A case of Helicobacter pylori-negative early gastric adenocarcinoma with gastrointestinal phenotype

AbstractA 40-year-old man with slightly depressed (0-IIc) type gastric cancer of the pyloric anterior gastric area underwent pre-operative screening for tetralogy of Fallot and endoscopic submucosal dissection (ESD) and was tested for Helicobacter pylori antigens and antibodies. Both tests were negative. He did not have a history of eradication. Pathological diagnosis of ESD showed a well-differentiated adenocarcinoma. The tumor was CD10-positive, MUC5AC-negative, and MUC6-confocal positive; it showed differentiation with gastrointestinal phenotype. Moreover, the tumor cells were lysozyme-positive, resembling Paneth cells. Mucosal glands exhibited intestinal metaplasia on the anal side of the tumor lesion. On the oral side of the tumor, metaplasia was non-existent, with normal pyloric glands present in the mucosal layer. The patient was not infected with H. pylori; however, intestinal metaplasia existed around the early gastric cancer. This suggested that the intestinal metaplasia occurred due to bile reflux, and the gastric neoplasia arose with the metaplasia without an H. pylori infection. This case may potentially help explain gastric cancer development in the absence of H. pylori infection.

Download Full-text

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

Canadian Journal of Gastroenterology ◽

10.1155/2005/732369 ◽

2005 ◽

Vol 19 (7) ◽

pp. 409-411 ◽

Cited By ~ 41

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.

Download Full-text

Association of family history of gastric cancer, intestinal metaplasia and high gastric juice ammonia in patients with Helicobacter pylori infection

Gastroenterology ◽

10.1016/s0016-5085(00)80697-6 ◽

2000 ◽

Vol 118 (4) ◽

pp. A1216

Author(s):

Premysl Bercik ◽

Elena F. Verdu ◽

Marek Ferkl ◽

Manfred Stolte ◽

Yoshio Wakatsuki ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Family History ◽

Intestinal Metaplasia ◽

Gastric Juice ◽

Helicobacter Pylori Infection ◽

History Of

Download Full-text

Clinical Recommendations of Russian Gastroenterological Association and RENDO Endoscopic Society on Diagnosis and Treatment of Gastritis and Duodenitis

Russian Journal of Gastroenterology Hepatology Coloproctology ◽

10.22416/1382-4376-2021-31-4-70-99 ◽

2021 ◽

Vol 31 (4) ◽

pp. 70-99

Author(s):

V. T. Ivashkin ◽

I. V. Maev ◽

T. L. Lapina ◽

E. D. Fedorov ◽

A. A. Sheptulin ◽

...

Keyword(s):

Gastric Cancer ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Chronic Gastritis ◽

Eradication Therapy ◽

Targeted Biopsy ◽

High Quality ◽

Familial History ◽

History Of ◽

H Pylori

Aim. The clinical guidelines are intended to supplement specialty decision-making for improved aid quality in patients with gastritis and duodenitis though acknowledging the latest clinical evidence and principles of evidencebased medicine.Key points. Gastritis is an inflammatory disease of stomach mucosa, with a separate definition of acute and chronic gastritis. Chronic gastritis is a cohort of chronic diseases uniting a typical morphology of persistent inflammatory infiltration, impaired cellular renewal with emergent intestinal metaplasia, atrophy and epithelial dysplasia of gastric mucosa. Oesophagogastroduodenoscopy (OGDS) or high-resolution OGDS with magnified or non-magnified virtual chromoendoscopy, including targeted biopsy for atrophy and intestinal metaplasia grading and neoplasia detection, are recommended to verify gastritis and duodenitis, precancer states and/or gastric mucosal changes. All chronic gastritis patients positive for H. рylori should undergo eradication therapy as aetiological and subsidiary for gastric cancer prevention. Chronic gastritis patients with symptoms of dyspepsia (epigastric pain, burning and congestion, early satiety), also combined with functional dyspepsia, are recommended proton pump inhibitors, prokinetics, rebamipide and bismuth tripotassium dicitrate in symptomatic treatment. With focal restricted intestinal metaplasia, follow-up is not required in most cases, mainly when advanced atrophic gastritis is ruled out in high-quality endoscopy with biopsy. However, a familial history of gastric cancer, incomplete intestinal metaplasia and persistent H. pylori infection render endoscopy monitoring with chromoendoscopy and targeted biopsy desirable once in three years. Patients with advanced atrophic gastritis should have high-quality endoscopy every 3 years, and once in 1–2 years if complicated with a familial history of gastric cancer.Conclusion. The recommendations condense current knowledge on the aetiology and pathogenesis of gastritis and duodenitis, as well as laboratory and instrumental diagnostic techniques, main approaches to aetiological H. pylori eradication and treatment of dyspeptic states.

Download Full-text

Association of interleukin 12B rs3212227 polymorphism with gastric cancer, intestinal metaplasia, and helicobacter pylori infection

Genetika ◽

10.2298/gensr2001115o ◽

2020 ◽

Vol 52 (1) ◽

pp. 115-126

Author(s):

Seda Orenay-Boyacioglu ◽

Elmas Kasap ◽

Hakan Yuceyar ◽

Mehmet Korkmaz

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Intestinal Metaplasia ◽

Clinical Features ◽

Statistical Significance ◽

Study Groups ◽

Interleukin 12 ◽

Allelic Frequencies ◽

Increased Risk ◽

H Pylori

Interleukin 12 (IL-12) has a key function in promoting Th1 immune response in the gastrointestinal mucosa. Although cytokine gene polymorphisms are associated with increased risk of gastric cancer (GC), studies on different geographic regions and ethnic groups are not able to draw a consistent result. The current case-control study aims to find out an association between a functional IL-12B rs3212227 polymorphism and the susceptibility and clinical features of the study groups, which are GC, Helicobacter pylori-infected and H. pylori-uninfected intestinal metaplasia (IM). In this study, IL-12B rs3212227 polymorphism was genotyped in 35 GC cases, 25 H. pylori-infected IM patients, 25 H. pylori-uninfected IM patients, and 25 control subjects. PCR-RFLP analysis was performed to find out and compare the polymorphism profiles of case biopsies. There was statistical significance in genotype distributions and allelic frequencies in GC patients with proximal arrest in stomach (p=0.042). The rs3212227 genotypes and allelic frequencies were not correlated with any of the study groups (p>0.05). Other clinical features examined in the GC patients were also not correlated with the rs3212227 genotypes and allelic frequencies (p>0.05). Current findings suggest that IL-12B rs3212227 polymorphism may play a role in GC development.

Download Full-text

Prevalence of cagA, vacA, babA2 and iceA Genes in Helicobacter pylori Strains Isolated from Colombian Patients with Functional Dyspepsia

Polish Journal of Microbiology ◽

10.33073/pjm-2012-004 ◽

2012 ◽

Vol 61 (1) ◽

pp. 33-40 ◽

Cited By ~ 18

Author(s):

AZUCENA ARÉVALO-GALVIS ◽

ALBA A. TRESPALACIOS-RANGEL ◽

WILLIAM OTERO ◽

MARCELA M. MERCADO-REYES ◽

RAÚL A. POUTOU-PIÑALES

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Molecular Markers ◽

High Risk ◽

Functional Dyspepsia ◽

Allelic Variants ◽

High Prevalence ◽

History Of ◽

H Pylori ◽

New Evidence

The clinical outcome of Helicobacter pylori infection has been particularly associated with virulence genotypes. These genotypes are useful as molecular markers in the identification of patients that are infected and at high risk for developing more severe gastric pathologies. Our main objective was to determine the prevalence of virulence genotypes cagA, vacA, iceA and babA2 of H. pylori, in patients with functional dyspepsia who are infected with the bacteria. H. pylori genotypes babA2 and cagA as well as vacA and iceA allelic variants were identified by PCR in 122 isolates resulting from 79 patients with functional dyspepsia. A high prevalence of genes cagA+ (71%), vacAs1am1 (34%), babA2 (57%) and iceA1 (87%) was found. The most frequent combined genotype found were cagA+/vacAs1am1/babA2+/iceA1 and cagA-/vacAs1am1/babA2+/iceA1, regardless of any family history of gastric cancer or MALT lymphoma. The very virulent genotype cagA+/vacAs1am1/babA2+/iceA1 prevailed in the studied patients with functional dyspepsia. Our results provide information about the prevalence of four of the more important virulent factors and constitute new evidence on the prevalence of the most virulent H. pylori genotype in patients with functional dyspepsia.

Download Full-text

Screening and eradication of Helicobacter pylori for gastric cancer prevention: the Taipei global consensus

Gut ◽

10.1136/gutjnl-2020-322368 ◽

2020 ◽

Vol 69 (12) ◽

pp. 2093-2112 ◽

Cited By ~ 1

Author(s):

Jyh-Ming Liou ◽

Peter Malfertheiner ◽

Yi-Chia Lee ◽

Bor-Shyang Sheu ◽

Kentaro Sugano ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Intestinal Metaplasia ◽

Eradication Therapy ◽

Population Level ◽

Cost Effective ◽

Current Evidence ◽

Global Consensus ◽

Vulnerable Subjects ◽

H Pylori

ObjectiveA global consensus meeting was held to review current evidence and knowledge gaps and propose collaborative studies on population-wide screening and eradication of Helicobacter pylori for prevention of gastric cancer (GC).Methods28 experts from 11 countries reviewed the evidence and modified the statements using the Delphi method, with consensus level predefined as ≥80% of agreement on each statement. The Grading of Recommendation Assessment, Development and Evaluation (GRADE) approach was followed.ResultsConsensus was reached in 26 statements. At an individual level, eradication of H. pylori reduces the risk of GC in asymptomatic subjects and is recommended unless there are competing considerations. In cohorts of vulnerable subjects (eg, first-degree relatives of patients with GC), a screen-and-treat strategy is also beneficial. H. pylori eradication in patients with early GC after curative endoscopic resection reduces the risk of metachronous cancer and calls for a re-examination on the hypothesis of ‘the point of no return’. At the general population level, the strategy of screen-and-treat for H. pylori infection is most cost-effective in young adults in regions with a high incidence of GC and is recommended preferably before the development of atrophic gastritis and intestinal metaplasia. However, such a strategy may still be effective in people aged over 50, and may be integrated or included into national healthcare priorities, such as colorectal cancer screening programmes, to optimise the resources. Reliable locally effective regimens based on the principles of antibiotic stewardship are recommended. Subjects at higher risk of GC, such as those with advanced gastric atrophy or intestinal metaplasia, should receive surveillance endoscopy after eradication of H. pylori.ConclusionEvidence supports the proposal that eradication therapy should be offered to all individuals infected with H. pylori. Vulnerable subjects should be tested, and treated if the test is positive. Mass screening and eradication of H. pylori should be considered in populations at higher risk of GC.

Download Full-text

CLINICAL, ENDOSCOPIC AND PATHOLOGICAL RESPONSES AFTER ERADICATION WITH RACM REGIMEN IN PATIENTS OF HELICOBACTER PYLORI-RELATED CHRONIC GASTRITIS

Journal of Medicine and Pharmacy ◽

10.34071/jmp.2016.2.2 ◽

2016 ◽

pp. 12-19

Author(s):

Thi Hoai Thai ◽

Van Huy Tran

Keyword(s):

Helicobacter Pylori ◽

Intestinal Metaplasia ◽

Chronic Gastritis ◽

Clinical Symptoms ◽

Epigastric Pain ◽

Bile Reflux ◽

Helicobacter Pylori Eradication ◽

Significant Change ◽

H Pylori ◽

Active Inflammation

Background: The clinical, endoscopic and histopathological responses after Helicobacter pylori eradication in patients of chronic gastritis were still inconstant. This study is aimed at: (1) evaluating of clinical variations, endoscopic images six months after Helicobacter pylori eradication by Rabeprazole-Amoxicillin—Metronidazole-Clarithromycin therapy for 14 days. (2) assessing histopathological response six months after H. pylori eradication. Method: prospective, consisting of 83 patients examined and treated in Danang hospital from 4/2014 to 6/2015. Results: There were improvements in clinical symptoms 6 months after H. pylori eradication: epigastric pain 85.5% vs. 7.2%); bloating (97.1% vs. 4.3%); indigestion (47.8% vs. 2.9%); weight loss (17.4% vs. 1.4%); anorexia (23.2% vs. 2.9%) (p< 0.01). However, there were no improvement regarding common lesions on endoscopy, edema (33.3% increase to 71%); flat erosion and elevated erosion (15.9% vs. 8.7%); atrophy (7.2%); haemorrhagic (5.8% vs. 0%); hypertrophic (7.2% vs. 0%); bile reflux (14.5% vs. 4.3%). Regarding histopathology: active inflammation accounted for a high proportion (63.8% vs. 27.5%); non-active inflammation (36.2% increase to 72.5%); atrophy (8.7% vs. 5.8%); dysplasia (26.1% vs. 1.4%), no significant change in intestinal metaplasia was found after treatment. Conclusions: There was an improvement in clinical symptoms and histopathological against inflammatory activity grade, dysplasia at the time before and after 6 months treatment H. pylori eradication. However, no significant change in mucosal atrophy and intestinal metaplasia was found. Key words: chronic gastritis; H. pylori; clinical, endoscopic and pathological responses

Download Full-text

Long-term persistence of gastric dysbiosis after eradication of Helicobacter pylori in patients who underwent endoscopic submucosal dissection for early gastric cancer

Gastric Cancer ◽

10.1007/s10120-020-01141-w ◽

2020 ◽

Author(s):

Toshio Watanabe ◽

Yuji Nadatani ◽

Wataru Suda ◽

Akira Higashimori ◽

Koji Otani ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Endoscopic Submucosal Dissection ◽

Eradication Therapy ◽

Bacterial Composition ◽

Submucosal Dissection ◽

History Of ◽

H Pylori

Abstract Background Gastric microbiome, other than Helicobacter pylori, plays a role in the tumorigenesis of gastric cancer (GC). Patients who undergo endoscopic submucosal dissection for early GC have a high risk of developing metachronous GC even after successful eradication of H. pylori. Thus, we investigated the microbial profiles and associated changes in such patients after the eradication of H. pylori. Methods A total of 19 H. pylori-infected patients with early GC who were or to be treated by endoscopic resection, with paired biopsy samples at pre- and post-eradication therapy, were retrospectively enrolled. Ten H. pylori-negative patients were enrolled as controls. Biopsy samples were analyzed using 16S rRNA sequencing. Results H. pylori-positive patients exhibited low richness and evenness of bacteria with the deletion of several genera, including Blautia, Ralstonia, Faecalibacterium, Methylobacterium, and Megamonas. H. pylori eradication partially restored microbial diversity, as assessed during a median follow-up at 13 months after eradication therapy. However, post-eradication patients had less diversity than that in the controls and possessed a lower abundance of the five genera mentioned above. The eradication of H. pylori also altered the bacterial composition, but not to the same extent as that in controls. The microbial communities could be clustered into three separate groups: H. pylori-negative, pre-eradication, and post-eradication. Conclusion Changes in dysbiosis may persist long after the eradication of H. pylori in patients with a history of GC. Dysbiosis may be involved in the development of both primary and metachronous GC after the eradication of H. pylori in such patients.

Download Full-text

Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis

BioMed Research International ◽

10.1155/2015/737621 ◽

2015 ◽

Vol 2015 ◽

pp. 1-9 ◽

Cited By ~ 18

Author(s):

Soichiro Sue ◽

Wataru Shibata ◽

Shin Maeda

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Signaling Pathways ◽

Intracellular Signaling ◽

Gastric Carcinogenesis ◽

Dependent Manner ◽

Intracellular Signaling Pathways ◽

H Pylori

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.

Download Full-text

Changes in Gastric Microbial Composition before and after Helicobacter pylori Eradication Therapy

The Korean Journal of Helicobacter and Upper Gastrointestinal Research ◽

10.7704/kjhugr.2020.0028 ◽

2020 ◽

Vol 20 (3) ◽

pp. 177-186

Author(s):

Chan Hyuk Park

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Microbial Diversity ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Diversity Index ◽

Eradication Therapy ◽

Cancer Development ◽

Microbial Composition ◽

H Pylori

Owing to advancements in next-generation sequencing and non-culture-based microbial research techniques, we have recognized that many bacterial taxa other than Helicobacter pylori (H. pylori) are present in the human stomach. Gastric microbial composition depends on gastric diseases, including gastritis, atrophic gastritis, intestinal metaplasia, and gastric cancer. Although H. pylori 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 H. pylori eradication, many investigators have studied the changes in the microbial composition in the stomach after H. pylori eradication. The gastric microbiome in patients with H. pylori infection typically shows abundance of H. pylori and a low microbial diversity index. If we treat H. pylori-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 H. pylori infection could be restored by H. pylori eradication therapy; however, there have been inconsistent findings of the abundant bacterial taxa after H. pylori 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 H. pylori eradication according to the severity of gastric inflammation.

Download Full-text