scholarly journals Effect of Helicobacter pylori on gastrointestinal microbiota: a population-based study in Linqu, a high-risk area of gastric cancer

Gut ◽  
2019 ◽  
Vol 69 (9) ◽  
pp. 1598-1607 ◽  
Author(s):  
Yang Guo ◽  
Yang Zhang ◽  
Markus Gerhard ◽  
Juan-Juan Gao ◽  
Raquel Mejias-Luque ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Chronic Atrophic Gastritis ◽  
Population Based ◽  
Shannon Index ◽  
Gastrointestinal Microbiota ◽  
Risk Area ◽  
High Risk Area ◽  
Microbial Dysbiosis ◽  
H Pylori

ObjectiveGastrointestinal microbiota may be involved in Helicobacter pylori-associated gastric cancer development. The aim of this study was to explore the possible microbial mechanisms in gastric carcinogenesis and potential dysbiosis arising from H. pylori infection.DesignDeep sequencing of the microbial 16S ribosomal RNA gene was used to investigate alterations in paired gastric biopsies and stool samples in 58 subjects with successful and 57 subjects with failed anti-H. pylori treatment, relative to 49 H. pylori negative subjects.ResultsIn H. pylori positive subjects, richness and Shannon indexes increased significantly (both p<0.001) after successful eradication and showed no difference to those of negative subjects (p=0.493 for richness and p=0.420 for Shannon index). Differential taxa analysis identified 18 significantly altered gastric genera after eradication. The combination of these genera into a Microbial Dysbiosis Index revealed that the dysbiotic microbiota in H. pylori positive mucosa was associated with advanced gastric lesions (chronic atrophic gastritis and intestinal metaplasia/dysplasia) and could be reversed by eradication. Strong coexcluding interactions between Helicobacter and Fusobacterium, Neisseria, Prevotella, Veillonella, Rothia were found only in advanced gastric lesion patients, and were absent in normal/superficial gastritis group. Changes in faecal microbiota included increased Bifidobacterium after successful H. pylori eradication and more upregulated drug-resistant functional orthologs after failed treatment.ConclusionH. pylori infection contributes significantly to gastric microbial dysbiosis that may be involved in carcinogenesis. Successful H. pylori eradication potentially restores gastric microbiota to a similar status as found in uninfected individuals, and shows beneficial effects on gut microbiota.

scholarly journals Evolutionarily-Related Helicobacter pylori Genotypes and Gastric Intraepithelial Neoplasia in a High-Risk Area of Northern Italy

2020 ◽  
Vol 8 (3) ◽  
pp. 324
Author(s):  
Sonia Toracchio ◽  
Rosario Alberto Caruso ◽  
Silvia Perconti ◽  
Luciana Rigoli ◽  
Enrico Betri ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Polymerase Chain Reaction ◽  
Helicobacter Pylori ◽  
High Risk ◽  
Intraepithelial Neoplasia ◽  
Northern Italy ◽  
Chain Reaction ◽  
Risk Area ◽  
High Risk Area ◽  
Polymerase Chain

Helicobacter pylori (Hp) is the major recognized risk factor for non-cardia gastric cancer (GC), but only a fraction of infected subjects develop GC, thus GC risk might reflect other genetic/environmental cofactors and/or differences in virulence among infectious Hp strains. Focusing on a high GC risk area of Northern Italy (Cremona, Lombardy) and using archived paraffin-embedded biopsies, we investigated the associations between the Hp vacA and cagA genotype variants and gastric intraepithelial neoplasia (GIN, 33 cases) versus non-neoplastic gastroduodenal lesions (NNGDLs, 37 cases). The glmM gene and the cagA and vacA (s and m) genotypes were determined by polymerase chain reaction (PCR) and sequencing. Hp was confirmed in 37/37 (100%) NNGDLs and detected in 9/33 GINs (27%), consistently with the well-known Hp loss in GC. CagA was detected in 4/9 Hp-positive GINs and in 29/37 NNGDLs. The vacA s1a and m1 subtypes were more common in GINs than in NNGDLs (6/7 vs. 12/34, p=0.014, for s1a; 7/7 vs. 18/34, p=0.020 for m1), with significant vacA s genotype-specific variance. The GIN-associated vacA s1a sequences clustered together, suggesting that aggressive Hp strains from a unique founder contribute to GC in the high-risk area studied.

scholarly journals Will Treatment of Helicobacter Pylori Infection in Childhood Alter the Risk of Developing Gastric Cancer?

2005 ◽  
Vol 19 (7) ◽  
pp. 409-411 ◽  
Author(s):  
Billy Bourke
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Precancerous Lesions ◽  
Positive Family History ◽  
Population Based ◽  
Screening Programs ◽  
History Of ◽  
Different Populations ◽  
H Pylori ◽  
Developed Nations

Helicobacter pylori has been classified as a group 1 carcinogen for gastric cancer. It is estimated that there is between a two- and sixfold increase in the risk of developing gastric cancer among infected patients. Among different populations, the risk of H pylori-infected individuals developing gastric cancer varies greatly. However, on a worldwide scale, gastric cancer is the second most common cause of cancer-related death. Therefore, H pylori eradication could help prevent up to three to four million gastric cancer deaths per year. H pylori is usually acquired in childhood. Because infected children have not harboured the organism for long enough to have developed precancerous lesions, childhood is theoretically an attractive time for H pylori eradication and, thus, could help prevent gastric cancer later in life. However, as H pylori prevalence and the incidence of gastric cancer are falling rapidly in developed nations, widespread population screening programs aimed at the eradication of H pylori in these countries would be enormously expensive. Therefore, except in groups with a high risk for development of gastric cancer (eg, Japanese or those with a strong positive family history of gastric cancer), a population-based test-and-treat policy is not justified.

scholarly journals Association of Helicobacter pylori infection and stomach cancer: our experience

2018 ◽  
Vol 5 (8) ◽  
pp. 2794
Author(s):  
N. G. Javan ◽  
Wormi Sharon
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Carcinoma ◽  
Stomach Cancer ◽  
Histopathological Examination ◽  
Chronic Atrophic Gastritis ◽  
Helicobacter Pylori Infection ◽  
Future Research ◽  
Gastric Cancer Prevention ◽  
H Pylori

Background: Infection with Helicobacter pylori (H. pylori) has been linked with chronic atrophic gastritis, an inflammatory precursor of gastric adenocarcinoma. There are data on the epidemiology, pathophysiology, and histology of this disease that show that Helicobacter pylori gastritis has an important role in gastric carcinogenesis. However, it has to be considered that only very few of those infected with Helicobacter pylori will develop gastric cancer. Hence, it will be a major target of future research to identify individuals who carry a greater risk for developing gastric cancer, and therefore may benefit from eradication of Helicobacter pylori in terms of gastric cancer prevention. Various studies revealed that approximately more than 50% of the world’s human population is infected by Helicobacter pylori. In underdeveloped countries, this association is shown to be much higher according to different studies.Methods: This study was conducted over a period of 36 months from 1st January 2014 till December 31st, 2016. All patients who underwent Gastrectomy during this period were taken. All specimens were investigated to see presence of helicobacter pylori by histological examination. A total of 50 Gastrectomy was performed by one surgical team over 36-month period.Results: Out of 50 patients, Helicobacter pylori positivity was seen in 33 (66%) cases by histopathological examination (HPE). Gastric cancer is more prevalent among males 31 (62%) as compared to 19 (38%) in females. It is more common among the older age group.Conclusions: Helicobacter pylori infection is higher in prevalence in cases of stomach cancer. Present study also showed that there is significant association of Helicobacter pylori infection with gastric carcinoma. Helicobacter pylori infection could be one of the etiological factors for gastric carcinoma.

Which genotype of Helicobacter pylori—cagA or cagE—Is better associated with gastric Cancer risk? Lessons from an extremely high-risk area in Iran

2020 ◽  
Vol 85 ◽  
pp. 104431 ◽  
Author(s):  
Seyedeh Zahra Bakhti ◽  
Saeid Latifi-Navid ◽  
Shokufe Gholizade Tobnagh ◽  
Kiana Yazdanbod ◽  
Abbas Yazdanbod
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
High Risk ◽  
Cancer Risk ◽  
Gastric Cancer Risk ◽  
Risk Area ◽  
High Risk Area

scholarly journals Pathways of Gastric Carcinogenesis, Helicobacter pylori Virulence and Interactions with Antioxidant Systems, Vitamin C and Phytochemicals

2020 ◽  
Vol 21 (17) ◽  
pp. 6451 ◽  
Author(s):  
James W. T. Toh ◽  
Robert B. Wilson
Keyword(s):  
Gastric Cancer ◽  
Ascorbic Acid ◽  
Helicobacter Pylori ◽  
Vitamin C ◽  
Atrophic Gastritis ◽  
Chronic Atrophic Gastritis ◽  
Gastric Carcinogenesis ◽  
Antioxidant Systems ◽  
H Pylori

Helicobacter pylori is a class one carcinogen which causes chronic atrophic gastritis, gastric intestinal metaplasia, dysplasia and adenocarcinoma. The mechanisms by which H. pylori interacts with other risk and protective factors, particularly vitamin C in gastric carcinogenesis are complex. Gastric carcinogenesis includes metabolic, environmental, epigenetic, genomic, infective, inflammatory and oncogenic pathways. The molecular classification of gastric cancer subtypes has revolutionized the understanding of gastric carcinogenesis. This includes the tumour microenvironment, germline mutations, and the role of Helicobacter pylori bacteria, Epstein Barr virus and epigenetics in somatic mutations. There is evidence that ascorbic acid, phytochemicals and endogenous antioxidant systems can modify the risk of gastric cancer. Gastric juice ascorbate levels depend on dietary intake of ascorbic acid but can also be decreased by H. pylori infection, H. pylori CagA secretion, tobacco smoking, achlorhydria and chronic atrophic gastritis. Ascorbic acid may be protective against gastric cancer by its antioxidant effect in gastric cytoprotection, regenerating active vitamin E and glutathione, inhibiting endogenous N-nitrosation, reducing toxic effects of ingested nitrosodimethylamines and heterocyclic amines, and preventing H. pylori infection. The effectiveness of such cytoprotection is related to H. pylori strain virulence, particularly CagA expression. The role of vitamin C in epigenetic reprogramming in gastric cancer is still evolving. Other factors in conjunction with vitamin C also play a role in gastric carcinogenesis. Eradication of H. pylori may lead to recovery of vitamin C secretion by gastric epithelium and enable regression of premalignant gastric lesions, thereby interrupting the Correa cascade of gastric carcinogenesis.

Beneficial effects of endoscopic screening on gastric cancer and its optimal screening interval: a population-based study

Endoscopy ◽  
2021 ◽  
Author(s):  
Wen-Qing Li ◽  
Xiang-Xiang Qin ◽  
Zhe-Xuan Li ◽  
Le-Hua Wang ◽  
Zong-Chao Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Early Detection ◽  
Population Based ◽  
Low Grade ◽  
Risk Area ◽  
Endoscopic Screening ◽  
Population Based Study ◽  
High Risk Area ◽  
Screening Interval ◽  
Optimal Screening

Background and study aims: The effectiveness of endoscopic screening on gastric cancer (GC) is less investigated and screening interval of repeated screening is yet to be optimized in China. Patients and methods: In a population-based prospective study, we included 375,800 subjects based on the Upper Gastrointestinal Cancer Early Detection Program in Linqu, a GC high-risk area in China, 14,670 of which underwent endoscopic screening(2012-2018). We assessed the associations of the risk of incident GC and GC-specific deaths with endoscopic screening and examined the changes in overall survival (OS) and disease-specific survival (DSS) of GCs by endoscopic screening. The optimal screening interval of repeated endoscopy for early detection of GC was explored. Results: Ever receiving endoscopic screening significantly decreased the risk of invasive GC(age and sex-adjusted RR=0.69, 95%CI:0.52-0.92) and GC-specific deaths(RR=0.33, 95%CI: 0.20-0.56), particularly for non-cardia GC. Repeated screening strengthened the beneficial effect on invasive GC-specific deaths by one-time screening. Among invasive GCs, screening-detected cases had significantly better OS(RR=0.18, 95%CI: 0.13-0.25) and DSS(RR=0.18, 95%CI: 0.13-0.25) than cases in the unscreened group, particularly for those receiving repeated endoscopy. For individuals with intestinal metaplasia or low-grade intraepithelial neoplasia, repeated endoscopy at an interval of less than two years, particularly within one year, significantly enhanced the detection of early GC, compared with repeated screening after two years(P-trend=0.02). Conclusion: Endoscopic screening prevented GC occurrence and death and improved its prognosis in a population-based study. Repeated endoscopy enhanced the effectiveness, for which screening interval needs to be defined in conformity with the severity of gastric lesions.

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