scholarly journals Rebamipide Improves Chronic Inflammation in the Lesser Curvature of the Corpus afterHelicobacter pyloriEradication: A Multicenter Study

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Tomoari Kamada ◽  
Motonori Sato ◽  
Tadashi Tokutomi ◽  
Tetsuo Watanabe ◽  
Takahisa Murao ◽  
...  

Background and Aim. Although many epidemiologic studies have shown thatHelicobacter pylorieradication has prophylactic effects on gastric cancer, it does not completely eliminate the risk of gastric cancer. We aimed to investigate the changes in histological gastritis in patients receiving rebamipide treatment afterH. pylorieradication.Methods. 206 patients who had undergoneH. pylorieradication were evaluated. Of these, 169 patients who achieved successful eradication were randomly allocated to 2 groups: the rebamipide group (n= 82) and the untreated group (n= 87). The primary endpoints were histopathological findings according to the updated Sydney system at the start of the study and after 1 year.Results. Final assessment for histological gastritis was possible in 50 cases from the rebamipide group and 53 cases from the untreated group. The activity and atrophy improved in both the rebamipide and untreated groups, and no significant intergroup differences were observed. Chronic inflammation affecting the lesser curvature of the corpus was significantly improved in the rebamipide group compared to in the untreated group (1.12±0.08versus1.35±0.08;P= 0.043).Conclusions. Rebamipide treatment afterH. pylorieradication alleviated chronic inflammation in the lesser curvature of the corpus compared to that in the untreated group. This trial is registered withUMIN000002369.

Pathogens ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 65
Author(s):  
Mariateresa Casarotto ◽  
Chiara Pratesi ◽  
Ettore Bidoli ◽  
Stefania Maiero ◽  
Raffaella Magris ◽  
...  

Helicobacter pylori (H. pylori) represents an independent risk factor for Gastric Cancer (GC). First Degree Relatives (FDR) of GC subjects and Autoimmune Gastritis (AG) patients are both at increased risk for GC. H. pylori genetic heterogeneity within the gastric niche of FDR and AG individuals has been little explored. To understand whether they exploit an increased H. pylori stability and virulence, 14 AG, 25 FDR, 39 GC and 13 dyspeptic patients (D) were investigated by a cultural PCR-based approach characterizing single colonies-forming-units. We chose three loci within the Cytotoxin-associated gene-A Pathogenicity Island (CagPAI) (cagA,cagE,virB11), vacA, homA and homB as markers of virulence with reported association to GC. Inflammatory/precancerous lesions were staged according to Sydney System. When compared to D, FDR, similarly to GC patients, were associated to higher atrophy (OR = 6.29; 95% CI:1.23–31.96 in FDR; OR = 7.50; 95% CI:1.67–33.72 in GC) and a lower frequency of mixed infections (OR = 0.16; 95% CI:0.03–0.81 in FDR; OR = 0.10; 95% CI:0.02–0.48 in GC). FDR presented also an increased neutrophil infiltration (OR = 7.19; 95% CI:1.16–44.65). Both FDR and GC carried a higher proportion of CagPAI+vacAs1i1mx+homB+ profiles (OR = 2.71; 95% CI: 1.66–4.41 and OR = 3.43; 95% CI: 2.16–5.44, respectively). Conversely, AG patients presented a lower frequency of subtypes carrying a stable CagPAI and vacAs1i1mx. These results underline different H. pylori plasticity in FDR and AG individuals, and thus, a different host-bacterium interaction capacity that should be considered in the context of eradication therapies.


2021 ◽  
Vol 51 (1) ◽  
Author(s):  
Andrea Carlin Ronquillo ◽  
Alex Ventura León ◽  
Jorge L Espinoza Ríos ◽  
Eduar A Bravo Paredes ◽  
Paúl Gómez Hinojosa ◽  
...  

Introduction. The operative link for gastritis assessment (OLGA) and the operative link on gastric intestinal metaplasia assessment (OLGIM) staging systems have been suggested to provide risk of assessment for gastric cancer. Objective. To evaluate the distribution of OLGA and OLGIM staging by age and Helicobacter pylori status. Material and methods. We studied 197 subjects undergoing elective upper gastrointestinal endoscopy. The presence of the H. pylori and histological changes were evaluated using the updated Sydney system. Stages III and IV of OLGA/OLGIM were considered high risk stages. Results. The H. pylori rate was 56.85% (112/197). High-risk OLGA/OLGIM cases were rare: 7/112 (6.5%) cases of OLGA in the H. pylori positive group and 6/85 (7%) in the H. pylori negative group; 5 (4.4%) cases of OLGIM in the H. pylori positive and 6 (7%) in the H. pylori negative. The proportion of advanced stages of OLGA and OLGIM increased with age (p < 0.001). High-risk OLGA was not found before age 40 regardless of the presence of H. pylori, but increased to 16.2%, 10.3%, 17.3% and 40.8% in subjects in the fourth, fifth, sixth and seventh decade of life respectively. The OLGIM high risk showed a similar trend: 0% before 40 years and up to 22.6% in people of 70 years. Conclusions. High-risk OLGA/OLGIM cases are infrequent before age 40 and increase significantly with age. No relation was found with the presence of the H. pylori. According to these protocols, only a fifth of the patients would strictly require endoscopic control.


2019 ◽  
Vol 45 (3) ◽  
pp. 170-174
Author(s):  
Rita Rani Barua ◽  
Sushanta Barua ◽  
Hena Rani Barua ◽  
Ajoy Kishore Barua ◽  
M.A. Jalil Ansari ◽  
...  

Background: Gastric cancer (GC) is the leading cause of cancer death in the world. Chronic inflammation is a predisposing factor of gastric carcinogenesis. TNF-α is a key pro-inflammatory cytokine secreted by macrophages and causes development of malignant diseases. It also plays an important role in chronic inflammation caused by Helicobacter Pylori. Therefore, TNF-α polymorphisms is studied in Helicobacter Pylori infected gastric cancer. Objective: To find out the high risk group of Helicobacter Pylori infected gastric cancer cases in Asian and Caucasian people. Methods: A total of 130 GC cases and 103 healthy controls from Jichi Medical School, Japan were studied. TNF-α genotype and allele frequency were studied by Restriction Fragment Length Polymorphism (RFLP). Results: Among the study population TNFa-308A was less frequent in Asian people than those of Caucasian. TNFa-238G allele was more frequent in H. pylori positive GC (p<0.036) cases. Conclusion: Findings of the study suggest that TNF-238G polymorphism of TNF-α gene may be closely associated with susceptibility to Helicobacter Pylori infected gastric cancer in Asian patients.  This might be due to high cytokine production by TNF-238G allele.


Author(s):  
Anjana M. L. ◽  
Kavitha Yevoor

Background: Helicobacter pylori has been established as a major etiological factor in the pathogenesis of chronic gastritis. The aim of the study was to interpret the histopathological changes in chronic gastritis using updated Sydney system and the association with H. pylori infection.Methods: This was a 3 years study in which 62 gastric endoscopic mucosal biopsies taken from patients presenting with dyspepsia were included. Slides were stained with routine H and E and Giemsa for H. pylori detection in chronic gastritis cases. Grading of the variables were done with reference to Sydney system of classification.Results: Out of 62 gastric biopsy specimens, 55 cases (88.7%) were histopathological diagnosed as chronic gastritis. Among chronic gastritis, 21 (38%) cases showed H. pylori and majority of these being moderately (2+) positive. 27 (49%) cases showed neutrophilic activity with most of them showed mild (1+) activity. Chronic inflammation was seen 52 (94.5%) with majority of these graded as moderate (2+). Intestinal metaplasia was seen in 8 (14.5%) of cases with majority being mild (1+). Atrophy was seen only in 3 (5.4%) of cases with majority being mild (1+). Significant statistical association was found between H. pylori and neutrophilic activity (p<0.001).Conclusions: Histological evaluation of chronic gastritis using updated Sydney system of classification helps in detection of H. pylori infection and prevents further progression of the disease. 


2015 ◽  
Vol 144 (2) ◽  
pp. 234-240 ◽  
Author(s):  
T. T. H. TRANG ◽  
H. NAGASHIMA ◽  
T. UCHIDA ◽  
V. MAHACHAI ◽  
R.-K. VILAICHONE ◽  
...  

SUMMARYIn order to evaluate the role of the RAD51 G135C genetic polymorphism on the risk of gastric cancer induced byHelicobacter pyloriinfection, we determined allele frequency and genotype distribution of this polymorphism in Bhutan – a population documented with high prevalence of gastric cancer and extremely high prevalence ofH. pyloriinfection. The status of RAD51 G135C was examined by restriction fragment length polymorphism analysis of PCR amplified fragments and sequencing. Histological scores were evaluated according to the updated Sydney system. G135C carriers showed significantly higher scores for intestinal metaplasia in the antrum than G135G carriers [mean (median) 0·33 (0)vs.0·08 (0),P= 0·008]. Higher scores for intestinal metaplasia of G135C carriers compared to those of G135G carriers were also observed inH. pylori-positive patients [0·3 (0)vs.0·1 (0),P= 0·002] andH. pylori-positive patients with gastritis [0·4 (0)vs.0·1 (0),P= 0·002] but were not found inH. pylori-negative patients. Our findings revealed that a combination ofH. pyloriinfection and RAD51 G135C genotype of the host showed an increasing score for intestinal metaplasia. Therefore, RAD51 G135C might be the important predictor for gastric cancer ofH. pylori-infected patients.


2019 ◽  
Vol 56 (4) ◽  
pp. 419-424 ◽  
Author(s):  
Michele Fernandes RODRIGUES ◽  
Maximiliano Ribeiro GUERRA ◽  
Angélica Vilela Rodrigues de ALVARENGA ◽  
Danillo Zeferino de Oliveira SOUZA ◽  
Rafaella Angélica Vieira e Silva COSTA ◽  
...  

ABSTRACT BACKGROUND: Helicobacter pylori infection is the most important risk factor for gastric atrophy and intestinal metaplasia, both considered gastric cancer precursor lesions. Therefore, the investigation of the occurrence of H. pylori infection, precursor lesions and associated factors guides the adoption of specific strategies for the control this type of cancer. OBJECTIVE: To evaluate the prevalence of H. pylori infection in patients undergoing upper digestive endoscopy, as well as the prevalence of intestinal metaplasia, atrophy and chronic inflammation and their association with H. pylori infection. METHODS: A retrospective study was performed based on reports of gastric endoscopic biopsies performed in a private laboratory affiliated to the Brazilian Public Health System (SUS). Patients were evaluated for age, gender and type of health service. The samples were evaluated for the presence of H. pylori, and also of chronic inflammation, intestinal metaplasia and glandular atrophy. RESULTS: Of a total of 4,604 patients (mean age 51±16.6), 63.9% were female and 63.1% coming from private health care service. The prevalence of H. pylori infection was 31.7% (n=1,459), and the percentage of infection was significantly higher in patients from public health service (42.0%) in relation to patients from private health service (25.6%). Among H. pylori (+) patients, a higher percentage of intestinal metaplasia (17.7% vs 13.3%) and glandular atrophy (17.6% vs 6.9%) were observed when compared to those H. pylori (-) (P<0.01). From the patients H. pylori (+) with at least one type of precursor lesion (n=418), 161 (38.5%) had metaplasia and chronic inflammation, 160 (38.3%) had atrophy and chronic inflammation and finally 97 (23.2%) presented metaplasia, atrophy and chronic inflammation simultaneously. CONCLUSION: The present study reinforces the association of H. pylori infection with gastric cancer precursor lesions in a Brazilian population, emphasizing the importance of infection prevention measures, as well as the treatment of infected patients, especially in regions with lower socioeconomic levels that show a higher prevalence of infection by H. pylori.


2001 ◽  
Vol 15 (9) ◽  
pp. 591-598 ◽  
Author(s):  
Manfred Stolte ◽  
Alexander Meining

In recent years, the importance of the histological diagnosis of gastritis on the basis of routinely obtained antral and corpus biopsies has increased enormously, which is owed not least of all to the discovery ofHelicobacter pylori. The introduction of the Sydney system made it possible, for the first time, to grade histological parameters, identify topographical distribution and, finally, make a statement about the etiopathogenesis of the gastritis. Of pathogenetic importance is, in the first instance, the differentiation between gastritis with and gastritis withoutH pyloriinfection. The group ofH pylori-associated gastritis can be further subdivided into forms of gastritis whose morphological distribution patterns usually identify them as sequelae ofH pyloriinfection, while the group of gastritis unassociated withH pylori, can be differentiated into autoimmune, chemically induced reactive gastritis, ex-H pylorigastritis,Helicobacter heilmanniigastritis, Crohn's gastritis and a number of special forms of gastritis.


2019 ◽  
Author(s):  
Nushka Ubhayawardana ◽  
Manjula Weerasekera ◽  
Kamani Samarasinghe ◽  
Sameera Premalal ◽  
Deepaka Weerasekera ◽  
...  

Abstract Objective Helicobacter pylori is a major cause for chronic gastritis and further it is associated with development of peptic ulcer disease and gastric cancer. Therefore, the objective of this study was to classify gastritis according to the updated Sydney system guidelines and find the association of H. pylori with each of graded variable. Number of 152 dyspeptic patients who underwent upper gastro-intestinal endoscopy at a Teaching Hospital were enrolled. Of the 2 biopsies collected one was used for PCR to detect H. pylori. The other biopsy was fixed in formalin followed by paraffin embedding and stained with H&E stain. Gastritis was classified microscopically according to the updated Sydney system. Results : Gastritis was reported over a wide age group ranging from 18-84 years with a mean age of 51 years. Based on histological findings, 12% of patients were diagnosed as H. pylori associated chronic active gastritis. There was no significant association between each graded variable and H. pylori positivity. Of the 152 dyspeptic patients 34 were positive by PCR for H. pylori infection. All the dyspeptic patients with H. pylori infection had chronic active gastritis, suggesting an etiologic role of the bacterium in the histologic lesion.


2017 ◽  
Vol 4 (S) ◽  
pp. 46
Author(s):  
Truong Xuan Bui

Gastric cancer is one of the leading cancer lesions in Vietnam. Up to now, Helicobacter pylori (H. pylori) infection is still remaining a major pathogenic factor in patients with peptic disorders in Vietnam. Aims: The aim of the study was evaluated the correlation between H. pylori infection with atrophic gastritis (AG), intestinal metaplasia (IM) and dysplasia (DP) in gastritis Vietnamese. Patients and Methods: A total of 161 gastritis patients including 105 males and 56 females with mean of age of 49.81 ± 11.32 years (21 - 79 years) were enrolled in the study. Upper GI endoscopy was evaluated in all patients and afterward gastric biopsy specimens were taken according to the recommendation of update Sydney system and modified Baylor. The gastric biopsy specimens were analyzed with skilled pathologist who did not know about clinico-endoscopic status. The confirmation of H. pylori infection was evaluated with urease test (clo-test) and Giemsa staining. Results: Of the 161 patients, 96 (59.6%) patients were infected with H. pylori, and about 72.05% (116/161) of patients was suffered from atrophic gastritis. The prevalence of atrophic gastritis in H. pylori infected patients (83/96, 86.45%) was significantly higher than that in non-infected patients (33/65, 50.76%), p = 0.041. In the study, the prevalence of intestinal metaplasia and dysplasia was 84/161 (52.17%) and 17/161 (10.55%), respectively. The prevalence of intestinal metaplasia in H. pylori infected patients was observed significantly higher than that in non-infected patients (61/96, 63.54% vs. 23/65, 35.38%, p = 0.044); and the prevalence of dysplasia in H. pylori infected patients was also higher than that in non-infected patients (14/96, 14.58% vs. 3/65, 4.61%, p = 0.073). Conclusion: In gastritis Vietnamese, H. pylori was related to atrophic gastritis, intestinal metaplasia and dysplasia, so gastritis Vietnamese infected with H. pylori could be categorized into high risk group for screening gastric cancer.


Background and aim: Helicobacter pylori (H. pylori) is an incriminated pathogen causing diseases in both animals and humans and considered a zoonotic pathogen. H. pylori infection is considered a cause of gastric cancer, which rests a significant health care challenge. This study analyzes the expression pattern of matrix metalloprotein 2 (MMP-2) in patients with Helicobacter pylori-associated gastritis and the effect of H. pylori on gastric cancer stem cells, as well as study the role of helicon bacteriosis in dog in transmission of H. pylori infection to human. Materials and methods: Fifty-five of each sample (gastric biopsy, blood and stool) were collected from patients suffering from dyspepsia, chronic vomiting and perforated peptic ulcers and also from apparent healthy dogs. The investigation detected H. pylori by serological and histopathological examination. Biopsies were stored in physiological saline for identification of H. pylori by conventional time PCR. MMP-2 and Gastric cancer stem cells were then identified by immunohistochemistry. Results: Serological identification for H. pylori Antigen and Antibodies revealed (63% human, 50% dogs) and (87% human, 90% dogs) respectively were positive. Genotyping of H. pylori based on 16S rRNA gene showed 54.5% of human and 35% of dogs were positive. Immunohistochemistry revealed strong expression of CD44 in H. pylori- associated gastric cancer cases, MMP-2 expression was observed in all neoplastic lesions associated with H. pylori infection. Conclusion: H. pylori infection affects gastric mucosa and induces changes in gastric stem cells altering their differentiation and increased expression of MMP’s and CD44with a resultant potentiation of oncogenic alteration. In addition the up-regulation of both markers could be an instrumental to interpret the origination of gastric cancer.


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