scholarly journals ID2012 Helicobacter pylori infection in relation to pre-cancerous lesions in gastritis Vietnamese

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.

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Soichiro Sue ◽  
Wataru Shibata ◽  
Shin Maeda

Helicobacter pylori(H. pylori) induces chronic gastric inflammation, atrophic gastritis, intestinal metaplasia, and cancer. Although the risk of gastric cancer increases exponentially with the extent of atrophic gastritis, the precise mechanisms of gastric carcinogenesis have not been fully elucidated.H. pyloriinduces genetic and epigenetic changes in gastric epithelial cells through activating intracellular signaling pathways in a cagPAI-dependent manner.H. pylorieventually induces gastric cancer with chromosomal instability (CIN) or microsatellite instability (MSI), which are classified as two major subtypes of gastric cancer. Elucidation of the precise mechanisms of gastric carcinogenesis will also be important for cancer therapy.


Author(s):  
Chan Hyuk Park

Owing to advancements in next-generation sequencing and non-culture-based microbial research techniques, we have recognized that many bacterial taxa other than <i>Helicobacter pylori (H. pylori)</i> are present in the human stomach. Gastric microbial composition depends on gastric diseases, including gastritis, atrophic gastritis, intestinal metaplasia, and gastric cancer. Although <i>H. pylori</i> is a major factor associated with gastric cancer development, other bacterial taxa may affect gastric carcinogenesis. Because the risk of gastric cancer development can be reduced through <i>H. pylori</i> eradication, many investigators have studied the changes in the microbial composition in the stomach after <i>H. pylori</i> eradication. The gastric microbiome in patients with <i>H. pylori</i> infection typically shows abundance of <i>H. pylori</i> and a low microbial diversity index. If we treat <i>H. pylori</i>-infected patients with antibiotics, microbial diversity increases, and the relative abundance also increases in many bacterial taxa. Several studies suggested that the microbial composition in patients with <i>H. pylori</i> infection could be restored by <i>H. pylori</i> eradication therapy; however, there have been inconsistent findings of the abundant bacterial taxa after <i>H. pylori</i> eradication in patients with atrophic gastritis and intestinal metaplasia. More studies are required to reach a definitive conclusion on restoration of the microbial composition after <i>H. pylori</i> eradication according to the severity of gastric inflammation.


2014 ◽  
Vol 63 (9) ◽  
pp. 1189-1196 ◽  
Author(s):  
Seiji Shiota ◽  
Modesto Cruz ◽  
José A. Jiménez Abreu ◽  
Takahiro Mitsui ◽  
Hideo Terao ◽  
...  

Although the incidence of gastric cancer in the Dominican Republic is not high, the disease remains a significant health problem. We first conducted a detailed analysis of Helicobacter pylori status in the Dominican Republic. In total, 158 patients (103 females and 55 males; mean age 47.1±16.2 years) were recruited. The status of H. pylori infection was determined based on four tests: rapid urease test, culture test, histological test and immunohistochemistry. The status of cagA and vacA genotypes in H. pylori was examined using PCR and gene sequencing. The overall prevalence of H. pylori infection was 58.9 %. No relationship was found between the H. pylori infection rate and the age range of 17–91 years. Even in the youngest group (patients aged <29 years), the H. pylori infection rate was 62.5 %. Peptic ulcer was found in 23 patients and gastric cancer was found in one patient. The H. pylori infection rate in patients with peptic ulcer was significantly higher than that in patients with gastritis (82.6 versus 54.5 %, P<0.01). The cagA-positive/vacA s1m1 genotype was the most prevalent (43/64, 67.2 %). Compared with H. pylori-negative patients, H. pylori-positive patients showed more severe gastritis. Furthermore, the presence of cagA was related to the presence of more severe gastritis. All CagA-positive strains had Western-type CagA. In conclusion, we found that H. pylori infection is a risk factor for peptic ulcer in the Dominican Republic. Patients with cagA-positive H. pylori could be at higher risk for severe inflammation and atrophy.


2019 ◽  
Vol 56 (3) ◽  
pp. 264-269
Author(s):  
Ariney Costa de MIRANDA ◽  
Cássio CALDATO ◽  
Mira Nabil SAID ◽  
Caio de Souza LEVY ◽  
Claudio Eduardo Corrêa TEIXEIRA ◽  
...  

ABSTRACT BACKGROUND: It is widely assumed that gender, age, gastritis and Helicobacter pylori , all have some degree of correlation and, therefore, can synergistically lead to the development of gastric cancer. OBJECTIVE: In this cross-sectional study, we expected to observe the above mentioned correlation in the analysis of medical records of 67 patients of both sexes (female, n=44), mean age ± standard deviation: 41±12 years old, all from Belém (capital of Pará State, Brazilian Amazon), a city historically known as one with the highest gastric cancer prevalence in this country. METHODS: All patients were submitted to upper gastrointestinal endoscopy for gastric biopsy histopathological analysis and rapid urease test. All diagnoses of gastritis were recorded considering its topography, category and the degree of inflammatory activity, being associated or not associated with H. pylori infection. RESULTS: The results show that no statistically relevant associations were found among the prevalences of the observed variables. CONCLUSION: The authors hypothesize that observed risk factors associated to gastric cancer might be lesser synergistic than is usually expected.


2020 ◽  
Author(s):  
Hossein Masoumi Asl ◽  
Ali Badamchi ◽  
Shima Javadinia ◽  
Siamak Khaleghi ◽  
Leila Tehraninia ◽  
...  

Helicobacter pylori (H. pylori) is a bacterium that resides in the human stomach, which is associated with gastroduodenal diseases. We investigate the prevalence of cagA, vacA, oipA, cagE1, cagE2 and dupA genotypes in H. pylori isolated from patients with Gastric ulcer, duodenal ulcer, and Gastric Cancer. Collected 74 samples from the Gastroenterology Unit of the Rasool Akram Hospital were included in this study. Gastric disorders were identified by endoscopy .gastric cancer was further confirmed by histopathology. H. pylori were detected by the urease test. Subsequently, DNA was extracted from gastric tissue of the subjects with the CLO-test yielded positive results. In general, 74 patients with a mean age of 53.45 years (Range 22 to 86-year-old), including 45 men and 29 women, were studied. Among 74 H. pylori-positive patients, 70 (94.5%) patients were positive for the cagA gene. About 95.8% (23/24) of the patients with gastric carcinoma were dupA positive and VacA gene (91.8%). The oipA genotype was detected in 71 (96%) of H.pylori positive samples. This gene was more common in patients with gastritis rather than cancer group. Also, 97.2% of 74 H. pylori isolates were cagE2-positive. In 25 patients with PUD, the occurrence percent of cagA+/VacA+, cagA+/Vac- , cagA- /VacA+ and cagA- /VaxA- genotypes were found 80%, 12%, 4.2% and 4.2 respectively. The results of the present study suggest that a high prevalence of virulent factors could contribute to the risk of developing gastroduodenal diseases.


2021 ◽  
Vol 6 (1) ◽  
pp. 53-57
Author(s):  
Miluska Castillo ◽  
Luis A. Bernabe ◽  
Carlos A. Castaneda ◽  
Nancy Suarez ◽  
Fernando Barreda ◽  
...  

Objective: The aim of this study was to determine the relationship between Helicobacter pylori (H. pylori) infection in relatives and patients with gastric cancer (GC).Methods: H. pylori infection was evaluated by the breath urease test in 171 relatives and by qPCR technique in gastric tissue of 61 patients (n=45 for GC and n=16 for non-GC). Results: There were included 137 relatives of GC patients and 34 of non-GC. The median age of the relatives of patients with a gastric tissue sample was 39 years (10-86). Infection was found in 60.2% (n=103) relatives. There were no higher H. pylori infection rates in relatives of patients with gastric cancer (62% vs 62.9%, p=0.33), H. pylori infection (60% vs 60%, p=0.96), or metaplasia (58.8% vs 61.8%, p=0.71). Conclusion: The prevalence of infection in relatives of GC patients is high in our population but not associated with H. pylori presence in the paired case.


2021 ◽  
Vol 12 ◽  
Author(s):  
Mariagrazia Piscione ◽  
Mariangela Mazzone ◽  
Maria Carmela Di Marcantonio ◽  
Raffaella Muraro ◽  
Gabriella Mincione

Worldwide, gastric cancer (GC) represents the fifth cancer for incidence, and the third as cause of death in developed countries. Indeed, it resulted in more than 780,000 deaths in 2018. Helicobacter pylori appears to be responsible for the majority of these cancers. On the basis of recent studies, and either alone or combined with additional etiological factors, H. pylori is considered a “type I carcinogen.” Over recent decades, new insights have been obtained into the strategies that have been adopted by H. pylori to survive the acidic conditions of the gastric environment, and to result in persistent infection, and dysregulation of host functions. The multistep processes involved in the development of GC are initiated by transition of the mucosa into chronic non-atrophic gastritis, which is primarily triggered by infection with H. pylori. This gastritis then progresses into atrophic gastritis and intestinal metaplasia, and then to dysplasia, and following Correa’s cascade, to adenocarcinoma. The use of antibiotics for eradication of H. pylori can reduce the incidence of precancerous lesions only in the early stages of gastric carcinogenesis. Here, we first survey the etiology and risk factors of GC, and then we analyze the mechanisms underlying tumorigenesis induced by H. pylori, focusing attention on virulence factor CagA, inflammation, oxidative stress, and ErbB2 receptor tyrosine kinase. Moreover, we investigate the relationships between H. pylori eradication therapy and other diseases, considering not only cardia (upper stomach) cancers and Barrett’s esophagus, but also asthma and allergies, through discussion of the “hygiene hypothesis. ” This hypothesis suggests that improved hygiene and antibiotic use in early life reduces microbial exposure, such that the immune response does not become primed, and individuals are not protected against atopic disorders, asthma, and autoimmune diseases. Finally, we overview recent advances to uncover the complex interplay between H. pylori and the gut microbiota during gastric carcinogenesis, as characterized by reduced bacterial diversity and increased microbial dysbiosis. Indeed, it is of particular importance to identify the bacterial taxa of the stomach that might predict the outcome of gastric disease through the stages of Correa’s cascade, to improve prevention and therapy of gastric carcinoma.


2006 ◽  
Vol 63 (3) ◽  
pp. 313-315 ◽  
Author(s):  
Ratko Tomasevic ◽  
Gradimir Golubovic ◽  
Miroslav Kiurski ◽  
Dragana Stankovic ◽  
Radoje Doder ◽  
...  

Introduction. Helicobacter pylori (H. pylori) infection is known to be the must common cause of chronic gastritis having some endoscopic and pathologic characteristies as determinated by the Sydney System for Gastritis Classification. The aim of our case report was to point out the relationship between an endoscopic finding of nodular antritis and the presence of H. pylori infection and active chronic gastritis. Case report. Our patient underwent upper gastrointestinal endoscopy for dyspeptic complaints and was diagnosed as having nodular antritis, but also underwent urease test and hystopathologic examination of antral mucosa, to determine the presence and density of H. pylori infection and the presence and severity of gastritis. After a course of anti H. pylori treatment, dyspepsia improved and new biopsy specimens obtained two months and six months afterwards revealed no pathological findings. Conclusion. The case report supported the association of H. pylori infection of lymphoid follicles with nodular gastric mucosis.


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