Helicobacter Pylori Infection in Endoscopic Biopsy Specimens of Gastric Cancer: A Preliminary Evaluation in a High Risk Population of Kashmir Valley

Objective: The aim of the present study was to assess the prevalence of Helicobacter pylori (H. pylori) infection in Kashmiri patients with gastric cancer and to compare this with a matched control population.Methods: Fifty patients with gastric cancer and thirty age/sex matched controls were included in the study. All the subjects were hailing from Kashmir Valley. For detection of H. pylori, biopsy specimens were used both from cases and controls.Results: An insignificant association was shown between H. pylori and both intestinal and diffuse type of gastric cancer.Conclusions: The data provides support against the significant association between H. pylori and gastric cancer in this part of world, a place where the age standardized incidence of gastric cancer is alarmingly high. We conclude that other factors like personal and special dietary habits of Kashmiri population may be more important for the development of gastric cancer.

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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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Use of a Novel Enzyme Immunoassay Based on Detection of Circulating Antigen in Serum for Diagnosis of Helicobacter pylori Infection

Clinical and Diagnostic Laboratory Immunology ◽

10.1128/cdli.11.4.775-779.2004 ◽

2004 ◽

Vol 11 (4) ◽

pp. 775-779 ◽

Cited By ~ 5

Author(s):

Abdelfattah M. Attallah ◽

Hisham Ismail ◽

Gellan G. Ibrahim ◽

Mohamed Abdel-Raouf ◽

Ahmed M. El-Waseef ◽

...

Keyword(s):

Helicobacter Pylori ◽

Endoscopic Biopsy ◽

Enzyme Linked Immunosorbent Assay ◽

Target Antigen ◽

Serum Samples ◽

Predictive Values ◽

Biopsy Specimens ◽

Significant Difference ◽

Circulating Antigen ◽

H Pylori

ABSTRACT Recently, noninvasive diagnostic tests for Helicobacter pylori infection have gained in significance. We have developed a sensitive and specific noninvasive immunoassay based on the detection of an H. pylori circulating antigen (HpCA) in sera from H. pylori-infected individuals. Monospecific antibody and Western blot analyses were used to demonstrate the presence of the target antigen in H. pylori cell lysate and serum samples. A novel enzyme-linked immunosorbent assay (ELISA) was developed for the detection of HpCA in serum. Endoscopic biopsy specimens from the gastric antra of 221 individuals (143 males and 78 females) with dyspeptic symptoms were evaluated for H. pylori infection, with culture used as a “gold standard” for diagnosis. The target H. pylori antigen was identified at 58 kDa. HpCA has been detected by ELISA with high degrees of sensitivity, specificity, and efficiency (>90%), and ELISA results show no significant difference (P > 0.05) from results of H. pylori culture of gastric biopsy specimens. The test's positive and negative predictive values were also high (95 and 86%, respectively). In conclusion, a sensitive and specific immunoassay was developed for the detection of HpCA in human serum. This test can be applied for noninvasive laboratory and field diagnoses of H. pylori infection.

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Helicobacter pylori infection in patients with early gastric cancer by the endoscopic phenol red test

Gut ◽

10.1136/gut.42.1.20 ◽

1998 ◽

Vol 42 (1) ◽

pp. 20-23 ◽

Cited By ~ 15

Author(s):

K Iseki ◽

M Tatsuta ◽

H Iishi ◽

M Baba ◽

S Ishiguro

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Early Gastric Cancer ◽

Phenol Red ◽

Ph Indicator ◽

Strong Risk Factor ◽

Biopsy Specimens ◽

Undifferentiated Adenocarcinoma ◽

H Pylori

Background—An endoscopic procedure that uses a pH indicator called phenol red to assess Helicobacter pyloriinfected gastric mucosa has recently been developed. This test makes it possible to take biopsy specimens from H pylori infected areas.Aim—This test was applied to patients with early gastric cancers to clarify the role of H pylori in gastric carcinogenesis.Subjects—Sixty five patients with early gastric cancer (50 with differentiated adenocarcinoma and 15 with undifferentiated adenocarcinoma).Methods—Patients with early gastric cancer underwent the endoscopic phenol red test before their operation. In this test, areas infected with H pylori can be observed as “coloured” areas where phenol red was turned from yellow to red.Results—H pylori infection was significantly (p<0.001) more frequent in patients with differentiated adenocarcinomas than in those with undifferentiated adenocarcinomas. Differentiated adenocarcinomas were usually located in areas of mucosa infected with H pylori, but undifferentiated adenocarcinomas were frequently located in non-infected areas.Conclusion—H pylori may be a strong risk factor for differentiated early gastric cancer.

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Helicobacter pylori-Induced Inflammation: Possible Factors Modulating the Risk of Gastric Cancer

Pathogens ◽

10.3390/pathogens10091099 ◽

2021 ◽

Vol 10 (9) ◽

pp. 1099

Author(s):

Sushil Kumar ◽

Girijesh Kumar Patel ◽

Uday C. Ghoshal

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Gut Microbiota ◽

Dietary Habits ◽

Tissue Injury ◽

Precancerous Lesions ◽

Gastric Carcinogenesis ◽

Future Research ◽

Intestinal Helminths ◽

H Pylori

Chronic inflammation and long-term tissue injury are related to many malignancies, including gastric cancer (GC). Helicobacter pylori (H. pylori), classified as a class I carcinogen, induces chronic superficial gastritis followed by gastric carcinogenesis. Despite a high prevalence of H. pylori infection, only about 1–3% of people infected with this bacterium develop GC worldwide. Furthermore, the development of chronic gastritis in some, but not all, H. pylori-infected subjects remains unexplained. These conflicting findings indicate that clinical outcomes of aggressive inflammation (atrophic gastritis) to gastric carcinogenesis are influenced by several other factors (in addition to H. pylori infection), such as gut microbiota, co-existence of intestinal helminths, dietary habits, and host genetic factors. This review has five goals: (1) to assess our current understanding of the process of H. pylori-triggered inflammation and gastric precursor lesions; (2) to present a hypothesis on risk modulation by the gut microbiota and infestation with intestinal helminths; (3) to identify the dietary behavior of the people at risk of GC; (4) to check the inflammation-related genetic polymorphisms and role of exosomes together with other factors as initiators of precancerous lesions and gastric carcinoma; and (5) finally, to conclude and suggest a new direction for future research.

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Helicobacter pylori Infection in Endoscopic Biopsy Specimens of Gastric Antrum: Laboratory Diagnosis and Comparative Efficacy of Three Diagnostic Tests

Diagnostic and Therapeutic Endoscopy ◽

10.1155/dte.6.25 ◽

1999 ◽

Vol 6 (1) ◽

pp. 25-29 ◽

Cited By ~ 2

Author(s):

G. M. Malik ◽

M. Mubarik ◽

S. A. Kadla

Keyword(s):

Helicobacter Pylori ◽

Diagnostic Yield ◽

Low Cost ◽

Endoscopic Biopsy ◽

Histopathological Analysis ◽

Test Procedures ◽

Biopsy Material ◽

Biopsy Specimens ◽

Urease Test ◽

H Pylori

Aims and objectives The present study was undertaken to compare the diagnostic yield of three available test procedures for detecting Helicobacter pylori (H. pylori) infection in endoscopic biopsies.Methods H. pylori infection was sought in 150 patients referred for upper gastrointestinal (GI) endoscopy. Multiple (about six) biopsy specimens were taken from pyloric antrum in each patient. Two biopsy specimens were subjected to one minute endoscopy room test – OMERT (a modified form of urease test), two were sent for histopathological analysis, where multiple sections were subjected to Giemsa staining and two were sent for microbiological evaluation after Gram's staining of heat fixed biopsy material.Results H. pylori positivity using histology, microbiology and OMERT was observed to be 33%, 30% and 27% respectively. However, overall 40% patients were infected when the results from three test procedures were combined, as H. pylori positivity was repeated more than once by these procedures separately. Histology was found to be superior to other two tests in our study, especially when multiple sections were examined, for the distribution of the organism was patchy. Amongst the infected, H. pylori was seen in only 30% of all 3–8 sections cut from a biopsy, whereas in 70% it was noted in a single section only.Conclusion The study revealed that histology has the highest detection rate and can be chosen as the “gold standard” amongst the three low cost test procedures available at present in our setup.

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

Biomedical Research and Therapy ◽

10.15419/bmrat.v4is.256 ◽

2017 ◽

Vol 4 (S) ◽

pp. 46

Author(s):

Truong Xuan Bui

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

High Risk Group ◽

Gastric Biopsy ◽

Biopsy Specimens ◽

Urease Test ◽

Sydney System ◽

H Pylori

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.

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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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The correlation between lncRNAs and Helicobacter pylori in gastric cancer

Pathogens and Disease ◽

10.1093/femspd/ftaa004 ◽

2019 ◽

Vol 77 (9) ◽

Author(s):

Narges Dastmalchi ◽

Seyed Mahdi Banan Khojasteh ◽

Mirsaed Miri Nargesi ◽

Reza Safaralizadeh

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Molecular Mechanisms ◽

Gastrointestinal Diseases ◽

Mechanisms Of Action ◽

Molecular Pathways ◽

Gastric Diseases ◽

Non Coding Rnas ◽

H Pylori ◽

The Relationship

ABSTRACT Helicobacter pylori infection performs a key role in gastric tumorigenesis. Long non-coding RNAs (lncRNAs) have demonstrated a great potential to be regarded as effective malignancy biomarkers for various gastrointestinal diseases including gastric cancer (GC). The present review highlights the relationship between lncRNAs and H. pylori in GC. Several studies have examined not only the involvement of lncRNAs in H. pylori-associated GC progression but also their molecular mechanisms of action. Among the pertinent studies, some have addressed the effects of H. pylori infection on modulatory networks of lncRNAs, while others have evaluated the effects of changes in the expression level of lncRNAs in H. pylori-associated gastric diseases, especially GC. The relationship between lncRNAs and H. pylori was found to be modulated by various molecular pathways.

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Helicobacter pylori Outer Membrane Vesicles and Extracellular Vesicles from Helicobacter pylori-Infected Cells in Gastric Disease Development

International Journal of Molecular Sciences ◽

10.3390/ijms22094823 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4823

Author(s):

María Fernanda González ◽

Paula Díaz ◽

Alejandra Sandoval-Bórquez ◽

Daniela Herrera ◽

Andrew F. G. Quest

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Outer Membrane ◽

Extracellular Vesicles ◽

Membrane Vesicles ◽

Outer Membrane Vesicles ◽

Host Cells ◽

Gastric Epithelium ◽

Infected Cells ◽

H Pylori

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.

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Role of TNF-α-Inducing Protein Secreted by Helicobacter pylori as a Tumor Promoter in Gastric Cancer and Emerging Preventive Strategies

Toxins ◽

10.3390/toxins13030181 ◽

2021 ◽

Vol 13 (3) ◽

pp. 181

Author(s):

Masami Suganuma ◽

Tatsuro Watanabe ◽

Eisaburo Sueoka ◽

In Kyoung Lim ◽

Hirota Fujiki

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Cell Surface Receptor ◽

Tumor Promoter ◽

Cancer Development ◽

Human Gastric Cancer ◽

Tnf Α ◽

Surface Receptor ◽

H Pylori ◽

Factor Α

The tumor necrosis factor-α (TNF-α)-inducing protein (tipα) gene family, comprising Helicobacter pylori membrane protein 1 (hp-mp1) and tipα, has been identified as a tumor promoter, contributing to H. pylori carcinogenicity. Tipα is a unique H. pylori protein with no similarity to other pathogenicity factors, CagA, VacA, and urease. American H. pylori strains cause human gastric cancer, whereas African strains cause gastritis. The presence of Tipα in American and Euro-Asian strains suggests its involvement in human gastric cancer development. Tipα secreted from H. pylori stimulates gastric cancer development by inducing TNF-α, an endogenous tumor promoter, through its interaction with nucleolin, a Tipα receptor. This review covers the following topics: tumor-promoting activity of the Tipα family members HP-MP1 and Tipα, the mechanism underlying this activity of Tipα via binding to the cell-surface receptor, nucleolin, the crystal structure of rdel-Tipα and N-terminal truncated rTipα, inhibition of Tipα-associated gastric carcinogenesis by tumor suppressor B-cell translocation gene 2 (BTG2/TIS21), and new strategies to prevent and treat gastric cancer. Thus, Tipα contributes to the carcinogenicity of H. pylori by a mechanism that differs from those of CagA and VacA.

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