Association of Helicobacter pylori infection and stomach cancer: our experience

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.

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Association of Helicobacter Pylori Infection and Stomach Cancer

Medical Journal of Shree Birendra Hospital ◽

10.3126/mjsbh.v12i2.12927 ◽

2015 ◽

Vol 12 (2) ◽

pp. 36-41 ◽

Cited By ~ 1

Author(s):

Narayan Thapa ◽

Kunda Bikram Shah ◽

Bharat Bahadur Bhandari ◽

Bhairab Kumar Hamal ◽

Amar Shrestha ◽

...

Keyword(s):

Helicobacter Pylori ◽

Stomach Cancer ◽

Histopathological Examination ◽

Helicobacter Pylori Infection ◽

Rapid Urease Test ◽

Diffuse Type ◽

Surgical Department ◽

Urease Test ◽

H Pylori ◽

Carcinoma Stomach

Introduction: Helicobacter pylori (H. Pylori) as a primary etiological factor in carcinoma stomach. Associationof H. Pylori in gastric cancer has been documented to be in more than 50% of cases. In underdevelopedcountries, this association is shown to be much higher according to different studies.Methods: A prospective observational study of 40 consecutive cases of carcinoma stomach was under takenin surgical department of Shree Birendra hospital and Bir hospital, for a period of two years 2009 to 2011.Location and pathological types of the lesion were noted and all specimens were investigated to see presenceof helicobacter pylori by rapid urease test (RUT) and histological examination.Results: Out of 40 patients, helicobacter pylori positivity was seen in 27 (67.5%) cases by both rapid ureasetest and Histopathological examination (HPE). Regarding the pathological types, out of 26 intestinal type of castomach, 20 (76.92%) cases were positive for H. pylori infection, whereas out of 14 diffuse type of ca stomach,7(50%) cases were positive for H. pylori. In 29 cases of distal ca stomach, H. pylori positivity was seen in 22(75.86%) cases, whereas in rest of the 11 cases the lesion involved other part of the stomach, H. pylori positivitywas seen in 5(45.45%) cases.Conclusion: Helicobacter pylori infection is higher in prevalence in cases of stomach cancer. Its associationwith intestinal histological type of stomach cancer is more common than diffuse type. There is higher prevalenceof Helicobacter pylori infection in distal carcinoma. doi: http://dx.doi.org/10.3126/mjsbh.v12i2.12927

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Helicobacter pylori Infection, Gastric Cancer and Gastropanel

Romanian Journal of Internal Medicine ◽

10.1515/rjim-2016-0025 ◽

2016 ◽

Vol 54 (3) ◽

pp. 151-156 ◽

Cited By ~ 1

Author(s):

Alexandra Loor ◽

D.L. Dumitraşcu

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Atrophic Gastritis ◽

Chronic Atrophic Gastritis ◽

Helicobacter Pylori Infection ◽

Invasive Test ◽

High Cancer Risk ◽

Important Challenge ◽

Reduction Of Mortality ◽

H Pylori

Abstract Gastric cancer (GC) is one of the most widespread types of cancer worldwide. Helicobacter pylori infection has been clearly correlated with gastric carcinogenesis. At present and in the near future, the most important challenge is and will be the significant reduction of mortality due to GC. That goal can be achieved through the identification of higher-risk patients, such as those with atrophic gastritis, intestinal metaplasia and dysplasia. In this review we intend to discuss the importance of diagnosing H. pylori infection and chronic atrophic gastritis in preventing gastric cancer, using a new non-invasive test called GastroPanel. This test is a classification algorithm including four biochemical parameters pepsinogen I and II (PGI and PGII), gastrin-17 (G17), and anti-Helicobacter pylori antibodies (Ig G anti-Hp) measured in fasting sera, which allows to classify patients as having atrophic or non-atrophic gastritis and to find whether gastritis is associated or not with H. pylori infection. GastroPanel is not a “cancer test”, but it can and should be used in the screening and diagnosis of subjects with a high cancer risk; still, a careful diagnostic made by superior digestive endoscopy is compulsory to find possible precancerous or cancerous lesions at an early and curable stage.

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Faculty Opinions recommendation of The benefit of mass eradication of Helicobacter pylori infection: a community-based study of gastric cancer prevention.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.717950070.793455324 ◽

2012 ◽

Author(s):

Steven Moss

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Cancer Prevention ◽

Helicobacter Pylori Infection ◽

Community Based ◽

Gastric Cancer Prevention

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Increased Production of Matrix Metalloproteinases in Helicobacter pylori Infection that Stimulates Gastric Cancer Stem Cells

International Journal of Veterinary Science ◽

10.37422/ijvs/20.043 ◽

2020 ◽

Keyword(s):

Gastric Cancer ◽

Stem Cells ◽

Helicobacter Pylori ◽

Cancer Stem Cells ◽

Histopathological Examination ◽

Physiological Saline ◽

Rrna Gene ◽

Peptic Ulcers ◽

Gastric Cancer Stem Cells ◽

H Pylori

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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Prospective Assessment of Helicobacter Pylori Infection and Gastric Pathologies in Sidi Bel Abbes region, Western Algeria

South Asian Journal of Experimental Biology ◽

10.38150/sajeb.7(5).p217-224 ◽

2018 ◽

Vol 7 (5) ◽

pp. 217-224

Author(s):

Zouaouia Chama ◽

Khedoudj Kanoun ◽

Fatima Zohra Elkadi ◽

Kara Turqui Douidi ◽

Noria Harir ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Histological Study ◽

Helicobacter Pylori Infection ◽

University Hospital ◽

Infection Prevalence ◽

Gastric Diseases ◽

Number Of Patients ◽

H Pylori ◽

The Impact

Helicobacter pylori infection concerns half of the world’s population, mainly in developing countries. It causes several gastrodudenal pathologies such as gastritis, ulcer and gastric adenocarcinoma. The aim of our study was to determine the prevalence of H.pylori infection and to assess the impact of different epidemiological factors as well as principal gastric diseases associ-ated to this infection. We underwent a prospective study during 18 months (month 2016-month 2017) which implicated 201 symptomatic patients for gastric fiboptic endoscopy at the level of Sidi Bel Abbes University hospital. We collected patients’ biopsies to perform a histological study and H. pylori culture. H. pylori identification was carried out based on bacteriological and biochemical analysis. The middle age of our population was (47.29 ±15.97ans) and the sex-ratio =0,8. The global prevalence of Helicobacter pylori infection is of 61.2% (123/201). This rate, after a statistic analysis, seems to be significantly related to age. It is particularly high especially for patients belonging to age range (20-30)-(51-60) years. The gender did not affect the infection prevalence that is more frequent in the gastritis case. We noticed also that HP infection prevalence was important in SBA the hospital. The range age (20-30)-(51-60) years had the highest prevalence of H. pylori and of gastritis which might be a risky ground of gastric cancer appearance. The ulcer pathology maximal rate concerned the group of 51 to 60 years. Above this age, this rate dropped whereas the number of patients suffering from gastric cancer, which presents an important rate in our study, increase for the group of 61-70 years.

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Canadian Helicobacter Study Group Consensus Conference: Update on the Approach to Helicobacter Pylori Infection in Children and Adolescents – an Evidence-Based Evaluation

Canadian Journal of Gastroenterology ◽

10.1155/2005/390932 ◽

2005 ◽

Vol 19 (7) ◽

pp. 399-408 ◽

Cited By ~ 77

Author(s):

Nicola L Jones ◽

Philip Sherman ◽

Carlo A Fallone ◽

Nigel Flook ◽

Fiona Smaill ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Proton Pump Inhibitor ◽

Proton Pump ◽

Consensus Conference ◽

Helicobacter Pylori Infection ◽

Diagnostic Tools ◽

Study Group ◽

Evidence Based ◽

H Pylori

As an update to previously published recommendations for the management of Helicobacter pylori infection, an evidence-based appraisal of 14 topics was undertaken in a consensus conference sponsored by the Canadian Helicobacter Study Group. The goal was to update guidelines based on the best available evidence using an established and uniform methodology to address and formulate recommendations for each topic. The degree of consensus for each recommendation is also presented. The clinical issues addressed and recommendations made were: population-based screening for H pylori in asymptomatic children to prevent gastric cancer is not warranted; testing for H pylori in children should be considered if there is a family history of gastric cancer; the goal of diagnostic interventions should be to determine the cause of presenting gastrointestinal symptoms and not the presence of H pylori infection; recurrent abdominal pain of childhood is not an indication to test for H pylori infection; H pylori testing is not required in patients with newly diagnosed gastroesophageal reflux disease; H pylori testing may be considered before the use of long-term proton pump inhibitor therapy; testing for H pylori infection should be considered in children with refractory iron deficiency anemia when no other cause has been found; when investigation of pediatric patients with persistent or severe upper abdominal symptoms is indicated, upper endoscopy with biopsy is the investigation of choice; the 13C-urea breath test is currently the best noninvasive diagnostic test for H pylori infection in children; there is currently insufficient evidence to recommend stool antigen tests as acceptable diagnostic tools for H pylori infection; serological antibody tests are not recommended as diagnostic tools for H pylori infection in children; first-line therapy for H pylori infection in children is a twice-daily, triple-drug regimen comprised of a proton pump inhibitor plus two antibiotics (clarithromycin plus amoxicillin or metronidazole); the optimal treatment period for H pylori infection in children is 14 days; and H pylori culture and antibiotic sensitivity testing should be made available to monitor population antibiotic resistance and manage treatment failures.

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Helicobacter Pylori Induce Gastric Upset

Journal of Medical Research and Surgery ◽

10.52916/jmrs214055 ◽

2021 ◽

pp. 1-1

Author(s):

Hazim Abdul Rahman Alhit

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Serum Antibody ◽

Endoscopic Biopsy ◽

Helicobacter Pylori Infection ◽

Gastric Epithelium ◽

Gastric Diseases ◽

Heterogeneous Distribution ◽

Cytotoxin Associated Gene A ◽

H Pylori

Editorial: Helicobacter pylori is a micro-aerophilic, helical-form gramnegative aggressive bacteria. Accordingly, the idiom “Helico” intimates its helical appearance, “bacter” symbolizes bacteria, while “pylori” denotes stomach due to the first and common site of this bacteria living. Further, Marshall B. and Warren R. observed and described it in 1982. Then, the followed investigators studied this bacterium in detail with its consequences and complexities [1]. Gastric upset (Indigestion), dyspepsia: means impaired gastric digestion. Accordingly, the patient complains of upper abdominal pain, heartburn, belching, nausea, even feeling earlier gastric fullness than expected while eating. Furthermore, there are many causes of indigestion like gastroesophageal reflux disease, ulcer disease, gastritis, and even gastric cancer. Hence, unexplained recent onset dyspepsia in older people may need additional examinations. Moreover, one of the common causes is Helicobacter pylori infection, which needs laboratory and endoscopic examination [2]. Argument Many theories investigated the etiology and pathogenesis of Helicobacter pylori infection, concerning chronic or acute gastritis. Hence, gastric upset is the main presentation of both types of gastritis. Evidences The genotype is valuable in determining the dominant Helicobacter pylori strains as the isolates were different genetically plus heterogeneous distribution. Accordingly, the vac and cag markers operate a significant function in defining clinical consequences. These virulence agents are present in a subset of Helicobacter pylori strains isolates like cagA, iceA, vacA, and ureC. Moreover, the cagA causes cytotoxins induction by the gastric epithelial cell as Interleukin 8 [3]. The molecular intercommunication researches exhibit that the act of acarus calamus in hindering biofilm formation in Helicobacter pylori is due to the inhibitory impact of phytobio-active component, β-sitosterol, on the quorum sensing molecules-ToxB, PhnB, DnaA, plus Sip. Consequently, this opinion may suggest the molecular mechanism of Helicobacter pylori in producing the acidrelated complaints and gives a clue to a new therapy [4]. Helicobacter pylori infection causes lncRNA risk impression linked to H. pylori in gastric cancer patients and can prognosticate the prediction of these patients [5]. There was a close relationship between raised serum IgE levels in Helicobacter pylori infected patients [6]. Counterargument The laboratory investigations of Helicobacter pylori infection depend on several factors like the fluctuations of serum antibody titers in a time series, the antigene detection in stool tests, the false-positive results of lab tests, or the manner of endoscopic biopsy collection. Furthermore, other factors like the variations in Cytotoxin-Associated Gene A (CagA) in East Asian patients. Moreover, the gastric nodularity or atrophy, the patient’s age, the severity of the gastric mucosal infection are causes of variations in Helicobacter pylori detection at the time of the investigation [7]. Refutation The significant markers of H. pylori, the presence of the vacuolating cytotoxin (vacA), the cytotoxin-associated gene A (cagA), which induced by the direct communication with gastric epithelium factor antigen (iceA gene), and the presence of urease C gene (ureC). Consequently, all these factors play the principal factors in deciding the gastric consequences of Helicobacter infections. Conclusion Helicobacter pylori induce gastric upset by several mechanisms to form numerous Gastric diseases.

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Transcriptome Analysis of the Inhibitory Effect of Astaxanthin on Helicobacter pylori-Induced Gastric Carcinoma Cell Motility

Marine Drugs ◽

10.3390/md18070365 ◽

2020 ◽

Vol 18 (7) ◽

pp. 365 ◽

Cited By ~ 1

Author(s):

Suhn Hyung Kim ◽

Hyeyoung Kim

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Gastric Carcinoma ◽

Cell Motility ◽

Cancer Progression ◽

Migration And Invasion ◽

Pcr Analysis ◽

Human Gastric Cancer ◽

Gastric Carcinoma Cell ◽

H Pylori

Helicobacter pylori (H. pylori) infection promotes the metastasis of gastric carcinoma cells by modulating signal transduction pathways that regulate cell proliferation, motility, and invasion. Astaxanthin (ASTX), a xanthophyll carotenoid, is known to inhibit cancer cell migration and invasion, however the mechanism of action of ASTX in H. pylori-infected gastric epithelial cells is not well understood. To gain insight into this process, we carried out a comparative RNA sequencing (RNA-Seq) analysis of human gastric cancer AGS (adenocarcinoma gastric) cells as a function of H. pylori infection and ASTX administration. The results were used to identify genes that are differently expressed in response to H. pylori and ASTX. Gene ontology (GO) analysis identified differentially expressed genes (DEGs) to be associated with cell cytoskeleton remodeling, motility, and/or migration. Among the 20 genes identified, those encoding c-MET, PI3KC2, PLCγ1, Cdc42, and ROCK1 were selected for verification by real-time PCR analysis. The verified genes were mapped, using signaling networks contained in the KEGG database, to create a signaling pathway through which ASTX might mitigate the effects of H. pylori-infection. We propose that H. pylori-induced upregulation of the upstream regulator c-MET, and hence, its downstream targets Cdc42 and ROCK1, is suppressed by ASTX. ASTX is also suggested to counteract H. pylori-induced activation of PI3K and PLCγ. In conclusion, ASTX can suppress H. pylori-induced gastric cancer progression by inhibiting cytoskeleton reorganization and reducing cell motility through downregulation of c-MET, EGFR, PI3KC2, PLCγ1, Cdc42, and ROCK1.

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