 2.0 ng/ml IL-1beta and by H pylori at a multiplicity of infection (MOI) of 50. The same IL-1beta and H pylori concentrations induced comparable increases in AGS cell caseinolytic activity at 60 kDa. MMP-3 monoclonal antibody immunoblots of AGS cell conditioned media detected immunoreactive bands at 71 kDa and 56 kDa. H pylori (MOI=50-100) induced dose dependent increases in both bands whereas IL-1beta (0.2-2 ng/ml) induced dose dependent increases only in the 71 kDa band, which was identified as a MMP-3/TIMP-3 (tissue inhibitor of metalloproteinases 3) heterodimer. AGS/H pylori conditioned media expressed 24 times more MMP-3 activity than AGS/IL-1beta conditioned media. There was a strong interaction between IL-1beta and H pylori on MMP-3 secretion. CONCLUSIONS We conclude that IL-1beta induces gastric epithelial cell MMP-3 secretion, contributing to epithelial tissue destruction during H pylori infection. However, other bacterial/host factors are needed to mediate the full gastric epithelial cell MMP-3 secretory response induced by H pylori infection.
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Affiliation(s)
- M Gööz
- Gastroenterology and Hepatology Division, Department of Medicine, Medical University of South Carolina, Charleston, SC, USA
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13
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Inamori M, Togawa JI, Takahashi K, Yoneda M, Fujisawa N, Iwasaki T, Ozawa Y, Kikuchi T, Muramatsu K, Chiguchi G, Matsumoto S, Kawamura H, Abe Y, Kirikoshi H, Kobayashi N, Sakaguchi T, Takamura T, Nakajima A, Ueno N, Sekihara H. Comparison of the effect on intragastric pH of a single dose of omeprazole or rabeprazole: which is suitable for on-demand therapy? J Gastroenterol Hepatol 2003; 18:1034-8. [PMID: 12911659 DOI: 10.1046/j.1440-1746.2003.03126.x] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/26/2023]
Abstract
BACKGROUND AND AIMS An ideal medication for heartburn should have the rapid onset of action needed for on-demand treatment. However, assessment of the onset of action of proton pump inhibitors has been largely subjective. We compared the inhibitory effect on gastric acid secretion of a single oral dose of omeprazole with that of rabeprazole. METHODS Fourteen Helicobacter pylori-negative men participated in this randomized, double-masked, two-way cross-over study. Intragastric pH was monitored continuously for 6 h after a single, randomly assigned 20 mg oral dose of either omeprazole or rabeprazole. After a 7-day washout period, the other drug was administered. Each patient's S-mephenytoin 4'-hydroxylase (CYP2C19) genotype was determined by polymerase chain reaction-restriction fragment length polymorphism. RESULTS Intragastric pH and pH holding time did not differ between treatments when the data were analyzed for the whole group without stratifying for CYP2C19 status. In CYP2C19 homozygous and heterozygous extensive metabolizers (10 subjects), rabeprazole maintained the intragastric at pH > 3 and> 4 for longer than omeprazole during both the 5 and 6 h study periods, and the average pH during the 6 h study period was higher with rabeprazole than with omeprazole. In these extensive metabolizers, rabeprazole maintained the pH > 2,> 3,> 3.5 and> 4 for longer during the 6 h study period than did omeprazole. CONCLUSIONS In H. pylori-negative men who are CYP2C19 homozygous or heterozygous extensive metabolizers, the intragastric pH after a single dose of 20 mg rabeprazole is higher during first 5-6 h than that after a single dose of 20 mg omeprazole.
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Affiliation(s)
- Masahiko Inamori
- The Third Department of Internal Medicine, Yokohama City University School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan.
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14
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Loffeld RJLF, van der Hulst RWM. Helicobacter pylori and gastro-oesophageal reflux disease: association and clinical implications. To treat or not to treat with anti-H. pylori therapy? Scand J Gastroenterol 2003:15-8. [PMID: 12408498 DOI: 10.1080/003655202320621391] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/10/2023]
Abstract
BACKGROUND It has been reported that patients are at risk of developing reflux oesophagitis after successful anti-Helicobacter pylori therapy, and the presence of the bacterium might be protective against the development of reflux oesophagitis. METHODS Review of the literature. RESULTS H. pylori is relevant to the management of oesophagitis because it increases the pH-elevating effect of proton-pump inhibitors. which increase the tendency of H. pylori gastritis to progress to atrophic gastritis, and because eradication of H. pylori increases the likelihood of oesophagitis. H. pylori increases basal gastrin levels, basal acid output, meal-stimulated maximal acid output and 24-h intragastric acidity. The effects on gastric acid production depend on the distribution of gastritis in the stomach. CONCLUSION H. pylori eradication may induce or exacerbate gastro-oesophageal reflux by its influence on gastric acidity and the antisecretory action of proton-pump inhibitors.
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Affiliation(s)
- R J L F Loffeld
- Dept. of Internal Medicine, De Heel Zaans Medisch Centrum, Zaandam, The Netherlands.
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15
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Manes G, Pieramico O, Uomo G, Mosca S, de Nucci C, Balzano A. Relationship of sliding hiatus hernia to gastroesophageal reflux disease: a possible role for Helicobacter pylori infection? Dig Dis Sci 2003; 48:303-7. [PMID: 12643607 DOI: 10.1023/a:1021927526790] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/09/2022]
Abstract
Sliding hiatal hernia is a common endoscopic finding with a prevalence that increases with the age of patients. Although nearly all patients with GERD have HH, only a minority of patients with hernia reports reflux symptoms. Our hypothesis is that H. pylori infection may be responsible for the high number of asymptomatic hernias. After exclusion of patients with peptic ulcer, 507 patients with an endoscopic diagnosis of hernia were considered. Patients were divided into three groups: A, < or = 45 years, 141 patients; B, 46-60 years, 144 patients; and C, > or = 61 years, 222 patients. Presence of reflux symptoms (questionnaire) and esophagitis, H. pylori status, and gastric histology were recorded. The prevalence of hernia in the total series was 11% in group A, 23% in B, and 38% in C. Aging was associated with a significant increase in H. pylori prevalence and corpus gastritis scores, and a parallel decrease of GERD symptom prevalence, which was 66.6% in group A, 52.1% in B, and 46.8% in C (P < 0.01). Taking the three groups together, prevalence of H. pylori infection was higher in patients without GERD than with GERD (66.4 vs 57.3%, P < 0.05), and higher in patients with nonerosive GERD than erosive GERD (62.8 vs 48.6%, P = 0.02); corpus gastritis scores were significantly higher in patients without GERD than those with GERD and in those with nonerosive than erosive GERD. In conclusion, H. pylori infection protects against development of GERD in subjects with hiatus hernia. This effect is significantly more evident in the elderly where, in spite of the high prevalence of hernia, only a small number of individuals develop GERD. The development of a corpus-predominant gastritis is probably responsible for this effect.
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Affiliation(s)
- Gianpiero Manes
- Department of Gastroenterology, Cardarelli Hospital, Naples, Italy
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16
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Gisbert JP, Pajares JM. [Prevalence of Helicobacter pylori infection in gastroesophageal reflux disease and Barretts esophagus]. Med Clin (Barc) 2002; 119:217-23. [PMID: 12200010 DOI: 10.1016/s0025-7753(02)73368-x] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/26/2022]
Affiliation(s)
- Javier P Gisbert
- Servicio de Aparato Digestivo, Hospital Universitario de La Princesa, Madrid, Spain.
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17
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Gudlaugsdottir S, van Dekken H, Stijnen T, Wilson JHP. Prolonged use of proton pump inhibitors, CagA status, and the outcome of Helicobacter pylori gastritis. J Clin Gastroenterol 2002; 34:536-40. [PMID: 11960065 DOI: 10.1097/00004836-200205000-00011] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]
Abstract
GOALS AND BACKGROUND To assess whether prolonged use of proton pump inhibitors (PPIs) in patients infected with Helicobacter pylori has adverse effects on gastritis. STUDY We studied 34 H. pylori-positive individuals with reflux esophagitis, Barrett esophagus, or nonulcer dyspepsia. Half of them were on maintenance treatment with PPIs (mean, 8 years) and half were not.H. pylori and CagA status were tested serologically. Gastric biopsies were classified histopathologically by the updated Sydney classification. RESULTS Proton pump inhibitors in H. pylori gastritis are associated with significantly less antral inflammation and lower H. pylori density, regardless of CagA status. There was a tendency toward more antral atrophy in patients with the CagA strain who were undergoing maintenance treatment with PPIs (p = 0.08), but there was an opposite tendency in CagA-negative individuals (p = 0.08). Intestinal metaplasia was seen more frequently in CagA-positive, treated individuals (p = 0.028). CONCLUSIONS These findings support the hypothesis that CagA status is important in the progression to atrophy and that maintenance treatment with PPIs accelerate this progression, while reducing inflammatory infiltration.
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Affiliation(s)
- Sunna Gudlaugsdottir
- Department of Internal Medicine, University Hospital Rotterdam, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands
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18
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Sobhani I, Canedo S, Alchepo B, Vissuzaine C, Chevalier C, Buyse M, Moizo L, Laigneau JP, Mignon M, Lewin JM, Bado A. Putative effect of Helicobacter pylori and gastritis on gastric acid secretion in cat. Am J Physiol Gastrointest Liver Physiol 2002; 282:G727-34. [PMID: 11897633 DOI: 10.1152/ajpgi.00282.2001] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
Helicobacter pylori may increase or inhibit gastric acid. We studied acid variations and plasma gastrin in cats harboring Helicobacter felis, harboring H. pylori, or free of gastric pathogens with reference to thioperamide (H(3) receptor antagonist) and SR-27417A (PAF receptor antagonist). In cats harboring H. felis, gastric mucosa were histologically normal. After H. felis eradication, pentagastrin-stimulated acid secretion was increased (40%) compared with the situation before eradication. Thioperamide abolished this inhibitory effect of H. felis, whereas SR-27417A did not. Basal and meal-stimulated plasma gastrin levels were not affected by eradication therapy. Acid secretion was inhibited (-80%) in week 3, increased from weeks 5 to 9, and remained constant for up to 42 weeks after H. pylori infection. SR-27417A had no effect on acid secretion before week 8 but inhibited it thereafter, and thioperamide increased it (20%) only before week 7 in those cats. Helicobacter inhibits gastric acid via an H(3) receptor pathway. Inflammatory mediators are thus involved in adaptation to the inhibitory effects of H. pylori on acid secretion.
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Affiliation(s)
- Iradj Sobhani
- INSERM Unité 410, Hôpital Bichat Claude Bernard, 75877 Cedex Paris 18, France.
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19
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De Block CEM, De Leeuw IH, Bogers JJPM, Pelckmans PA, Ieven MM, Van Marck EAE, Van Hoof V, Máday E, Van Acker KL, Van Gaal LF. Helicobacter pylori, parietal cell antibodies and autoimmune gastropathy in type 1 diabetes mellitus. Aliment Pharmacol Ther 2002; 16:281-9. [PMID: 11860411 DOI: 10.1046/j.1365-2036.2002.01186.x] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
BACKGROUND Fifteen to 20% of type 1 diabetic patients exhibit parietal cell antibodies (PCA), which are associated with autoimmune gastritis, hypochlorhydria, iron deficiency and pernicious anaemia. AIM To examine whether Helicobacter pylori infection could explain the high prevalence of PCA and autoimmune gastropathy in diabetes. If so, H. pylori eradication could prevent autoimmune gastritis. METHODS In 229 type 1 diabetics (M/F: 135/94; age: 41 +/- 12 years) PCA were measured. H. pylori infection was assessed by serology, urea breath test in all and by histology (updated Sydney system) in 88 subjects. Pentagastrin tests were performed in 42 patients. RESULTS Sixty-nine patients were PCA-positive. H. pylori infection was present in 72 patients and was negatively associated with HLA-DQA1*0103-B1*0603 (OR=0.12, P=0.015) and positively with DQA1*0501-B1*0201 (OR=1.9, P=0.032). PCA-positivity was linked to HLA-DQA1*0501-B1*0301 (OR=3.9, P=0.017). A link between H. pylori and PCA was observed when PCA-positivity was defined as a titre > or = 1/20 (OR=2.0, P=0.03), but not if > or =1/40 was the cut-off point. PCA-positivity, but not H. pylori infection, was associated with iron deficiency anaemia (OR=2.7, P=0.008), pernicious anaemia (OR= 33.5, P < 0.0001), hypochlorhydria (OR=12.1, P=0.0008) and autoimmune gastritis (OR=12.5, P < 0.0001). CONCLUSIONS The HLA-bound susceptibility of H. pylori and PCA differed. PCA-positivity but not ongoing H. pylori infection is associated with autoimmune gastritis. Low titres of PCA might reflect H. pylori infection rather than autoimmune gastropathy.
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Affiliation(s)
- C E M De Block
- Department of Endocrinology-Diabetology, University of Antwerp, University Hospital Antwerp, Wilrijkstraat 10, B-2650 Edegem, Belgium.
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20
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Sanduleanu S, Jonkers D, de Bruïne A, Hameeteman W, Stockbrügger RW. Changes in gastric mucosa and luminal environment during acid-suppressive therapy: a review in depth. Dig Liver Dis 2001; 33:707-19. [PMID: 11785719 DOI: 10.1016/s1590-8658(01)80050-5] [Citation(s) in RCA: 31] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/09/2023]
Abstract
Acid-suppressive therapy and subsequent changes in gastric mucosa and luminal environment rank highly amongst the investigated issues in gastroenterology over the past two to three decades. Herewith, we present an overview of these intragastric changes, particularly during long-term administration of acid-suppresive medication and concurrent infection with Helicobacter pylori. Current evidence indicates that: i) Long-term acid suppression facilitates the development of fundic ECL cell hyperplasia, especially in the presence of Helicobacter pylori. No neoplastic changes directly attributable to acid suppression have so far been demonstrated in humans. ii) Acid-suppressive therapy increases the risk of enteric infections. iii) Acid-suppressive therapy does not alter fat and mineral bioavailability, but may decrease the absorption of protein-bound vitamin B12. iv) Acid suppression invariably results in intragastric overgrowth of non-Helicobacter pylori bacterial species. The concurrent infection with Helicobacter pylori may promote this bacterial overgrowth and the intragastric formation of N-nitrosamines. v) Acid-suppressive therapy alters the natural course of Helicobacter pylori gastritis, transforming the antral-predominant pattern into a body-predominant pattern, which in turn may progress to body gland atrophy. The pathophysiology of this phenomenon is currently under investigation. vi) In view of the potential adverse effects of acid suppression in the presence of Helicobacter pylori, the screen-and-treat strategy is advocated for Helicobacter pylori in subjects considered for long-term treatment.
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Affiliation(s)
- S Sanduleanu
- Department of Gastroenterology/Hepatology, University Hospital, Maastricht, The Netherlands.
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21
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Rokkas T, Ladas SD, Liatsos C, Panagou E, Karameris A, Raptis SA. Effectiveness of acid suppression in preventing gastroesophageal reflux disease (GERD) after successful treatment of Helicobacter pylori infection. Dig Dis Sci 2001; 46:1567-72. [PMID: 11478511 DOI: 10.1023/a:1010616710501] [Citation(s) in RCA: 7] [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
There is evidence that Helicobacter pylori eradication might predispose to gastroesophageal reflux disease (GERD). The aim of this prospective study was to examine the effectiveness of antisecretory treatment, after successful H. pylori eradication, in preventing GERD, since no data exist so far. Eighty initially H. pylori(+) patients, without GERD at the time of H. pylori eradication [50 peptic ulcer (PU) and 30 nonulcer (NU), 55 men, 25 women, median age 38 years, range 19-57], after successful H. pylori eradication were randomized to recieve either omeprazole 20 mg daily (group A) or no treatment (group B) for one year. All patients underwent upper gastrointestinal endoscopy at 0, 6, and 12 months or when GERD symptoms occurred. There were 40 patients in each group, and there were no statistically significant differences between the two groups in terms of sex, age, body weight, ulcer/no ulcer ratio, and other demographic data. Seven patients from group A and five patients from group B were lost to follow-up, and therefore there were 33 and 35 patients in groups A and B, respectively, who completed the study. One of 33 patients in group A (3%) and 10/35 (28.5%) in group B developed GERD symptoms during follow-up (P = 0.0022). The respective values for esophagitis were 0/33 (0%) and 6/35 (17.1%) (P = 0.0083). In conclusion, antisecretory treatment in H. pylori(+) patients, after successful eradication, is effective in preventing GERD.
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Affiliation(s)
- T Rokkas
- Gastroenterology Unit, 401 Army General Hospital, Athens, Greece
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22
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Padol IT, Moran AP, Hunt RH. Effect of purified lipopolysaccharides from strains of Helicobacter pylori and Helicobacter felis on acid secretion in mouse gastric glands in vitro. Infect Immun 2001; 69:3891-6. [PMID: 11349056 PMCID: PMC98418 DOI: 10.1128/iai.69.6.3891-3896.2001] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022] Open
Abstract
As a bacterial product, Helicobacter pylori lipopolysaccharide (LPS) can originate in close proximity to parietal cells, but the role of this uniquely structured endotoxin on acid secretion has not been fully investigated and remains unclear. The purpose of this study was to test the direct effect of purified LPS (tested range, 0.1 to 100 microg/ml) from various strains of H. pylori and from one Helicobacter felis strain on histamine- and carbachol-stimulated acid secretion in vitro using mouse gastric glands and the accumulation of [(14)C]aminopyrine. In addition, we investigated whether H. pylori LPS can interfere with two native antisecretory substances, prostaglandin E(2) (PGE(2)) and somatostatin, which may contribute to bacterial pathogenicity. Except for the LPS from H. pylori SS1 (Sydney strain), which gave a statistically significant increase in both histamine- and carbachol-stimulated acid output (38 and 24%, respectively; P < 0.05), no effect of the tested LPS was observed on acid secretion. H. pylori LPS purified from a patient isolate did not affect the potency or the efficacy of the inhibitory dose response curve to PGE(2) or somatostatin. Bacterial interstrain variation in the direct stimulatory effect of Helicobacter-derived LPS on acid secretion was observed, which probably reflects the molecular structure of LPS and the potential to contribute to virulence. Importantly, the data showed that H. pylori LPS did not have any direct antisecretory properties. It can be speculated that the acid stimulatory properties of LPS from H. pylori SS1 may contribute to the gastric damage observed in the mouse model of H. pylori infection.
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Affiliation(s)
- I T Padol
- Intestinal Disease Research Programme, McMaster University, Hamilton, Ontario, Canada
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23
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Rokkas T, Ladas SD, Triantafyllou K, Liatsos C, Petridou E, Papatheodorou G, Karameris A, Raptis SA. The association between CagA status and the development of esophagitis after the eradication of Helicobacter pylori. Am J Med 2001; 110:703-7. [PMID: 11403754 DOI: 10.1016/s0002-9343(01)00723-9] [Citation(s) in RCA: 22] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/25/2023]
Abstract
BACKGROUND Strains of Helicobacter pylori with the cytotoxine-associated gene A (cagA) are linked to severe forms of gastroduodenal disease. Although eradication of H. pylori may predispose to the development of reflux esophagitis, the effects of CagA status on risk of esophagitis after successful H. pylori treatment are not known. METHODS We studied 50 consecutive patients without esophagitis in whom H. pylori was eradicated successfully. CagA status was determined by immunoblotting sera from patients against H. pylori antigens. Patients underwent upper gastrointestinal endoscopy before eradication and 6, 12, 18, and 24 months after eradication or when reflux symptoms occurred. Biopsy specimens of the antrum and corpus were evaluated for gastritis before H. pylori eradication and at the end of the study. The sum of the scores for acute and chronic inflammation (both measured on a 0 [absent] to 3 [severe] scale) comprised the total gastritis severity score. RESULTS In a multivariate proportional hazards regression analysis, positive CagA serology (hazard ratio [HR] = 10, 95% confidence interval [CI]: 1.3 to 81) and moderate-to-severe corpus gastritis (total severity score > or =4) before eradication (HR = 2.3, 95% CI: 1.2 to 6.1) were independent risk factors for the development of esophagitis after H. pylori eradication. CONCLUSION Patients infected with strains of H. pylori that are cagA-positive are at increased risk of developing esophagitis after eradication of H. pylori.
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Affiliation(s)
- T Rokkas
- Gastroenterology Unit, 401 Army General Hospital, Athens, Greece
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24
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Beil W, Sewing KF, Busche R, Wagner S. Helicobacter pylori augments the acid inhibitory effect of omeprazole on parietal cells and gastric H(+)/K(+)-ATPase. Gut 2001; 48:157-62. [PMID: 11156634 PMCID: PMC1728211 DOI: 10.1136/gut.48.2.157] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
BACKGROUND In duodenal ulcer patients, intragastric acidity during omeprazole treatment is significantly lower before Helicobacter pylori eradication than after cure. AIMS To determine if H pylori enhances the acid inhibitory potency of omeprazole in isolated parietal cells and on H(+)/K(+)-ATPase. METHODS Rat parietal cells and pig gastric membrane vesicles enriched in H(+)/K(+)-ATPase activity were incubated with H pylori and the H pylori fatty acid cis 9,10-methyleneoctadecanoic acid (MOA), and the inhibitory effects of omeprazole on parietal cell acid production, H(+)/K(+)-ATPase enzyme activity, and ATPase mediated proton transport were assessed. RESULTS In isolated parietal cells, H pylori and MOA increased the acid inhibitory potency of omeprazole 1.8 fold. H pylori did not affect the inhibitory potency of omeprazole on H(+)/K(+)-ATPase enzyme activity. In proton transport studies, H pylori (intact bacteria and sonicate) and MOA accelerated the onset of the inhibitory effect of omeprazole and enhanced the proton dissipation rate in response to omeprazole. H. pylori itself increased proton permeability at the vesicle membrane. CONCLUSION Our results show that H pylori augments the acid inhibitory potency of omeprazole in parietal cells and enhances omeprazole induced proton efflux rate from gastric membrane vesicles. We suggest that omeprazole unmasks the permanent effect of H pylori on proton permeability at the apical parietal cell membrane, which is counteracted in the absence of a proton pump inhibitor by a reserve H(+)/K(+)-ATPase capacity.
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Affiliation(s)
- W Beil
- Department of General Pharmacology, Hannover Medical School, Hannover, Germany.
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25
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Martínek J, Kuzela L, Spicák J, Vavrecka A. Review article: the clinical influence of Helicobacter pylori in effective acid suppression-implications for the treatment of gastro-oesophageal reflux disease. Aliment Pharmacol Ther 2000; 14:979-90. [PMID: 10930891 DOI: 10.1046/j.1365-2036.2000.00805.x] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
The relationship between gastro-oesophageal reflux disease (GERD) and Helicobacter pylori is unclear. Recent data indicate that H. pylori probably exerts a protective effect against GERD. In recent years, the interaction between H. pylori, proton pump inhibitors and GERD has been widely studied. Currently available proton pump inhibitors produce significantly higher intragastric pH in H. pylori-positive patients than in those who are H. pylori negative, and this phenomenon may be clinically relevant. The mechanisms responsible for this difference in efficacy are not fully understood, although there are two major theories. Ammonia, produced by H. pylori, is able to neutralize gastric acid, and thus apparently increase the effect of acid suppressive agents (the 'ammonia theory'). The other theory is that decrease in acid output is due to the development of corpus gastritis during treatment with a proton pump inhibitor (the 'gastritis theory'). Treatment strategies to overcome this lowered sensitivity to acid suppression are to increase the frequency/dose of a proton pump inhibitor or to add an H2-receptor antagonist in the evening-but both have pharmaco-economic implications. An agent that could provide adequate pH control regardless of H. pylori status would be highly beneficial in the treatment of GERD, and may also lower treatment costs.
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Affiliation(s)
- J Martínek
- IKEM, Clinic of Hepatogastroenterology, Praha, Czech Republic; Clinic of Gastroenterology, St. Cyril and Method's Hospital, Bratislava, Slovak Republic.
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26
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Haruma K, Hamada H, Mihara M, Kamada T, Yoshihara M, Sumii K, Kajiyama G, Kawanishi M. Negative association between Helicobacter pylori infection and reflux esophagitis in older patients: case-control study in Japan. Helicobacter 2000; 5:24-9. [PMID: 10672048 DOI: 10.1046/j.1523-5378.2000.00003.x] [Citation(s) in RCA: 62] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
BACKGROUND Recent studies have clarified a close association between H. pylori infection and gastritis, peptic ulcer disease, and gastric cancer, but there is little information concerning the relationship between H. pylori infection and reflux esophagitis (RE). We investigated the relationship between H. pylori, RE, and corpus gastritis. SUBJECTS AND METHODS Ninety-five patients with RE and 190 sex- and age-matched asymptomatic healthy controls demonstrating no localized lesions in the upper GI tract were studied and evaluated for H. pylori infection, histologic gastritis, serum gastrin, and pepsinogens (PGs). RESULTS H. pylori infection was significantly lower in RE patients than in asymptomatic controls (41% vs. 76%, p <.01). Histologic gastritis of both the antrum and corpus was significantly less frequent (antrum; p <.01, corpus; p <. 01), and serum levels of PGI and the PG I/II ratio were significantly higher in RE patients than in controls (PGI; p <.05, PG I/II ratio; p <.01). When the subjects were divided into two age groups (59 years of age and younger and 60 years of age and older), a significant difference was found only among patients over 60 years of age (29% vs. 85%, p <.01). Among subjects in this age group, gastritis in both the antrum and corpus were significantly milder in RE patients than in controls. Although the prevalence of H. pylori infection was similar between the two groups of patients under 59 years of age, corpus gastritis was significantly milder in patients than in controls (p <.05). CONCLUSIONS A significantly low prevalence of H. pylori infection was found in RE patients over 60 years of age but not in those under 59 in comparison with sex- and age-matched controls. The relative lack of corpus gastritis might play a role in the pathogenesis of RE in our population through preservation of the acid secretion area.
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Affiliation(s)
- K Haruma
- Gastrointestinal Unit, First Department of Internal Medicine, Hiroshima University School of Medicine, and Department of Internal Medicine, Hiroshima Mitsubishi Hospital, Hiroshima, Japan
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27
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Abstract
The nature of the relationship between Helicobacter pylori (Hp) infection and gastroesophageal reflux disease (GERD) remains unclear. This article reviews the current body of knowledge regarding the association between these two common entities. The authors examine the potential interactions of Hp and GERD from epidemiologic and pathophysiologic viewpoints and summarize and critique the prevalence and eradication studies that have been performed to date. Special consideration is given to the possible effects that long-term use of proton pump inhibitors may have on Hp gastritis.
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Affiliation(s)
- D C Metz
- Division of Gastroenterology, University of Pennsylvania Health System, Philadelphia, USA
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28
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Murayama Y, Miyagawa J, Shinomura Y, Kanayama S, Yasunaga Y, Nishibayashi H, Yamamori K, Higashimoto Y, Matsuzawa Y. Morphological and functional restoration of parietal cells in helicobacter pylori associated enlarged fold gastritis after eradication. Gut 1999; 45:653-61. [PMID: 10517899 PMCID: PMC1727706 DOI: 10.1136/gut.45.5.653] [Citation(s) in RCA: 28] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
BACKGROUND/AIM Helicobacter pylori infections are associated with hypochlorhydria in patients with pangastritis. It has previously been shown that eradication of H pylori leads to an increase in acid secretion in H pylori associated enlarged fold gastritis, suggesting that H pylori infection affects parietal cell function in the gastric body. The aim of this study was to evaluate the effects of H pylori infection on parietal cell morphology and function in hypochlorhydric patients. PATIENTS/METHODS The presence of H pylori infection, mucosal length, and inflammatory infiltration were investigated in six patients with enlarged fold gastritis and 12 patients without enlarged folds. Parietal cell morphology was examined by immunohistochemistry using an antibody against the alpha subunit of H(+),K(+)-ATPase and electron microscopy. In addition, gastric acid secretion and fasting serum gastrin concentration were determined before and after the eradication of H pylori. RESULTS In the H pylori positive patients with enlarged fold gastritis, fold width, foveolar length, and inflammatory infiltration were increased. In addition, the immunostaining pattern of H(+), K(+)-ATPase was less uniform, and the percentage of altered parietal cells showing dilated canaliculi with vacuole-like structures and few short microvilli was greatly increased compared with that in H pylori positive patients without enlarged folds. After eradication, fold width, foveolar length, and inflammatory infiltrates decreased and nearly all parietal cells were restored to normal morphology. On the other hand, altered parietal cells were negligible in H pylori negative patients. In addition, the basal acid output and tetragastrin stimulated maximal acid output increased significantly from 0.5 (0.5) to 4.1 (1.5) mmol/h and from 2.5 (1.2) to 13.8 (0.7) mmol/h (p<0.01), and fasting serum gastrin concentrations decreased significantly from 213.5 (31.6) to 70.2 (7.5) pg/ml (p<0.01) after eradication in patients with enlarged fold gastritis. CONCLUSION The morphological changes in parietal cells associated with H pylori infection may be functionally associated with the inhibition of acid secretion seen in patients with enlarged fold gastritis.
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Affiliation(s)
- Y Murayama
- Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan
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29
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Lin HJ, Tseng GY, Hsieh YH, Perng CL, Lee FY, Chang FY, Lee SD. Will Helicobacter pylori affect short-term rebleeding rate in peptic ulcer bleeding patients after successful endoscopic therapy? Am J Gastroenterol 1999; 94:3184-8. [PMID: 10566712 DOI: 10.1111/j.1572-0241.1999.01516.x] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
OBJECTIVE Helicobacter pylori (H. pylori) can augment the pH-increasing effect of omeprazole in patients with peptic ulcer. A high intragastric pH may be helpful in preventing recurrent hemorrhage by stabilizing the blood clot at the ulcer base of bleeding peptic ulcer patients. Therefore, we hypothesized that omeprazole may reduce short-term rebleeding rate in these patients with H. pylori infection after initial hemostasis had been obtained. METHODS Between July 1996 and December 1998, 65 bleeding peptic ulcer patients (24 gastric ulcer, 41 duodenal ulcer) who had obtained initial hemostasis with endoscopic therapy were enrolled in this trial. Thirty (46.2%) of them were found to have H. pylori infection by a rapid urease test and pathological examination. For all studied patients, omeprazole was given 40 mg intravenously every 6 h for 3 days. Thereafter, omeprazole was given 20 mg per os (p.o.) once daily for 2 months. A pH meter was inserted in the fundus of each patient under fluoroscopic guidance after intravenous omeprazole had been administered. The occurrence of rebleeding episode was observed for 14 days. RESULTS In patients with H. pylori infection, intragastric pH (median, 95% confidence interval [CI]: 6.54, 5.90-6.68) was higher than in those without H. pylori infection (6.05, 5.59-6.50, p < 0.001). However, the patients with rebleeding (2 vs 3), volume of blood transfusion (median, range: 1000 ml, 0-2250 vs 750, 0-2000), number of operations (0 vs 1), mortality caused by bleeding (0 vs 0), and hospital stay (median, range: 6 days, 3-14 vs 7, 5-16) were not statistically different from those without H. pylori infection. CONCLUSIONS Omeprazole does increase intragastric pH in bleeding peptic ulcer patients with H. pylori infection. However, the presence of H. pylori infection does not affect the short-term rebleeding rate in these patients.
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Affiliation(s)
- H J Lin
- Department of Medicine, Veterans General Hospital-Taipei, Taiwan, Republic of China
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30
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Abstract
Greater than one-half of the world's population harbors Helicobacter pylori. The majority of infected individuals, however, remain asymptomatic, with only 10% to 20% developing diseases, including peptic ulcer disease, gastric cancer, and gastric mucosa-associated lymphoid tissue lymphoma. This article reviews host factors that may predispose an individual to both the acquisition of H. pylori infection and subsequent clinical outcome. Individuals with specific blood group antigens and human leukocyte antigen genotypes may be more susceptible to H. pylori infection. Additional factors, such as the age of acquisition, the host immune response, the site of infection, acid secretion, and interactions with nonhost factors (including bacterial virulence factors and environmental influences) may play a role in determining clinical outcome. Further investigation is required to clarify the mechanisms by which these interactions occur and, more critically, to determine their relative importance. This knowledge will enable the identification of individuals at risk of developing clinical disease with H. pylori infection.
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Affiliation(s)
- T N Nguyen
- Division of Gastroenterology, McGill University, Montreal, Quebec, Canada
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31
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van Herwaarden MA, Samsom M, van Nispen CH, Mulder PG, Smout AJ. The effect of Helicobacter pylori eradication on intragastric pH during dosing with lansoprazole or ranitidine. Aliment Pharmacol Ther 1999; 13:731-40. [PMID: 10383501 DOI: 10.1046/j.1365-2036.1999.00531.x] [Citation(s) in RCA: 49] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
BACKGROUND The antisecretory effect of omeprazole on intragastric pH is decreased in the absence of Helicobacter pylori. AIM To investigate the effect of H. pylori eradication on intragastric pH during lansoprazole or ranitidine dosing in 41 asymptomatic H. pylori-positive subjects. METHOD Two groups of healthy H. pylori-positive volunteers were investigated. One group was dosed with lansoprazole 30 mg at 08.00 hours for at least 8 days, before and after 2 weeks of placebo-controlled double-blind eradication therapy using ranitidine bismuth citrate 400 mg b.d. and clarithromycin 500 mg b.d. The other group was dosed with ranitidine 300 mg at 23.00 hours for at least 8 days using the same trial design. An upper endoscopy was performed to establish H. pylori status by rapid urease test, culture and histology before both periods of dosing. Twenty-four hour intragastric pH recording was performed on the final day of all periods of dosing. RESULTS H. pylori eradication significantly decreased the intragastric pH reached during lansoprazole treatment throughout all periods of the day. Intragastric pH during ranitidine treatment was not affected by H. pylori eradication, except for the late-night period. CONCLUSION H. pylori eradication has a more pronounced effect on the acid-inhibiting properties of lansoprazole than on those of ranitidine.
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Affiliation(s)
- M A van Herwaarden
- Gastrointestinal Research Unit, Departments of Gastroenterology and Surgery, University Hospital Utrecht.
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32
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Tani N, Watanabe Y, Suzuki T, Muramatsu S, Miyazawa M, Kimura N, Miwa T. Effects of inflammatory cytokines induced by Helicobacter pylori infection on aminopyrine accumulation in parietal cells isolated from guinea pigs. Dig Dis Sci 1999; 44:686-90. [PMID: 10219823 DOI: 10.1023/a:1026645321698] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
The effects of inflammatory cytokines induced by Helicobacter pylori infection on acid secretion have not been well defined. The purpose of this study was to investigate the direct effects of these cytokines on parietal cells isolated from guinea pigs. We examined the effects of human recombinant IL-1beta (0.05-100 ng/ml), IL-8 (2-256 ng/ml), and TNF-alpha (0.625-80 ng/ml) on acid secretion stimulated by three secretagogues (10(-4) M histamine, 10(-4) M carbachol, and 10(-5) M tetragastrin) and on basal acid secretion from isolated parietal cells, which was measured by the aminopyrine accumulation method. None of three cytokines showed any significant effects on stimulated or basal acid secretion from isolated guinea pig parietal cells. We concluded that inflammatory cytokines induced by Helicobacter pylori infection may affect acid secretion through mechanisms other than direct actions on parietal cells.
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Affiliation(s)
- N Tani
- Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan
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33
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Gillen D, Wirz AA, Neithercut WD, Ardill JE, McColl KE. Helicobacter pylori infection potentiates the inhibition of gastric acid secretion by omeprazole. Gut 1999; 44:468-75. [PMID: 10075952 PMCID: PMC1727447 DOI: 10.1136/gut.44.4.468] [Citation(s) in RCA: 96] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/01/2023]
Abstract
BACKGROUND Omeprazole has a greater intragastric pH elevating effect in Helicobacter pylori positive than negative subjects. Ammonia production by H pylori has been suggested as a probable mechanism. AIMS To assess the effect of H pylori status on gastric acid secretion during omeprazole treatment, and to examine the possible role of ammonia neutralisation of intragastric acid in increased omeprazole efficacy in infected subjects. METHODS Twenty H pylori positive and 12 H pylori negative healthy volunteers were examined before and six to eight weeks after commencing omeprazole 40 mg/day. On both occasions plasma gastrin and acid output were measured basally and in response to increasing doses of gastrin 17 (G-17). Gastric juice ammonium concentrations were also measured. RESULTS Prior to omeprazole, measurements were similar in the H pylori positive and negative subjects. During omeprazole, median basal intragastric pH was higher in the H pylori positive (7.95) versus negative (3.75) subjects (p<0.002). During omeprazole basal, submaximal (180 pmol/kg/h G-17), and maximal acid outputs (800 pmol/kg/h G-17) were lower in H pylori positive subjects (0.0, 3.6, 6.0 mmol/h respectively) versus negative subjects (0.3, 14.2, 18.6 mmol/h) (p<0.03 for each). This effect was not explained by neutralisation by ammonia. CONCLUSION The presence of H pylori infection leads to a more profound suppression of acid secretion during omeprazole treatment. The effect cannot be explained by neutralisation of intragastric acid by bacterial ammonia production and its precise mechanism has to be explained.
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Affiliation(s)
- D Gillen
- University Department of Medicine and Therapeutics, Western Infirmary, Glasgow G11 6NT, UK
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34
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Konturek PC, Brzozowski T, Konturek SJ, Stachura J, Karczewska E, Pajdo R, Ghiara P, Hahn EG. Mouse model of Helicobacter pylori infection: studies of gastric function and ulcer healing. Aliment Pharmacol Ther 1999; 13:333-46. [PMID: 10102967 DOI: 10.1046/j.1365-2036.1999.00476.x] [Citation(s) in RCA: 38] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
BACKGROUND Helicobacter pylori infection in humans is a major risk factor for peptic ulcer, but studies on the relation between H. pylori infection and gastric pathology are limited due to a deficiency of convenient animal models resembling this infection in humans. METHODS We studied the effects of inoculation of conventional BALB/c mice with CagA and VacA positive (type I) H. pylori or CagA and VacA negative H. pylori (type II) strains on gastric secretion and healing of chronic acetic acid-induced ulcers in mouse stomachs. The ulcer area, gastric blood flow, plasma interleukin (IL)-1beta and IL-12, as well as plasma gastrin and gastric luminal somatostatin were determined. Gastric mucosal biopsy samples were also taken for assessment of the presence of viable H. pylori using a rapid urease test, H. pylori-culture and the RT-PCR analysis of the signal for H. pylori CagA. RESULTS Gastric acid and pepsin secretion was reduced by over 50% immediately after H. pylori inoculation and accompanied by a significant increment in plasma gastrin and fall in gastric luminal somatostatin content observed over all test days, particularly in mice infected with type I H. pylori. The area of ulcers in vehicle-treated controls decreased significantly starting from day 2 after ulcer induction and then continued to decline for a further 14 days to heal almost completely after 28 days. In contrast, the ulcers were present until day 28 in all mice infected with type I or type II H. pylori strains, being significantly larger, especially with type I H. pylori infection. The gastric blood flow at the ulcer margin and ulcer crater in vehicle-treated mice gradually increased with decreasing ulcer size, after 14 and 28 days reaching a value which was not significantly different from that in vehicle-administered mice. In contrast, the gastric blood flow in type I H. pylori and, to a lesser extent, in type II H. pylori infected mice was significantly lower than in vehicle controls, both at the margin and at the crater of ulcers at all tested days. Histological changes such as oedema or congestion of surface epithelium were found after 7 days whereas mucosal inflammatory infiltration appeared after 14 days with a further increase after 28 days, especially in type I H. pylori and to a lesser extent in type II H. pylori infected mice. Plasma IL-1beta and IL-12 were significantly elevated at all tested days of ulcer healing and their increments were significantly higher in type I than in type II H. pylori infection. CONCLUSIONS Conventional mice with gastric ulcers can be successfully infected by both toxigenic and nontoxigenic H. pylori strains, and this infection causes an immediate suppression of gastric secretion and markedly delays the healing of ulcers due to the fall in mucosal microcirculation in the ulcer region, cytokine release and an impairment in the gastrin-somatostatin link that appears to be independent of gastritis and more pronounced with infection of toxigenic than nontoxigenic strains.
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Affiliation(s)
- P C Konturek
- Department of Medicine I, University of Erlangen-Nuremberg, Erlangen, Germany
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35
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Haruma K, Mihara M, Okamoto E, Kusunoki H, Hananoki M, Tanaka S, Yoshihara M, Sumii K, Kajiyama G. Eradication of Helicobacter pylori increases gastric acidity in patients with atrophic gastritis of the corpus-evaluation of 24-h pH monitoring. Aliment Pharmacol Ther 1999; 13:155-62. [PMID: 10102944 DOI: 10.1046/j.1365-2036.1999.00459.x] [Citation(s) in RCA: 110] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
BACKGROUND Recent studies have shown that the eradication of Helicobacter pylori results in a gastric acid secretion which decreases to normal levels in patients with duodenal ulcer disease. The aim of this study was to evaluate the effect of eradication of H. pylori in a 24-h study of gastric acidity in patients with atrophic gastritis of the corpus. METHODS Intragastric acidity was measured by continuous 24-h pH monitoring, and the histology of the gastric antrum and corpus were evaluated in 14 H. pylori-positive patients with histologically proven atrophic gastritis of the corpus (10 men, 4 women; mean age, 57 years) before and 1 year after anti-H. pylori therapy. RESULTS H. pylori was absent in 13 of 14 patients 1 year after treatment. Both gastritis and atrophy scores were significantly lower after eradication therapy (P < 0.01). The 24-h median pH and the percentage of 24-h pH readings above 4.0 units were significantly decreased after eradication therapy (from 5.12 +/- 0.36 to 2.69 +/- 0.21, and from 65.5 +/- 6.6% to 28.2 +/- 6.1%, P < 0.01, respectively.) CONCLUSION Eradication of H. pylori increases 24-h gastric acidity in patients with atrophic gastritis of the corpus. Improvement of the histology of the gastric antrum and corpus may lead to the normalization of gastric acidity.
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Affiliation(s)
- K Haruma
- Gastrointestinal Unit, First Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima, Japan.
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36
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Gillen D, Wirz AA, Ardill JE, McColl KE. Rebound hypersecretion after omeprazole and its relation to on-treatment acid suppression and Helicobacter pylori status. Gastroenterology 1999; 116:239-47. [PMID: 9922302 DOI: 10.1016/s0016-5085(99)70118-6] [Citation(s) in RCA: 123] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/25/2022]
Abstract
BACKGROUND & AIMS There have been conflicting reports regarding acid secretion after treatment with omeprazole. This study examined acid secretion after treatment with omeprazole and its relation to Helicobacter pylori status and on-treatment gastric function. METHODS Twelve H. pylori-negative and 9 H. pylori-positive subjects were examined before, on, and at day 15 after an 8-week course of 40 mg/day omeprazole. On each occasion, plasma gastrin, intragastric pH, and acid output were measured basally and in response to increasing doses of gastrin 17. RESULTS In the H. pylori-negative subjects at day 15 after omeprazole treatment, basal acid output was 82% higher (P < 0.007) and maximal acid output 28% higher (P < 0.003) than before omeprazole. The degree of increase in maximal acid output was related to both on-treatment pH and on-treatment fasting gastrin levels, being 48.0% in subjects with an on-treatment pH of >4 vs. 21. 0% in those with a pH of <4 (P < 0.02) and 49.2% in subjects with an on-treatment gastrin of >25 ng. L-1 vs. 19.8% in those with a fasting gastrin of <25 ng. L-1 (P < 0.006). At day 15 after omeprazole treatment, the H. pylori-positive subjects showed a heterogeneous response with some having increased acid output and others persisting suppression. CONCLUSIONS Rebound acid hypersecretion occurs in H. pylori-negative subjects after omeprazole treatment. Its severity is related to the degree of elevation of pH on treatment. Persisting suppression of acid secretion masks the phenomenon in H. pylori-positive subjects.
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Affiliation(s)
- D Gillen
- University Department of Medicine & Therapeutics, Western Infirmary, Glasgow, Scotland
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37
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Williams MP, Sercombe J, Hamilton MI, Pounder RE. A placebo-controlled trial to assess the effects of 8 days of dosing with rabeprazole versus omeprazole on 24-h intragastric acidity and plasma gastrin concentrations in young healthy male subjects. Aliment Pharmacol Ther 1998; 12:1079-89. [PMID: 9845397 DOI: 10.1046/j.1365-2036.1998.00418.x] [Citation(s) in RCA: 140] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/21/2022]
Abstract
BACKGROUND Rabeprazole (LY307640, E3810) is a new, potent, proton pump inhibitor. A single daily 20 mg dose significantly decreases 24-h intragastric acidity. There are no data currently available directly comparing the effect of rabeprazole on 24-h acidity with established proton pump inhibitors. AIM To compare the effects of rabeprazole 20 mg o.m. and omeprazole 20 mg o.m. on 24-h intragastric acidity and plasma gastrin concentration in a randomized, double-blind, placebo-controlled trial, in healthy H. pylori-negative subjects. METHODS Twenty-four healthy male volunteers, negative for H. pylori infection by serology and 13C-urea breath test, were studied on the 1st and 8th day of dosing with either placebo, rabeprazole 20 mg or omeprazole 20 mg, once each morning, in a crossover fashion. On days 1 and 8, hourly intragastric acidity was measured by gastric aspiration for 24 h from 08.00 hours. On day 8, plasma gastrin concentrations were also measured hourly from 08.00 to 24.00 hours, then every 2 h thereafter. RESULTS A single dose of both rabeprazole and omeprazole significantly decreased 24-h intragastric acidity compared with placebo. The 24-h acidity on day 1 was significantly decreased for rabeprazole compared with omeprazole (331 vs. 640 mmol.h/L, P < 0.001), resulting in a significantly higher median 24-h intragastric pH and longer times at which intragastric pH was > 3 and > 4. On day 8 of dosing, the decrease in 24-h intragastric acidity was greater with rabeprazole than with omeprazole, but the difference was not statistically significant (160 vs. 218 mmol.h/L, P = 0.1). However, 24-h plasma gastrin concentration (1687 vs. 1085 pmol.h/L. P < 0.01) and percentage time that intragastric pH was > 3 (69 vs. 59%, P = 0.008) and > 4 (60 vs. 51%, P = 0.03) were significantly greater. CONCLUSIONS Rabeprazole 20 mg once daily has a significantly faster onset of antisecretory activity than omeprazole 20 mg once daily. After 8 days the differences in intragastric pH > 3 and > 4 holding times persisted, but there was no significant difference in 24-h acidity.
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Affiliation(s)
- M P Williams
- University Department of Medicine, Royal Free and University College Medical School, London, UK
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38
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Furuta T, Takashima M, Arai H, Hanai H, Kaneko E. Helicobacter pylori infection and progression of gastric atrophy and intestinal metaplasia. Scand J Gastroenterol 1998; 33:1005. [PMID: 9759961 DOI: 10.1080/003655298750027074] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]
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Beil W, Birkholz C, Wagner S, Sewing KF. Helicobacter pylori fatty acid cis 9,10-methyleneoctadecanoic acid increases [Ca2+]i, activates protein kinase C and stimulates acid secretion in parietal cells. Prostaglandins Leukot Essent Fatty Acids 1998; 59:119-25. [PMID: 9774175 DOI: 10.1016/s0952-3278(98)90090-4] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/09/2023]
Abstract
The effect of the Helicobacter pylori (H. pylori) fatty acid cis 9,10-methyleneoctadecanoic acid (MOA) on gastric acid secretion was studied in isolated guinea-pig parietal cells. MOA (1 and 3 micromol/l) stimulated basal and enhanced histamine- and dibutyryl cyclic AMP-stimulated acid secretion in parietal cells. MOA increased intracellular free [Ca2+]i concentration in a concentration-dependent manner. The source of [Ca2+]i was extracellular as demonstrated by depletion of [Ca2+]i with EGTA. Furthermore, MOA caused activation of parietal cell protein kinase C (PKC). The effect of MOA upon PKC activation was [Ca2+]i-dependent but did not require phosphatidylserine as phospholipid co-factor. Similarly to the effect of diolein, MOA increased the stimulatory effect of phosphatidylserine at low [Ca2+]i concentrations. Treatment of parietal cells with MOA caused translocation of PKC from the cytosol to the membrane-associated cell fraction. We propose that MOA stimulates parietal cell acid secretion presumably by an increase of cytosolic free [Ca2+]i concentrations and PKC activation.
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Affiliation(s)
- W Beil
- Department of General Pharmacology, Hannover Medical School, Germany
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40
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41
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Gillen D, el-Omar EM, Wirz AA, Ardill JE, McColl KE. The acid response to gastrin distinguishes duodenal ulcer patients from Helicobacter pylori-infected healthy subjects. Gastroenterology 1998; 114:50-7. [PMID: 9428218 DOI: 10.1016/s0016-5085(98)70632-8] [Citation(s) in RCA: 77] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
BACKGROUND & AIMS Helicobacter pylori-induced hypergastrinemia is accompanied by increased acid secretion in patients with duodenal ulcer (DU) but not in infected healthy volunteers. The aim of this study was to investigate the mechanism underlying this difference. METHODS Thirty-four H. pylori-negative and 20 H. pylori-positive healthy volunteers and 15 H. pylori-positive patients with DU were studied. Maximal acid output and sensitivity to gastrin (gastrin concentration required to achieve 50% maximal acid output) were assessed by examining the dose response to gastrin 17. Inhibitory control was tested by comparing the maximal acid response to cholecystokinin octapeptide with that for gastrin 17. RESULTS Sensitivity to gastrin was similar in patients with DU (median, 69.5 ng.L-1; range, 26.2-142) and H. pylori-negative healthy volunteers (median, 82.2 ng.L-1; range, 17.7-410); H. pylori-positive healthy volunteers were less sensitive than either (164.5 ng.L-1; range, 44.8 to > 3360 ng.L-1). Patients with DU had higher maximal acid output (51.2 mmol.h-1; range, 30.8-73.7 mmol.h-1) than either infected healthy volunteers (37.8 mmol.h-1; range, 0.0-65.0 mmol.h-1; P < 0.04) or uninfected healthy volunteers (35.3 mmol.h-1; range, 21.3-67.3 mmol.h-1; P < 0.002). The maximal acid output in both groups of healthy subjects was similar. The proportion of maximal acid output to gastrin 17 achieved by cholecystokinin was similar in patients with DU (36.6%; range, 21.5%-58.2%) and H. pylori-negative healthy volunteers (28.7%; range, 5.9%-85.8%). CONCLUSIONS A combination of decreased sensitivity to gastrin in infected healthy volunteers and increased maximal acid secretory capacity in patients with DU underlies their different acid response to H. pylori-induced hypergastrinemia.
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Affiliation(s)
- D Gillen
- University Department of Medicine and Therapeutics, Western Infirmary, Glasgow, Scotland
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Calam J, Gibbons A, Healey ZV, Bliss P, Arebi N. How does Helicobacter pylori cause mucosal damage? Its effect on acid and gastrin physiology. Gastroenterology 1997; 113:S43-9; discussion S50. [PMID: 9394759 DOI: 10.1016/s0016-5085(97)80010-8] [Citation(s) in RCA: 79] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients with gastric cancer and their relatives. Investigation of the basic mechanisms may show how H. pylori causes different diseases in different persons. Infection of the gastric antrum increases gastrin release. Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor alpha and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible. The infection also diminishes mucosal expression of somatostatin. Exposure of canine D cells to tumor necrosis factor alpha in vitro reproduces this effect. These changes in gastrin and somatostatin increase acid secretion and lead to duodenal ulceration. But the acid response depends on the state of the gastric corpus mucosa. The net effect of corpus gastritis is to decrease acid secretion. Specific products of H. pylori inhibit parietal cells. Also, interleukin 1 beta, which is overexpressed in H. pylori gastritis, inhibits both parietal cells and histamine release from enterochromaffin-like cells. H. pylori also promotes gastric atrophy, leading to loss of parietal cells. Factors such as a high-salt diet and a lack of dietary antioxidants, which also increase corpus gastritis and atrophy, may protect against duodenal ulcers by decreasing acid output. However, the resulting increase of intragastric pH may predispose to gastric cancer by allowing other bacteria to persist and produce carcinogens in the stomach.
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Affiliation(s)
- J Calam
- Department of Gastroenterology, Imperial College School of Medicine, Hammersmith Hospital, London, England.
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43
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Labenz J, Malfertheiner P. Helicobacter pylori in gastro-oesophageal reflux disease: causal agent, independent or protective factor? Gut 1997; 41:277-80. [PMID: 9378377 PMCID: PMC1891487 DOI: 10.1136/gut.41.3.277] [Citation(s) in RCA: 95] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Affiliation(s)
- J Labenz
- Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University, Magdeburg, Germany
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Yasunaga Y, Shinomura Y, Kanayama S, Higashimoto Y, Yabu M, Miyazaki Y, Murayama Y, Nishibayashi H, Kitamura S, Matsuzawa Y. Mucosal interleukin-1 beta production and acid secretion in enlarged fold gastritis. Aliment Pharmacol Ther 1997; 11:801-9. [PMID: 9305492 DOI: 10.1046/j.1365-2036.1997.00200.x] [Citation(s) in RCA: 22] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
BACKGROUND We have previously shown that eradication of Helicobacter pylori increases acid secretion in H. pylori-associated enlarged fold gastritis. AIM To investigate whether locally produced interleukin-1 beta is possibly involved in the inhibition of acid secretion in H. pylori gastritis. METHODS IL-1 beta release from the gastric body mucosa was determined by short-term culture of biopsy specimens in 13 patients with enlarged fold gastritis (all H. pylori-positive), five H. pylori-positive and 10 H. pylori-negative patients without enlarged folds. The acid-inhibitory effect of locally produced IL-1 beta was examined by [14C]-aminopyrine uptake assay using isolated rabbit gastric glands. RESULTS IL-1 beta release was significantly greater in patients with enlarged fold gastritis, significantly correlated with both basal and tetragastrin-stimulated acid outputs in the H. pylori-positive patients (r = -0.591 and r = -0.641, respectively; P < 0.01), and significantly decreased with concomitant increases in acid secretions after eradication of H. pylori. [14C]-aminopyrine uptake was inhibited by IL-1 beta in a dose-dependent manner. CONCLUSIONS Increased production of IL-1 beta caused by H. pylori infection is possibly involved in the inhibition of acid secretion in enlarged fold gastritis.
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Affiliation(s)
- Y Yasunaga
- Second Department of Internal Medicine, Osaka University Medical School, Japan
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Gutierrez O, Melo M, Segura AM, Angel A, Genta RM, Graham DY. Cure of Helicobacter pylori infection improves gastric acid secretion in patients with corpus gastritis. Scand J Gastroenterol 1997; 32:664-8. [PMID: 9246705 DOI: 10.3109/00365529708996515] [Citation(s) in RCA: 91] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
BACKGROUND For more than 30 years it has been known that gastric acid secretion is inversely related to the extent and severity of corpal gastritis. We therefore evaluated the effect of cure of Helicobacter pylori infection on basal and pentagastrin-stimulated acid secretion. METHODS Basal acid output (BAO) and maximal acid output (MAO) were assessed in 11 H. pylori-infected dyspeptic patients (8 women and 3 men; mean age, 28 years) before and after successful anti-H. pylori therapy. RESULTS The gastritis index was significantly lower after therapy and was associated with an increase in both BAO and MAO after cure of the H. pylori infection (BAO from 0.3 mmol/h and MAO from 4.8 mmol/h to 19 mmol/ h). Basal and stimulated acid concentrations also increased (29.1 +/- 36.6 to 54 +/- 31 mmol/l and 72.5 +/- 46 to 120.1 +/- 30 mmol/l, respectively, for basal and stimulated acid concentrations; P < 0.05 for peak and MAO, P = 0.07 for BAO). CONCLUSION Gastric acid secretion increased into the normal range after successful treatment of H. pylori infection, suggesting that gastric function can recover to normal or almost normal after cure of H. pylori infection.
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Affiliation(s)
- O Gutierrez
- Dept. of Gastroenterology, Hospital San Juan de Dios Universidad Nacional de Colombia, Bogotu, Colombia
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Affiliation(s)
- Z Healey
- Department of Gastroenterology, Royal Postgraduate Medical School, Hammersmith Hospital, London
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Taguchi Y, Kaito M, Gabazza EC, Takaji S, Shibata T, Oka S, Ikemura N, Nakao K, Hashimoto Y, Imoto I. Helicobacter pylori inhibits the secretory activity of gastric parietal cells in patients with chronic gastritis. An ultrastructural study. Scand J Gastroenterol 1997; 32:656-63. [PMID: 9246704 DOI: 10.3109/00365529708996514] [Citation(s) in RCA: 18] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
BACKGROUND Previous in vitro studies suggested that Helicobacter pylori may inhibit the acid secretion of gastric parietal cells. The aim of this study was to investigate ultrastructurally the influence of H. pylori infection on the gastric parietal cell function in vivo. METHODS This study comprised 28 patients with chronic gastritis. Biopsy specimens were taken from the gastric body in all cases and examined by electron microscopy. Gastric parietal cells were counted in each ultrathin section and classified into secretory and non-secretory types. The pH of the gastric juice was also measured in all patients. RESULTS The number of parietal cells in the secretory phase was significantly lower in H. pylori-infected (n = 16) patients than in those (n = 12) without H. pylori infection. The intragastric pH was significantly higher in patients with H. pylori-associated gastritis than in those without H. pylori infection. Parietal cells in secretory phase tended to decrease in proportion to the activity of the gastric mucosal inflammation. CONCLUSIONS The results of this investigation suggests that H. pylori-associated gastritis is related to a decreased secretory activity of the gastric parietal cells.
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Affiliation(s)
- Y Taguchi
- Third Dept. of Internal Medicine, Mie University School of Medicine, Japan
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Annibale B, Marignani M, Azzoni C, D'Ambra G, Caruana P, D'Adda T, Delle Fave G, Bordi C. Atrophic body gastritis: distinct features associated with Helicobacter pylori infection. Helicobacter 1997; 2:57-64. [PMID: 9432330 DOI: 10.1111/j.1523-5378.1997.tb00060.x] [Citation(s) in RCA: 69] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
BACKGROUND Usually, atrophic body gastritis has been considered an autoimmune disease characterized by the presence of parietal cell antibodies. Previous investigations into the role of Helicobacter pylori infection have obtained conflicting results. The aim of this study was to investigate the prevalence and role of H. pylori in a prospectively investigated population of patients with corpus-predominant atrophic gastritis. PATIENTS AND METHODS A consecutive series of 67 newly diagnosed cases of atrophic body gastritis was derived from a screening of 326 patients with unexplained anemia or dyspepsia. Criteria for diagnosis were fasting hypergastrinemia, pentagastrin-resistant achlorhydria, and histological confirmation of body atrophy. In all 67 patients, H. pylori infection was evaluated independently by histological assay and urease test. The gastritis status of both the fundic and antral mucosa were graded according to the Sydney system. Parietal cell and intrinsic factor antibodies also were determined. RESULTS Active H. pylori infection was present in 26.8% of our patients and allowed us to identify a patient's subpopulation with a significantly smaller degree of body mucosa damage as shown by functional parameters (gastrin, gastric acid secretion, pepsinogen I) and histological assessment. In this subpopulation, a higher prevalence of gastric cancer familial history was found. Presence of parietal cell antibodies showed a similar prevalence in H. pylori-positive and H. pylori-negative patients (61.1% vs. 69.4%) and was not associated with significant functional and histological differences. Cure of infection determined an evident improvement of corporal atrophy as well as a reduction of hypergastrinemia. CONCLUSION Active H. pylori infection, a potential cause of oxyntic gland atrophy, is found in one-fourth of patients with newly diagnosed atrophic body gastritis.
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Affiliation(s)
- B Annibale
- Gastroenterology Unit, University La Sapienza Rome, Italy
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Haque M, Hirai Y, Yokota K, Mori N, Jahan I, Ito H, Hotta H, Yano I, Kanemasa Y, Oguma K. Lipid profile of Helicobacter spp.: presence of cholesteryl glucoside as a characteristic feature. J Bacteriol 1996; 178:2065-70. [PMID: 8606185 PMCID: PMC177906 DOI: 10.1128/jb.178.7.2065-2070.1996] [Citation(s) in RCA: 87] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/31/2023] Open
Abstract
The lipid and fatty acid profiles of eight Helicobacter spp. (H. nemestrinae, H. acinonyx, H. canis, Helicobacter sp. strain CLO-3, "H. rappini" [Flexispira rappini], H. pametensis, Helicobacter sp. strain Bird-B, and Helicobacter sp. strain Bird-C) and the fatty acid profiles of five additional species (H. pylori, H. felis, H. muridarum, H. mustelae, and H. fennelliae) were analyzed and compared. A heterologous fatty acid profile was observed among the Helicobacter spp., and on that basis the species could be divided into two groups. Group A had 19-carbon cyclopropane fatty acid (19:0cyc) and tetradecanoic acid (14:0) as the major fatty acids, and group B characteristically lacked the 19:0cyc and had hexadecanoic acid (16:0) and octadecenoic (18:1) acids as the major fatty acids. The species of group A are primarily gastric colonizers, and those of group B are primarily intestinal colonizers. Seven of the eight species studied showed the unusual and characteristic presence of cholesteryl glucosides (CGs), and most of these seven showed a very large amount (9.7 to 27.4% of the weight of total extractable lipid). The types of CGs and their distribution in different species were as follows: cholesteryl-6-O-acyl-alpha-D-glucopyranoside (cholesteryl-6-O-tetradecanoyl-alpha-D-glucopyranoside in H. nemestrinae and mainly cholesteryl-6-O-dodecanoyl-alpha-D-glucopyranoside in "H. rappini"), cholesteryl-alpha-D-glucopyranoside (H. nemestrinae, H. acinonyx, H. canis, Helicobacter sp. strain CLO-3, and "H. rappini"), and cholesteryl-6-O-phosphatidyl-alpha-D-glucopyranoside (H. nemestrinae, H. acinonyx, H. canis, and Helicobacter sp. strain CLO-3). Besides this, we could also detect cholesteryl acyl glucoside in H. acinonyx, cholesteryl glucoside in Helicobacter sp. strains Bird-B and -C, and cholesteryl phosphatidyl glucoside in "H. rappini" and Helicobacter sp. strain Bird-C. A selective accumulation of free cholesterol was observed in the neutral lipid fractions. On the basis of the detection of CGs in 11 of the 13 species studied so far, the presence of CGs appears to be a characteristic feature of the genus Helicobacter. In view of this and also because of a simple and rapid detection method described herein, the CGs can be used as a valuable chemotaxonomic marker.
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Affiliation(s)
- M Haque
- Department of Bacteriology, Okayama University Medical School, Japan
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Cave DR. Helicobacter pylori and its interaction with chief and parietal cells. THE YALE JOURNAL OF BIOLOGY AND MEDICINE 1996; 69:91-8. [PMID: 9041695 PMCID: PMC2588978] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
Helicobacter pylori has been shown, along with other Helicobacter species to produce effector molecules that induce substantial physiological changes on acid and pepsin secretion. The effects are clinically evident, and long-term achlorhydria may be a risk factor for gastric cancer. Further identification and characterization of the factors may lead to additional understanding of gastric physiology.
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Affiliation(s)
- D R Cave
- St. Elizabeth's Medical Center, Boston, Massachusetts 02135, USA
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