Determine the Prevalence of cagA and Baba of Helicobacter Pylori Isolated from Gastric Atrophic Patients

2021 ◽  
Vol 15 (6) ◽  
pp. 1620-1622
Author(s):  
Muhammad Nazir ◽  
Talal Safdar ◽  
Mushtaq Ahmad ◽  
Muhammad Ikram ◽  
Nisar Khan Sajid ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Atrophy ◽  
P Value ◽  
Caga Gene ◽  
Medical Sciences ◽  
Acute Gastritis ◽  
H Pylori ◽  
Standard Techniques ◽  
Gastroduodenal Disorders

Objective: The aim of this study is to determine the prevalence of cagA and babA of helicobacter pylori isolated from gastric atrophic patients. Study Design: Descriptive/Analytical Place and Duration: The study was conducted at Medicine/Gastroenterology department of Khyber Teaching Hospital and Peshawar Institute of Medical Sciences, Peshawar for six months duration from March 2020 to August 2020. Methods: Total one hundred and twenty patients of both genders were presented in this study. Patients were aged between 20-80 years of age. Patients detailed demographics age, sex and body mass index were recorded after taking informed written consent. All patients of gastroduodenal disorders were undergone for isolation of bacteria by using standard techniques. Complete data was analyzed by SPSS 22.0 version. Results: Total 50 (41.7%) patients were males and 70 (58.3%) patients were females. Mean age of the patients were 41.96 ± 16 years with mean BMI 25.24 ± 4.8 kg/m2. Frequency of H pylori was isolated in 30 (25%) patients in which 13 patients had atrophic gastritis, 9 patients had gastric ulcer and 8 patients had acute gastritis. Prevalence of cagA gene was 16 (53.33%) and babA was 10 (33.33%) in H. pylori isolated patients. Significantly difference with p value <0.05 was observed between cagA positive strains and patients of gastric atrophic. The involvement of gastric atrophic patients was not correlated to the babA gene. Conclusion: We concluded in this study that different cagA positive H. pylori can be retrieved from gastric atrophy patients. Keywords: Gastric atrophy, Gastric cancer, cagA, babA, Helicobacter pylori

scholarly journals Epstein–Barr Virus and Helicobacter Pylori Co-Infection in Non-Malignant Gastroduodenal Disorders

Pathogens ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 104 ◽  
Author(s):  
Ramsés Dávila-Collado ◽  
Oscar Jarquín-Durán ◽  
Le Thanh Dong ◽  
J. Luis Espinoza
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Infection Rate ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Ebv Infection ◽  
Pubmed Database ◽  
Epstein Barr ◽  
H Pylori ◽  
Gastroduodenal Disorders

Epstein–Barr virus (EBV) and Helicobacter pylori (H. pylori) are two pathogens associated with the development of various human cancers. The coexistence of both microorganisms in gastric cancer specimens has been increasingly reported, suggesting that crosstalk of both pathogens may be implicated in the carcinogenesis process. Considering that chronic inflammation is an initial step in the development of several cancers, including gastric cancer, we conducted a systematic review to comprehensively evaluate publications in which EBV and H. pylori co-infection has been documented in patients with non-malignant gastroduodenal disorders (NMGDs), including gastritis, peptic ulcer disease (PUD), and dyspepsia. We searched the PubMed database up to August 2019, as well as publication references and, among the nine studies that met the inclusion criteria, we identified six studies assessing EBV infection directly in gastric tissues (total 949 patients) and three studies in which EBV infection status was determined by serological methods (total 662 patients). Due to the substantial methodological and clinical heterogeneity among studies identified, we could not conduct a meta-analysis. The overall prevalence of EBV + H. pylori co-infection in NMGDs was 34% (range 1.8% to 60%). A higher co-infection rate (EBV + H. pylori) was reported in studies in which EBV was documented by serological methods in comparison with studies in which EBV infection was directly assessed in gastric specimens. The majority of these studies were conducted in Latin-America and India, with most of them comparing NMGDs with gastric cancer, but there were no studies comparing the co-infection rate in NMGDs with that in asymptomatic individuals. In comparison with gastritis caused by only one of these pathogens, EBV + H. pylori co-infection was associated with increased severity of gastric inflammation. In conclusion, only relatively small studies testing EBV and H. pylori co-infection in NMGDs have been published to date and the variable report results are likely influenced by geographic factors and detection methods.

DETERMINATION OF HELICOBACTER PYLORI CAGA GENE AND VACA GENOTYPES IN PATIENTS WITH GASTRIC CANCER

2013 ◽  
pp. 118-125
Author(s):  
Quy Hung Le ◽  
Thi Minh Thi Ha
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Signet Ring Cell ◽  
Tubular Adenocarcinoma ◽  
Negative Group ◽  
Caga Gene ◽  
Positive Group ◽  
Histopathological Classification ◽  
Vaca Gene ◽  
H Pylori

Background: H. pylori is the first cause of gastric cancer (GC). However, the role of cagA gene and vacA gene in GC is still controversial. This study is aimed at determining the rates of H. pylori infection, cagA gene, vacA genotypes in patients with GC; and evaluating the relationship between cagA gene, vacA genotypes and endoscopic and histopathological features of gastric cancer. Patients and methods: Fifty eight GC patients and one hundred and sixteen non-GC patients (controls) were enrolled. Infection of H. pylori was determined by PCR. cagA gene and vacA genotypes were determined by Multiplex PCR. Results: The rate of H. pylori was found in 55.2% in GC group. The rate of cagA gene and vacA gene in GC patients H. pylori positive were found in 78.1% and 100%, respectively. vac A genotypes s1/m1, s1/m2 and s1/m1m2 were found in 34.4%; 50% and 15.6%, respectively. The risk of GC of cagA positive group was higher than cagA negative group, with OR = 4,5; 95%CI = 1.6-12.2. The risk of GC of vacA s1/m1, cagA positive group was higher than vacA s1/m1, cagA negative group, OR = 7.1; 95%CI = 1.4-36. A statistically significative difference of rate of cagA positive was found between Borrmann III/IV group (100%) and Borrmann I/II group (46.2%). A statistically significative difference of rate of cagA positive was found between the tubular adenocarcinoma group (100%) and signet-ring cell carcinoma (44.4%, p = 0,002), and mucinous adenocarcinoma (50%, p =0,024). Conclusion: Gene cagA and vacA s1/m1 genotype were both risk factors in GC. A significative differences of rate of cagA positive were found between Borrmann groups, and between groups of WHO histopathological classification. Key words: cagA gene and vacA genotype, Helicobacter pylori, gastric cancer

Amplification of 3′ repeat sequences in the Helicobacter pylori CagA gene is associated with gastric atrophy and gastric cancer

1998 ◽  
Vol 114 ◽  
pp. A707
Author(s):  
Y. Yamaoka ◽  
T. Kodama ◽  
K. Kashima ◽  
D.Y. Graham ◽  
A.R. Sepulveda
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Atrophy ◽  
Caga Gene ◽  
Repeat Sequences

scholarly journals Rejuvenation of Helicobacter pylori–Associated Atrophic Gastritis Through Concerted Actions of Placenta-Derived Mesenchymal Stem Cells Prevented Gastric Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Jong Min Park ◽  
Young Min Han ◽  
Ki Baik Hahm
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Helicobacter Pylori ◽  
Mesenchymal Stem Cells ◽  
Atrophic Gastritis ◽  
Conditioned Medium ◽  
Gastric Atrophy ◽  
Control Group ◽  
Therapeutic Effects ◽  
H Pylori

Chronic Helicobacter pylori infection causes gastric cancer via the progression of precancerous chronic atrophic gastritis (CAG). Therefore, repairing gastric atrophy could be a useful strategy in preventing H. pylori–associated gastric carcinogenesis. Although eradication of the bacterial pathogen offers one solution to this association, this study was designed to evaluate an alternative approach using mesenchymal stem cells to treat CAG and prevent carcinogenesis. Here, we used human placenta-derived mesenchymal stem cells (PD-MSCs) and their conditioned medium (CM) to treat H. pylori–associated CAG in a mice/cell model to explore their therapeutic effects and elucidate their molecular mechanisms. We compared the changes in the fecal microbiomes in response to PD-MSC treatments, and chronic H. pylori–infected mice were given ten treatments with PD-MSCs before being sacrificed for end point assays at around 36 weeks of age. These animals presented with significant reductions in the mean body weights of the control group, which were eradicated following PD-MSC treatment (p &lt; 0.01). Significant changes in various pathological parameters including inflammation, gastric atrophy, erosions/ulcers, and dysplastic changes were noted in the control group (p &lt; 0.01), but these were all significantly reduced in the PD-MSC/CM-treated groups. Lgr5+, Ki-67, H+/K+-ATPase, and Musashi-1 expressions were all significantly increased in the treated animals, while inflammatory mediators, MMP, and apoptotic executors were significantly decreased in the PD-MSC group compared to the control group (p &lt; 0.001). Our model showed that H. pylori–initiated, high-salt diet–promoted gastric atrophic gastritis resulted in significant changes in the fecal microbiome at the phylum/genus level and that PD-MSC/CM interventions facilitated a return to more normal microbial communities. In conclusion, administration of PD-MSCs or their conditioned medium may present a novel rejuvenating agent in preventing the progression of H. pylori–associated premalignant lesions.

scholarly journals Estimation of the degree of gastric mucosal atrophy based on serum pepsinogen levels after eradication of Helicobacter pylori

2020 ◽  
Author(s):  
Takahiro Suzuki ◽  
Tomohiro Higuchi ◽  
Takuma Kagami ◽  
Mihoko Yamade ◽  
Shinya Tani ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Serum Levels ◽  
Gastric Atrophy ◽  
Mucosal Inflammation ◽  
Serum Pepsinogen ◽  
Mucosal Atrophy ◽  
Gastric Mucosal Atrophy ◽  
H Pylori

Abstract Background Serum pepsinogen (PG) levels correlate with the degree of gastric mucosal inflammation and atrophy, which correlate with gastric cancer risk, in patients infected with Helicobacter pylori (H. pylori). Serum PG levels change after eradication of H. pylori, but it is not known if there are corresponding changes in the gastric mucosa. We examined whether the degree of gastric atrophy correlated with PG levels measured after eradication of H. pylori. Methods We retrospectively examined the relationship between gastric atrophy and serum levels of PG I, PG II and PG I/II ratios measured after eradication of H. pylori. The degree of gastric mucosal atrophy before H. pylori eradication was scored (0, 1, 2) according to the Kyoto classification of gastritis. Results A total of 430 treated patients were enrolled. Serum levels of PG I (ρ = − 0.362 and P < 0.001), PG II (ρ = − 0.158 and P = 0.001) and PG I/II ratio (ρ = − 0.337 and P < 0.001) all correlated negatively with atrophy scores. When PG I/II was less than 3.4, 5.4 or 6.7, the probability of the open type of gastric atrophy was estimated to be 75%, 50%, or 25%, respectively. Conclusion Our results suggest that serum PG levels measured after H. pylori eradication can be used to estimate the degree of gastric mucosal atrophy and are useful for selecting individuals with a high risk of gastric cancer after H. pylori eradication.

scholarly journals Prevalence, diversity and disease association of Helicobacter pylori in dyspeptic patients from Pakistan

2013 ◽  
Vol 7 (03) ◽  
pp. 220-228 ◽  
Author(s):  
Adnan Khan ◽  
Amber Farooqui ◽  
Yasir Raza ◽  
Faisal Rasheed ◽  
Hamid Manzoor ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Disease Burden ◽  
Detection Rate ◽  
East Asian ◽  
Disease Association ◽  
Gastric Biopsy ◽  
Caga Gene ◽  
H Pylori ◽  
Type Strains

Introduction: The etiological association of Helicobacter pylori with gastric ulcer (GU), gastric cancer (GC), and duodenal ulcer (DU) is well-known. Understanding the epidemiology of H. pylori facilitates the estimation of disease burden in a certain population. This study presents the diversity of H. pylori genotypes and their association with different clinical outcomes among dyspeptic patients in Pakistan over a period of four years. Methodology: Gastric biopsy samples from a total of 450 dyspeptic individualswere subjected to PCR, genotypingand histology. Results: A total of 201 (45%) cases were found positive for H. pylori. The detection rate was high in GU (91%), DU (86%) and GC (83%) cases compared with those cases who had intact gastric mucosa (18%). Histology revealed the presence of infection in 68% of cases of mild/chronic nonspecific gastritis with others belonging to the GU sequel. cagA gene carriage was observed in 104 (51%) cases or mostly from DU, GU and GC groups, of which 97 were Western type strains while 3 were East-Asian type strains that are rarely observed in South Asia. vacA allelic variant s1am1 was most commonly observed, followed by s1am2, and s1bm1, with direct correlation in diseased cases (gastritis, GU, DU and GC). Prevalent genotypic combinations were s1am1/cagA- in gastritis and s1am1/cagA+ in DU, GU, and GC. Conclusions: Our study indicates the predominant circulation of Western type cagA and vacAs1am1 type H. pylori strains in Pakistan.

scholarly journals Risk of gastric cancer in the second decade of follow-up after Helicobacter pylori eradication

2019 ◽  
Vol 55 (3) ◽  
pp. 281-288 ◽  
Author(s):  
Susumu Take ◽  
Motowo Mizuno ◽  
Kuniharu Ishiki ◽  
Chiaki Kusumoto ◽  
Takayuki Imada ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Incidence Rate Ratio ◽  
Gastric Atrophy ◽  
Diffuse Type ◽  
Gastric Cancer Risk ◽  
Helicobacter Pylori Eradication ◽  
H Pylori ◽  
Diffuse Type Gastric Cancer

Abstract Background and aims Eradication of Helicobacter pylori reduces the risk of gastric cancer. In this study, we investigated the risk beyond 10 years after eradication of H. pylori. Methods We conducted a retrospective cohort study of 2737 patients who had yearly endoscopic follow-up after cure of H. pylori infection. For comparison of gastric cancer risk in the second decade of follow-up with that in the first decade, we calculated standardized incidence ratios (SIRs) by dividing the number of observed cases of gastric cancer in the second decade of follow-up by that of expected cases which was estimated using the incidence rate ratio of age in the first decade. Results During the follow-up for as long as 21.4 years (mean 7.1 years), gastric cancer developed in 68 patients (0.35% per year). The SIRs for diffuse-type gastric cancer was infinity (0 expected case and 4 observed cases) in patients with mild gastric mucosal atrophy and 10.9 (95% confidence interval 4.53–26.1) with moderate atrophy, whereas no significant increase of SIRs was observed in intestinal-type cancer regardless of the grade of baseline gastric atrophy or in diffuse-type cancer in patients with severe atrophy even though who had the highest risk. Conclusions The longer the follow-up, the greater the risk of developing diffuse-type gastric cancer becomes in patients with mild-to-moderate gastric atrophy at baseline. Endoscopic surveillance should be continued beyond 10 years after cure of H. pylori irrespective of the severity of gastric atrophy.

scholarly journals Lack of association between gastric cancer and hopQ alleles in Helicobacter pylori

Genetika ◽  
2016 ◽  
Vol 48 (3) ◽  
pp. 893-902 ◽  
Author(s):  
Elham Kazemi ◽  
Danial Kahrizi
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Acute Inflammation ◽  
Outer Membrane Proteins ◽  
Healthy Individuals ◽  
Specific Primers ◽  
Stomach Acid ◽  
H Pylori ◽  
Peripheral Cells ◽  
Gastroduodenal Disorders

Helicobacter pylori use a number of mechanisms to survive in the stomach lumen. The presence of these bacteria in the stomach can lead to gastritis and reduction in stomach acid production. Acute inflammation can directly damage to the peripheral cells that are responsible for the secretion of acid. The risk of developing gastric carcinoma is associated to heterogeneity of Helicobacter pylori virulence factors (such as cagA). The HopQ is one of the outer membrane proteins involved in bacterial adherence to gastric mucosa and has been suggested to also play a role in the virulence of H. pylori. This gene has been shown in two types. The purpose of the current study was to investigate the association between different H. pylori virulence hopQ alleles (types I and II) and patients with gastroduodenal disorders. For this purpose 58 stomach biopsies the of patients with gastric cancer and 100 saliva samples from healthy individuals were collected. Then genomic DNA was purified and PCR for was done for desired genes via specific primers. The H. pylori infections were diagnosed by PCR for GlmM gene. Then frequencies of hopQI+, hopQII+ and hopQI+ hopQII+ genotypes were determined in H. pylori infected cases. Statistical analysis showed that there were not significant differences between healthy and diseased ones for genotypes hopQI+, hopQII+ and hopQI+ hopQII+.

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

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.

Helicobacter Pylori Infection in Sjögren’s Syndrome: Co-incidence or Causality?

2019 ◽  
Vol 15 (3) ◽  
pp. 238-241
Author(s):  
Massoud Saghafi ◽  
Nafiseh Abdolahi ◽  
Reza Orang ◽  
Mohammad Reza Hatef ◽  
Mohammad Hadi Molseghi
Keyword(s):  
Helicobacter Pylori ◽  
Serum Level ◽  
Sjögren’S Syndrome ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Control Group ◽  
P Value ◽  
H Pylori ◽  
Sjögren‘S Syndrome

Background and Aim: Lymphoid cell infiltration and destruction of exocrine glands, specifically lacrimal and salivary glands are characteristics of Sjogren’s syndrome (SS). An etiological role has been proposed for Helicobacter pylori (H. pylori), interacting in the clinical course and complications of SS (including gastric cancer and lymphoma). The aim of this study was to identify the probable correlation between H. pylori infection and Sjogren’s syndrome (SS). Methods: In this case-control study, ELISA method was used to determine serum level of IgA and IgM anti H. pylori antibody in 43 subjects with SS according to the international criteria and 95 healthy subjects as control. SPSS-17 was used to analyze data with t-test. P value <.05 were considered significant. Results: Serum level of IgM (34.9% vs. 10.5%, p-value= 0.001) and IgA (67.4% vs. 46.3% p value= 0.021) anti H. pylori antibody were significantly higher in SS patients compared to the control group. There was a positive correlation between age and H. pylori infection (r=0.2, Pvalue= 0.05). Conclusion: Patients with SS had a higher prevalence of H. pylori infection compared to the normal population. Eradication of H. pylori is recommended particularly in older patients with SS.

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