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1.
Rev. bras. ciênc. vet ; 27(2): 74-79, abr./jun. 2020. il.
Article in Portuguese | LILACS, VETINDEX | ID: biblio-1378256

ABSTRACT

O objetivo deste trabalho foi relacionar os achados anatomopatológicos das lesões gástricas subclínicas de ocorrência natural em leitões com a presença, ou não, de Helicobacter spp. por meio da imuno-histoquímica. Foram utilizados 48 leitões de linhagem genética comercial. Os animais foram adquiridos em uma granja comercial, com peso médio de 34 Kg e idade média de 79 dias; após o abate, seus estômagos foram coletados e avaliados. Avaliações histopatológicas e imuno-histoquímicas foram realizadas em amostras das regiões anatômicas aglandular e glandular. Macroscopicamente, 34 (70,83%) leitões apresentaram lesões na região aglandular, enquanto que em 14 animais (29,17%) não foram encontradas alterações nesta região. Dos estômagos com lesão, 14 foram classificados como grau 1, seis como grau 2 e 14 como grau 3. Microscopicamente, 44 amostras (91,66%) apresentaram paraqueratose. Deste total, 22 apresentaram a forma discreta, 20 a moderada e dois a acentuada. Na avaliação macroscópica da porção glandular, 41 (85,4%) animais apresentaram alteração em pelo menos uma das três regiões, e em somente sete (14,6%) não foram encontradas lesões em nenhuma delas. Em 14 deles, houve aumento da atividade mucípara, em dois, houve erosão e, em cinco, hiperemia. As lesões na região glandular do estômago foram mais extensas no antro e no cárdia, seguidas do fundo. Em relação à análise imuno-histoquímica, 21 (43,8%) amostras tiveram resultados negativos em todas as regiões, e 24 (50%) foram positivas em pelo menos uma delas, sendo que nenhuma foi positiva em todas. Os achados anatomopatológicos demonstraram relação estatística com a bactéria e, sua imunomarcação não associada à lesão em certas regiões gástricas, demonstra seu caráter saprofítico e oportunista.


The aim of this study was to relate the anatomopathological findings of naturally occurring subclinical gastric lesions in piglets, with or without Helicobacter spp. through immunohistochemistry. Forty-eight piglets of commercial genetic lineage were used. The animals were acquired in a commercial farm, with an average weight of 34 kg and an average age of 79 days, and after slaughter, their stomachs were collected and evaluated. Samples from the glandular and aglandular anatomical regions were evaluated. Macroscopically, 34 (70.83%) samples had lesions on aglandular region, while 14 (29.17%) nothing had. Of the injured stomachs, 14 were classified as grade 1, six as grade 2 and 14 as grade 3. Microscopically, 44 samples (91.66%) showed parakeratosis. Of these, 22 showed a discreet manner, 20 moderate and two severe. In the glandular region, in 41 (85.4%) samples there was a change in at least one of the three regions, and only seven animals (14.6%) showed no change in any of the three. Fourteen samples showed increased muciparous activity, two showed erosion and five hyperemia. The lesions were higher in antral regions and cardic, followed the fundus. In relation to immunohistochemistry, 21(43.8%) samples were negative in all areas, 24 (50%) were positive in at least one, and none were positive in all. The anatomopathological findings showed a statistical relationship with the bacteria, and its immunostaining, not associated with gastric lesions in certain regions, demonstrates its saprophytic and opportunistic character.


Subject(s)
Animals , Stomach Ulcer/veterinary , Swine/anatomy & histology , Helicobacter Infections/veterinary , Helicobacter/pathogenicity , Stomach/microbiology , Immunohistochemistry/veterinary , Bacterial Zoonoses/diagnosis
4.
Article in English | WPRIM | ID: wpr-762452

ABSTRACT

Evaluation of diagnostic tests requires reference standards, which are often unavailable. Latent class analysis (LCA) can be used to evaluate diagnostic tests without reference standards, using a combination of observed and estimated results. Conditionally independent diagnostic tests for Helicobacter pylori infection are required. We used LCA to construct a reference standard and evaluate the capability of non-invasive tests (stool antigen test and serum antibody test) to diagnose H. pylori infection compared with the conventional method, where histology is the reference standard. A total of 96 healthy subjects with endoscopy histology results were enrolled from January to July 2016. Sensitivity and specificity were determined for the LCA approach (i.e., using a combination of three tests as the reference standard) and the conventional method. When LCA was used, sensitivity and specificity were 83.8% and 99.4% for histology, 80.0% and 81.9% for the stool antigen test, and 63.6% and 89.3% for the serum antibody test, respectively. When the conventional method was used, sensitivity and specificity were 75.8% and 71.1% for the stool antigen test and 77.7% and 60.7% for the serum antibody test, respectively. LCA can be applied to evaluate diagnostic tests that lack a reference standard.


Subject(s)
Diagnosis , Diagnostic Tests, Routine , Endoscopy , Healthy Volunteers , Helicobacter pylori , Helicobacter , Methods , Sensitivity and Specificity
5.
Journal of Gastric Cancer ; : 225-233, 2019.
Article in English | WPRIM | ID: wpr-764484

ABSTRACT

PURPOSE: Gastric adenocarcinoma of the fundic gland type (chief cell predominant type) (GA-FG-CCP) was first reported as a rare adenocarcinoma found in the normal fundic mucosa. Recent studies have proposed the possibility that GA-FG-CCPs were also generated in the atrophic mucosa after Helicobacter pylori (HP) eradication therapy. However, little is known on the endoscopic findings of GA-FG-CCP generated in the atrophic mucosa due to its extreme rarity. MATERIALS AND METHODS: A total of 8 patients who underwent endoscopic submucosal resection and were diagnosed with GA-FG-CCP generated in the HP-uninfected mucosa (4 cases, HP-uninfected group) or HP-eradicated atrophic mucosa (4 cases, HP-eradicated group) were retrospectively analyzed, and their endoscopic findings, including magnifying endoscopy with narrow band imaging (M-NBI), and pathological features were compared. RESULTS: While GA-FG-CCPs in the 2 groups displayed similar macroscopic appearance, M-NBI demonstrated that characteristic microvessels (tapered microvessels like withered branches) were specifically identified in the HP-eradicated group. Pathological investigation revealed that a decreasing number of fundic glands and thinned foveolar epithelium covering tumor ducts were thought to lower the thickness of the covering layer over tumor ducts in the HP-eradicated group. Moreover, dilation of vessels just under the surface of the lesions contributed to the visualization of microvessels by M-NBI. CONCLUSIONS: The change in background mucosa due to HP infection influenced the thickness of the covering layer over the tumor ducts and M-NBI finding of GA-FG-CCP.


Subject(s)
Adenocarcinoma , Endoscopy , Epithelium , Helicobacter pylori , Helicobacter , Humans , Microvessels , Mucous Membrane , Narrow Band Imaging , Retrospective Studies , Stomach Neoplasms
6.
Article in English | WPRIM | ID: wpr-764309

ABSTRACT

BACKGROUND: Helicobacter pylori infection is a major risk factor in the development of gastric cancer. H. pylori infection of gastric epithelial cells increases the levels of reactive oxygen species (ROS), activates oncogenes, and leads to β-catenin-mediated hyper-proliferation. β-Carotene reduces ROS levels, inhibits oxidant-mediated activation of inflammatory signaling and exhibits anticancer properties. The present study was carried out to determine if β-carotene inhibits H. pylori-induced cell proliferation and the expression of oncogenes c-myc and cyclin E by reducing the levels of β-catenin and phosphorylated glycogen synthase kinase 3β (p-GSK3β). METHODS: Gastric epithelial AGS cells were pre-treated with β-carotene (5 and 10 μM) for 2 hours prior to H. pylori infection and cultured for 6 hours (for determination of the levels of p-GSK3β, GSK3β, and β-catenin) and 24 hours (for determination of cell viability and protein levels of c-myc and cyclin E). Cell viability was determined by the MTT assay and protein levels were determined via western blot-based analysis. RESULTS: β-Carotene inhibited H. pylori-induced increases in the percentage of viable cells, phosphorylated GSK3β (p-GSK3β), and the levels of β-catenin, c-myc and cyclin E. CONCLUSIONS: β-Carotene inhibits H. pylori-induced hyper-proliferation of gastric epithelial cells by suppressing β-catenin signaling and oncogene expression.


Subject(s)
beta Carotene , beta Catenin , Cell Proliferation , Cell Survival , Cyclin E , Cyclins , Epithelial Cells , Glycogen Synthase Kinases , Helicobacter pylori , Helicobacter , Oncogenes , Reactive Oxygen Species , Risk Factors , Stomach Neoplasms
7.
Article in English | WPRIM | ID: wpr-764294

ABSTRACT

BACKGROUND: Helicobacter pylori increases production of reactive oxygen species (ROS), which activates inflammatory and carcinogenesis-related signaling pathways in gastric epithelial cells. Therefore, reducing ROS, by upregulating antioxidant enzyme, such as superoxide dismutase (SOD), may be a novel strategy to prevent H. pylori-associated gastric diseases. Astaxanthin is an antioxidant carotenoid that prevents oxidative stress-induced cell injury. The present study was aimed to determine whether H. pylori decreases SOD activity by changing the levels of SOD1/SOD2 and whether astaxanthin prevents changes in SOD levels and activity in H. pylori-infected gastric epithelial AGS cells. METHODS: AGS cells were pre-treated with astaxanthin for 3 hours prior to H. pylori infection and cultured for 1 hour in the presence of H. pylori. SOD levels and activity were assessed by Western blot analysis and a commercial assay kit, respectively. Mitochondrial ROS was determined using MitoSOX fluorescence. RESULTS: H. pylori decreased SOD activity and the SOD2 level, but increased mitochondrial ROS in AGS cells. The SOD1 level was not changed by H. pylori infection. Astaxanthin prevented H. pylori-induced decreases in the SOD2 level and SOD activity and reduced mitochondrial ROS in AGS cells. CONCLUSIONS: Consumption of astaxanthin-rich food may prevent the development of H. pylori-associated gastric disorders by suppressing mitochondrial oxidative stress.


Subject(s)
Blotting, Western , Epithelial Cells , Fluorescence , Helicobacter pylori , Helicobacter , Oxidative Stress , Reactive Oxygen Species , Stomach Diseases , Superoxide Dismutase , Superoxides
8.
Article in Korean | WPRIM | ID: wpr-785900

ABSTRACT

In order to investigate the antioxidant effect of alkylhydroxide peroxidase (ahpC) of Helicobacter pylori (H. pylori) 26695, an ahpC-deficient mutant (H. pylori 26695 ahpC::cat) was generated. ahpC-deficient mutant was grown slowly at lower pressure of oxygen (5% oxygen) compared to the H. pylori 26695. Whole cell proteins isolated form H. pylori 26695 and H. pylori 26695 ahpC::cat were analyzed by MALDI-TOF and tandem-MS. The expression of 15 proteins, including Ppa, HypB, GrpE, Elp, RecA, GroES, Mda66, RibE, NapA, GlnA, BioB, TrxB, Tsf, FumC and Icd, was more than doubled in H. pylori 26695 ahpC::cat. Production of 10 proteins such as UreG, FabE, Adk, Pnp, OorC, AtpA, AtpD, Nqq3, Pfr, and TagD decreased below 50% in H. pylori 26695 ahpC::cat compared to the H. pylori 26695. In microarray analysis, 9 genes including sul1, amiE, frxA, fecA, hyuA, and katA increased in transcription level in H. pylori 26695 ahpC::cat compared to H. pylori 26695. A total of 24 genes, including flaB, protein kinase C inhibitor, cag16, pabC, and sabA, reduced in transcription. 27 genes, including HP0889, showed common expression changes in ahpC, katA, and sodB-deficient mutations. As a result of this study, there were not many genes whose expression was commonly changed by the deletion of each of the three major antioxidant enzymes of H. pylori. These results showed the functions and regulation of the three antioxidant enzymes were different in H. pylori.


Subject(s)
Antioxidants , Helicobacter pylori , Helicobacter , Microarray Analysis , Oxygen , Peroxidase , Protein Kinase C , Proteome , Ribes
9.
Article in Korean | WPRIM | ID: wpr-742135

ABSTRACT

BACKGROUND/AIMS: The Helicobacter pylori (H. pylori) eradication rate of standard triple therapy is unsatisfactory in Korea, and sequential therapy (SQT) has been suggested to be a practical first-line alternative regimen. The aim of this prospective study was to document changes in annual eradication rates of SQT. METHODS: A total of 983 H. pylori-positive subjects were enrolled from 2010 to 2018 and their data were subjected to intention-to-treat (ITT) and per-protocol (PP) analysis. All subjects received 10-day sequential therapy consisting of 40 mg esomeprazole and 1 g amoxicillin b.i.d for 5 days followed by 40 mg esomeprazole b.i.d, 500 mg clarithromycin b.i.d and 500 mg metronidazole t.i.d for 5 days. The 13C-urea breath test, rapid urease test (CLO test®), and histology were used to confirm eradication. Compliance and side effects were also investigated. RESULTS: ITT and PP eradication rates of SQT were 69.9% (687 of 983) and 87.1% (657 of 754), respectively. The annual eradication rate of ITT remained consistent over the 8-year study period (p for trend=0.167), whereas PP analysis showed the eradication rate increased (p for trend=0.042). The overall adverse event rate for SQT was 41.7% (410 subjects). CONCLUSIONS: Despite high antibiotic resistance rates in Korea, the eradication rate of SQT did not decrease over the 8-year study period.


Subject(s)
Amoxicillin , Breath Tests , Clarithromycin , Compliance , Drug Resistance, Microbial , Esomeprazole , Helicobacter pylori , Helicobacter , Intention to Treat Analysis , Korea , Metronidazole , Prospective Studies , Urease
10.
Article in English | WPRIM | ID: wpr-738995

ABSTRACT

BACKGROUND/AIMS: The association between Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) or low-dose aspirin therapy as a risk factor for peptic ulcer bleeding (PUB) remains unclear. This study investigated the risk of PUB associated with H. pylori infection and NSAID or low-dose aspirin therapy in patients with PUD. MATERIALS AND METHODS: This case-control study investigated 340 patients with PUB between 2012 and 2016. The control group comprised age and sex-matched patients with endoscopically documented non-bleeding ulcers. Using logistic regression analysis, the adjusted odds ratio (AOR) was calculated for the risk of PUB. RESULTS: Of the patients investigated, 57.9% in the study group and 51.8% in the control group were diagnosed with H. pylori infection (P=0.106). Logistic regression analysis showed synergistic interaction between H. pylori infection and low-dose aspirin therapy. Multivariate analysis showed that low-dose aspirin (AOR 3.92, P < 0.001), NSAIDs (AOR 2.98, P=0.001), warfarin (AOR 14.57, P=0.011), gastric ulcer (compared with duodenal ulcer) (AOR 1.65, P=0.01), and smoking (AOR 1.97, P=0.004) increased the risk of PUB compared with the risk of PUD. CONCLUSIONS: Both NSAIDs and aspirin are independent risk factors for bleeding in patients with PUD. Additionally, low-dose aspirin therapy concomitant with H. pylori infection produced a synergistic effect. Therefore, H. pylori eradication may be crucial in aspirin users. Moreover, a proton pump inhibitor should be prescribed in patients with a history of bleeding ulcers who need long-term NSAID treatment.


Subject(s)
Anti-Inflammatory Agents, Non-Steroidal , Aspirin , Case-Control Studies , Helicobacter pylori , Helicobacter , Hemorrhage , Humans , Logistic Models , Multivariate Analysis , Odds Ratio , Peptic Ulcer , Proton Pumps , Risk Factors , Smoke , Smoking , Stomach Ulcer , Ulcer , Warfarin
11.
Article in English | WPRIM | ID: wpr-738994

ABSTRACT

BACKGROUND/AIMS: Gastrointestinal glandular stem cells renew every 8 years. New stem cells with impeded housekeeping gene methylation have unstable phenotypes and are prone to transform into malignant cells. Age-related changes in methylation in the gastric mucosa were evaluated to define the period of cancer-prone stem cell replacement. MATERIALS AND METHODS: Endoscopic biopsy specimens of normal-appearing gastric mucosa were obtained from 148 Helicobacter pylori-negative controls, 124 H. pylori-positive controls, and 69 gastric cancer patients with closed-type mucosal atrophy. Methylation-variable sites of two stomach-specific genes (TFF2 and TFF3) and four housekeeping genes (CDH1, ARRDC4, MMP2, and CDKN2A) were analyzed using radioisotope-labeled methylation-specific polymerase chain reaction. Age-related methylation was evaluated depending on the gastric mucosal atrophy at 2-year intervals. RESULTS: TFF2 methylation peaked periodically at 40 to 41, 48 to 49, 56 to 57, and 64 to 65 years of age in H. pylori-negative controls. Periodic peaks of TFF2 methylation were also found in H. pylori-positive controls. Housekeeping-gene methylation troughed at 48 to 49, 56 to 57, and 68 to 69 years of age in cancer patients. Trough methylation of CDH1 and ARRDC4 was lower in cancer patients than in H. pylori-positive controls. CONCLUSIONS: Methylation peaks of stomach-specific TFF2 in controls and methylation troughs of housekeeping genes in cancer patients were found every 8 years. Periodic methylation patterns may be used to identify individuals at high risk for gastric cancer.


Subject(s)
Adult Stem Cells , Atrophy , Biopsy , DNA Methylation , Gastric Mucosa , Genes, Essential , Helicobacter , Humans , Methylation , Mucous Membrane , Phenotype , Polymerase Chain Reaction , Stem Cells , Stomach Neoplasms
12.
Yonsei Medical Journal ; : 38-47, 2019.
Article in English | WPRIM | ID: wpr-719689

ABSTRACT

PURPOSE: Helicobacter pylori (HP)-infected gastric cancer (GC) is known to be a fatal malignant tumor, but the molecular mechanisms underlying its proliferation, invasion, and migration remain far from being completely understood. Our aim in this study was to explore miR-1915 expression and its molecular mechanisms in regulating proliferation, invasion, and migration of HP-infected GC cells. MATERIALS AND METHODS: Quantitative real-time PCR and western blot analysis were performed to determine miR-1915 and receptor for advanced glycation end product (RAGE) expression in HP-infected GC tissues and gastritis tissues, as well as human gastric mucosal cell line GES-1 and human GC cell lines SGC-7901 and MKN45. CCK8 assay and transwell assay were performed to detect the proliferation, invasion, and migration capabilities. MiR-1915 mimics and miR-1915 inhibitor were transfected into GC cells to determine the target relationship between miR-1915 and RAGE. RESULTS: MiR-1915 was under-expressed, while RAGE was over-expressed in HP-infected GC tissues and GC cells. Over-expressed miR-1915 could attenuate cellular proliferation, invasion, and migration capacities. RAGE was confirmed to be the target gene of miR-1915 by bioinformatics analysis and luciferase reporter assay. Moreover, HP-infected GC cellular proliferation, invasion, and migration were inhibited after treatment with pcDNA-RAGE. CONCLUSION: MiR-1915 exerted tumor-suppressive effects on cellular proliferation, invasion, and migration of HP-infected GC cells via targeting RAGE, which provided an innovative target candidate for treatment of HP-infected GC.


Subject(s)
Blotting, Western , Cell Line , Cell Proliferation , Computational Biology , Gastritis , Helicobacter pylori , Helicobacter , Humans , Luciferases , Rage , Real-Time Polymerase Chain Reaction , Stomach Neoplasms , Up-Regulation
13.
Article in English | WPRIM | ID: wpr-766105

ABSTRACT

PURPOSE: Several studies have shown that the oral cavity is a secondary location for Helicobacter pylori colonization and that H. pylori is associated with the severity of periodontitis. This study investigated whether H. pylori had an effect on the periodontium. We established an invasion model of a standard strain of H. pylori in human periodontal ligament fibroblasts (hPDLFs), and evaluated the effects of H. pylori on cell proliferation and cell cycle progression. METHODS: Different concentrations of H. pylori were used to infect hPDLFs, with 6 hours of co-culture. The multiplicity of infection in the low- and high-concentration groups was 10:1 and 100:1, respectively. The Cell Counting Kit-8 method and Ki-67 immunofluorescence were used to detect cell proliferation. Flow cytometry, quantitative real-time polymerase chain reaction, and western blots were used to detect cell cycle progression. In the high-concentration group, the invasion of H. pylori was observed by transmission electron microscopy. RESULTS: It was found that H. pylori invaded the fibroblasts, with cytoplasmic localization. Analyses of cell proliferation and flow cytometry showed that H. pylori inhibited the proliferation of periodontal fibroblasts by causing G2 phase arrest. The inhibition of proliferation and G2 phase arrest were more obvious in the high-concentration group. In the low-concentration group, the G2 phase regulatory factors cyclin dependent kinase 1 (CDK1) and cell division cycle 25C (Cdc25C) were upregulated, while cyclin B1 was inhibited. However, in the high-concentration group, cyclin B1 was upregulated and CDK1 was inhibited. Furthermore, the deactivated states of tyrosine phosphorylation of CDK1 (CDK1-Y15) and serine phosphorylation of Cdc25C (Cdc25C-S216) were upregulated after H. pylori infection. CONCLUSIONS: In our model, H. pylori inhibited the proliferation of hPDLFs and exerted an invasive effect, causing G2 phase arrest via the Cdc25C/CDK1/cyclin B1 signaling cascade. Its inhibitory effect on proliferation was stronger in the high-concentration group.


Subject(s)
Blotting, Western , CDC2 Protein Kinase , Cell Count , Cell Cycle , Cell Proliferation , Coculture Techniques , Colon , Cyclin B1 , Cytoplasm , Fibroblasts , Flow Cytometry , Fluorescent Antibody Technique , G2 Phase , Helicobacter pylori , Helicobacter , Humans , Methods , Microscopy, Electron, Transmission , Mouth , Periodontal Ligament , Periodontitis , Periodontium , Phosphorylation , Real-Time Polymerase Chain Reaction , Serine , Tyrosine
15.
Article in English | WPRIM | ID: wpr-765065

ABSTRACT

Detection of early-stage gastric cancer improves the prognosis of patients. Endoscopic submucosal dissection (ESD) is a curative and stomach-preserving treatment for early gastric cancer (EGC) associated with a low risk of lymph node metastasis. However, several studies have reported missed diagnosis of gastric cancer. Therefore, endoscopists are required to learn accurate diagnostic skills to eliminate endoscopic blind spots. A systematic screening protocol to map the entire stomach without blind spots reduces the risk of missed lesions. Knowledge of the features of EGC or dysplasia is essential to identify suspicious lesion. Information of the common sites of occurrence of EGC can also enable a detailed endoscopic examination to improve detection rates. Previous reports investigating the location of gastric cancers resected by ESD or surgery showed that the antrum and lesser curvature of stomach were predominantly affected. Helicobacter pylori-induced atrophic changes advance from the antrum to the corpus along the lesser curvature, predominantly affecting these areas. Gastric cancers in the antrum and the lower corpus are also commonly missed during screening examination. Therefore, a careful examination of the lower third stomach is warranted to avoid missing synchronous and metachronous gastric lesions. Knowledge of the location of EGC enables accurate endoscopic examination and detection of EGC in early stage.


Subject(s)
Diagnosis , Endoscopy , Helicobacter , Humans , Lymph Nodes , Mass Screening , Neoplasm Metastasis , Optic Disk , Prognosis , Stomach , Stomach Neoplasms
16.
17.
Gut and Liver ; : 628-641, 2019.
Article in English | WPRIM | ID: wpr-763887

ABSTRACT

BACKGROUND/AIMS: Insufficient systematic reviews were conducted in the previous meta-analyses about the prevalence of Helicobacter pylori infection in patients with chronic kidney disease (CKD). The aim of this study was to evaluate the prevalence of H. pylori infection in patients with CKD. METHODS: A systematic review of studies that evaluated the prevalence of H. pylori infection in patients with CKD compared to a control group was performed. Only studies with adult patients were included, and studies with renal transplant recipients or diabetic nephropathy patients were excluded. Random-effects model meta-analyses with sensitivity analyses and subgroup analyses were conducted to confirm the robustness of the main result. A meta-regression analysis was conducted to explore the influence of potential heterogeneity on the outcomes. The methodological quality of the included publications was evaluated using the Risk of Bias Assessment tool for Nonrandomized Studies. Publication bias was also assessed. RESULTS: In total, 47 studies were identified and analyzed. The total prevalence of H. pylori infection was 48.2% (1,968/4,084) in patients with CKD and 59.3% (4,097/6,908) in the control group. Pooled analysis showed a significantly lower prevalence of H. pylori infection in patients with CKD (vs control group: odds ratio, 0.64; 95% confidence interval, 0.52 to 0.79). Sensitivity analyses revealed consistent results, and meta-regression analysis showed no significant confounders. No publication bias was detected. CONCLUSIONS: The results of this study suggest a lower prevalence of H. pylori infection in patients with CKD.


Subject(s)
Adult , Bias , Diabetic Nephropathies , Helicobacter pylori , Helicobacter , Humans , Odds Ratio , Population Characteristics , Prevalence , Publication Bias , Renal Insufficiency, Chronic , Transplant Recipients
18.
Gut and Liver ; : 483-497, 2019.
Article in English | WPRIM | ID: wpr-763878

ABSTRACT

Antibiotic resistance is the most important factor leading to the failure of eradication regimens. This review focuses on the prevalence of Helicobacter pylori primary and secondary resistance to clarithromycin, metronidazole, amoxicillin, levofloxacin, tetracycline, and multidrug in Vietnam. We searched the PubMed, EMBASE, Vietnamese National Knowledge Infrastructure, and Vietnamese Biomedical databases from January 2000 to December 2016. The search terms included the following: H. pylori infection, antibiotic (including clarithromycin, metronidazole, amoxicillin, levofloxacin, tetracycline, and multidrug) resistance in Vietnam. The data were summarized in an extraction table and analyzed manually. Finally, Excel 2007 software was used to create charts. Ten studies (three studies in English and seven in Vietnamese) were included in this review. A total of 308, 412, 523, 408, 399, and 268 H. pylori strains were included in this review to evaluate the prevalence of H. pylori primary resistance to amoxicillin, clarithromycin, metronidazole, levofloxacin, tetracycline, and multidrug resistance, respectively. Overall, the primary resistance rates of amoxicillin, clarithromycin, metronidazole, levofloxacin, tetracycline, and multidrug resistance were 15.0%, 34.1%, 69.4%, 27.9%, 17.9% and 48.8%, respectively. Secondary resistance rates of amoxicillin, clarithromycin, metronidazole, levofloxacin, tetracycline, and multidrug resistance were 9.5%, 74.9%, 61.5%, 45.7%, 23.5% and 62.3%, respectively. In Vietnam, primary and secondary resistance to H. pylori is increasing over time and affects the effectiveness of H. pylori eradication.


Subject(s)
Amoxicillin , Asians , Bismuth , Clarithromycin , Drug Resistance, Microbial , Drug Resistance, Multiple , Helicobacter pylori , Helicobacter , Humans , Levofloxacin , Metronidazole , Prevalence , Tetracycline , Vietnam
19.
Gut and Liver ; : 506-514, 2019.
Article in English | WPRIM | ID: wpr-763876

ABSTRACT

BACKGROUND/AIMS: The validity of ¹³C-urea breath test (¹³C-UBT) for Helicobacter pylori detection is influenced by atrophic gastritis. The aim of this study was to evaluate the effect of citric acid on the accuracy of ¹³C-Urea breath test after H. pylori eradication therapy in a region where atrophic gastritis is common. METHODS: In this prospective study, H. pylori-positive patients received ¹³C-UBT after H. pylori eradication regimen. They were classified into citric acid group and control group. To determine diagnostic accuracy of ¹³C-UBT, patients were offered invasive methods. RESULTS: A total of 1,207 who successfully took H. pylori-eradication regimen received UBT. They were assigned into the citric acid group (n=562) and the control group (n=645). The mean ¹³C-UBT value of the citric acid group was 10.3±26.4‰, which was significantly (p<0.001) higher than that of that control group (5.1‰±12.6‰). Of these patients 122 patients were evaluated by endoscopic biopsy methods. Based on invasive tests, the accuracy, sensitivity, specificity, positive predictive value, and negative predictive value of ¹³C-UBT for the citric acid group were 83.3%, 91.7%, 81.3%, 55.0%, and 97.5%, respectively. Those of the control group were 87.7%, 90.9%, 88.2%, 62.5%, and 97.8%, respectively. They were not significantly different between the two groups. Although the presence of gastric atrophy and intestinal metaplasia (IM) decreased the accuracy, the decrease was not significant. CONCLUSIONS: In a country with high prevalence of atrophic gastritis or IM, false positivity remained common despite the use of citric acid in ¹³C-UBT.


Subject(s)
Atrophy , Biopsy , Breath Tests , Citric Acid , Diagnosis , Gastritis, Atrophic , Helicobacter pylori , Helicobacter , Humans , Metaplasia , Prevalence , Prospective Studies , Sensitivity and Specificity
20.
Gut and Liver ; : 531-540, 2019.
Article in English | WPRIM | ID: wpr-763873

ABSTRACT

BACKGROUND/AIMS: This nationwide, multicenter prospective randomized controlled trial aimed to compare the efficacy and safety of 10-day concomitant therapy (CT) and 10-day sequential therapy (ST) with 7-day clarithromycin-containing triple therapy (TT) as first-line treatment for Helicobacter pylori infection in the Korean population. METHODS: Patients with H. pylori infection were assigned randomly to 7d-TT (lansoprazole 30 mg, amoxicillin 1 g, and clarithromycin 500 mg twice daily for 7 days), 10d-ST (lansoprazole 30 mg and amoxicillin 1 g twice daily for the first 5 days, followed by lansoprazole 30 mg, clarithromycin 500 mg, and metronidazole 500 mg twice daily for the remaining 5 days), or 10d-CT (lansoprazole 30 mg, amoxicillin 1 g, clarithromycin 500 mg, and metronidazole 500 mg twice daily for 10 days). The primary endpoint was eradication rate by intention-to-treat (ITT) and per-protocol (PP) analyses. RESULTS: A total of 1,141 patients were included. The 10d-CT protocol achieved a markedly higher eradication rate than the 7d-TT protocol in both the ITT (81.2% vs 63.9%) and PP analyses (90.6% vs 71.4%). The eradication rate of the 10d-ST protocol was superior to that of the 7d-TT protocol (76.3% vs 63.9%, ITT analysis; 85.0% vs 71.4%, PP analysis). No significant differences in adherence or serious side effects were found among the three treatment arms. CONCLUSIONS: The 10d-CT and 10d-ST regimens were superior to the 7d-TT regimen as standard first-line treatment in Korea.


Subject(s)
Amoxicillin , Arm , Clarithromycin , Disease Eradication , Helicobacter pylori , Helicobacter , Humans , Korea , Lansoprazole , Metronidazole , Prospective Studies
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