Association of Helicobacter pylori vacA polymorphisms with the risk of gastric precancerous lesions in a Moroccan population

Introduction: Helicobacter pylori infection is the major risk factor of atrophic gastritis and intestinal metaplasia. The vacA gene is one of the most virulence factors of H. pylori and genetic diversity in its s, m, i, and d regions is associated with gastric lesions severity. This study aimed to investigate the association of vacA s, m, i, and d regions with the risk of atrophic gastritis and intestinal metaplasia in a Casablanca population. Methodology: A total of 210 patients suffering from gastric lesions (chronic gastritis, atrophic gastritis, and intestinal metaplasia) were enrolled. The type of lesion was diagnosed by histological examination. Detection of H. pylori infection and genotyping of vacA regions were carried out by PCR. Results: The prevalence of H. pylori was 95%. The most common vacA genotypes were s2 (51.5%), m2 (77%), i2 (60.5%), and d2 (58.5%). VacA s1, m1, and i1 genotypes were associated with a high risk of intestinal metaplasia, while the vacA d1 genotype increases the risk of atrophic gastritis and intestinal metaplasia. The most common vacA combination was s2/m2/i2/d2 (52%), and it was more detected in chronic gastritis. The moderate virulent vacA combination (s1/m2/i1/d1) increases the risk of atrophic gastritis, while the most virulent vacA combination (s1/m1/i1/d1) increases the risk of intestinal metaplasia. Conclusions: Genotyping of vacA d region might be a reliable marker for the identification of vacA virulent strains that represent a high risk of developing precancerous lesions (atrophic gastritis and intestinal metaplasia).

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Review of Research on Routes of Helicobacter pylori Infection

Infection International ◽

10.1515/ii-2017-0105 ◽

2015 ◽

Vol 4 (2) ◽

pp. 45-49

Author(s):

Hang Li

Keyword(s):

Helicobacter Pylori ◽

Drinking Water ◽

Peptic Ulcer ◽

Gastric Mucosa ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Gastric Adenocarcinoma ◽

Precancerous Lesions ◽

Natural Environments ◽

H Pylori

AbstractIn recent years, many scholars conducted in-depth research onHelicobacter pyloriand identified it as an important pathogen of chronic gastritis and peptic ulcer.H. pylorialso causes also and contributes to precancerous lesions (atrophic gastritis and intestinal metaplasia) and is closely related to occurrence and development of gastric adenocarcinoma and gastric mucosa-associated lymphoma. This study summarizes biological characteristics, epidemic status, and infection route ofH. pyloriand reviews research on roles of natural environments, especially drinking water, during infection.

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Significance of Helicobacter pylori Eradication on Atrophic Gastritis and Intestinal Metaplasia

The Korean Journal of Helicobacter and Upper Gastrointestinal Research ◽

10.7704/kjhugr.2020.0018 ◽

2020 ◽

Vol 20 (2) ◽

pp. 107-116

Author(s):

Kichul Yoon ◽

Nayoung Kim

Keyword(s):

Helicobacter Pylori ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Precancerous Lesions ◽

Eradication Therapy ◽

Diffuse Type ◽

Helicobacter Pylori Eradication ◽

Predicting Factors ◽

Point Of No Return ◽

H Pylori

There has been an accumulation of data regarding the chemopreventive effects of Helicobacter pylori (H. pylori) eradication. However, it remains unclear how H. pylori infection causes gastric cancer (GC) and how H. pylori eradication can prevent GC. Atrophic gastritis (AG) and intestinal metaplasia (IM) are known as precancerous lesions which mainly lead to intestinal-type GC but to some extent, can also lead to diffuse-type GC. The most important mechanism of AG/IM is H. pylori-induced chronic gastritis. Thus, the reversibility of AG and IM by H. pylori eradication therapy is very important in the prevention of GC. There have been many studies providing data supporting the improvement of AG by the eradication of H. pylori to some extent. In contrast, IM has been regarded as “the point of no return.” However, more recent studies have implied the improvement of IM after eradication, suggesting the importance of early eradication therapy in reversible histological status. In this review, we focused on the reversibility of AG and IM by H. pylori eradication and tried to investigate the predicting factors for the improvement of AG and IM including age, sex, smoking, and diet, as well as H. pylori infection.

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Prevalence of High-Risk Groups for Gastric Carcinoma – A Biopsy Finding

Nepalese Medical Journal ◽

10.3126/nmj.v1i2.21600 ◽

2018 ◽

Vol 1 (2) ◽

pp. 82-85

Author(s):

Geetika KC ◽

Shiva Raj KC ◽

Purnima Gyawali

Keyword(s):

Risk Factors ◽

Helicobacter Pylori ◽

High Risk ◽

Gastric Carcinoma ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Total Study Population ◽

Female Ratio ◽

High Risk Factors ◽

H Pylori

Introduction: Gastric carcinoma is leading cause of death world wide including Nepal. The 5 years survival rate of gastric carcinoma (25%) has drastically decreased compared to early gastric cancers (90-90%) hence implying the need for early detection. Atrophic gastritis and intestinal metaplasia are considered as major high-risk factors and is a precancerous lesion along with Helicobacter pylori. This study tries to look at the distribution of atrophy and intestinal metaplasia across age and gender and their occurrence in Helicobacter pylori positive cases.Materials and methods: It is Cross-sectional study of a retrospectively collected data at KIST medical college and GRP poly clinic private limited from April 2008 till March 2018. Total of 10,683 cases were included. The slides were stained with Hematoxilin and Eosin stain and Giemsa stain and evaluated by two pathologists. Statistical analysis was done using SPSS vs 21.Results: Total numbers of cases studied were 10,683 with male to female ratio of 1.04:1. The most common age group of the study was 18-40 years (n=6206; 58.8%). Atrophy was seen in 81 (0.8 %) cases, Intestinal metaplasia in 298 (2.8 %) cases and Helicobacter Pylori was positive in 4459 (42.2%) cases. The incidence of atrophic gastritis was more in H. pylori positive group 54 (0.5%) group where as intestinal metaplasia was more in H. pylori negative 190(1.8%) group.Conclusion: Atrophic gastritis and intestinal metaplasia, high-risk factors for gastric carcinoma, were not the common findings. Atrophic gastritis was seen in 0.8% and intestinal metaplasia was seen in 2.8% of the total study population.

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Chronic gastritis and Helicobacter pylori in digestive form of Chagas' disease

Revista do Instituto de Medicina Tropical de São Paulo ◽

10.1590/s0036-46651993000200002 ◽

1993 ◽

Vol 35 (2) ◽

pp. 117-121 ◽

Cited By ~ 9

Author(s):

A. J. A. Barbosa ◽

D. M. M. Queiroz ◽

A. M. M. F. Nogueira ◽

M. J. A. Roquette Reis ◽

E. N. Mendes ◽

...

Keyword(s):

Helicobacter Pylori ◽

Gastric Mucosa ◽

Atrophic Gastritis ◽

Chagas Disease ◽

Chronic Gastritis ◽

Antral Mucosa ◽

Common Cause ◽

Superficial Gastritis ◽

H Pylori ◽

Inflammatory Changes

Patients with the digestive form of Chagas'disease frequently present chronic gastritis. As the microorganism Helicobacter pylori is now accepted as the most common cause of human chronic gastritis, the present work was undertaken to verify a possible relationship between the presence of this bacterium and inflammatory changes of antral mucosa in chagasic patients. Seventeen chagasics, with megaesophagus and or megacolon were studied. Fragments from two different regions of antral mucosa were obtained by endoscopy, fixed in 4% neutral formaldehyde and embedded in paraffin. The sections were stained by haematoxylin and eosin for histology analysis, and by carbolfuchsin for H. pylori identification. H. pylori was found in 16 (94.1%) chagasic patients, all of them presenting chronic gastritis. Superficial gastritis was seen in 9 (52.9%) while atrophic gastritis was present in 8 (47.1%) patients. H. pylori was present on gastric mucosa of 8 (100%) patients with atrophic gastritis and of 8 (88.8%) patients with superficial gastritis. We concluded that the microorganism H. pylori should be considered a possible factor connected with the etiopathogenesis of chronic superficial and atrophic gastritis frequently observed in patients with the digestive form of Chagas' disease.

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Role of endoscopy in suspicion of atrophic gastritis with and without intestinal metaplasia in comparison to histopathology

Acta Gastro Enterologica Belgica ◽

10.51821/84.1.208 ◽

2021 ◽

Vol 84 (1) ◽

pp. 9-17

Author(s):

H Ibrahim ◽

A Shams El-Deen ◽

ZA Kasemy ◽

M Saad ◽

AA Sakr

Keyword(s):

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Sensitivity And Specificity ◽

Chronic Gastritis ◽

Gastrointestinal Symptoms ◽

High Sensitivity ◽

High Specificity ◽

Poor Correlation ◽

Gastric Lesions ◽

Low Sensitivity

Background and study aims : Atrophic gastritis (AG) and intestinal metaplasia (IM) are established premalignant gastric lesions. Many studies documented a poor correlation between esophagogastroduodenoscopy (EGD) and histopathological (HP) findings of precancerous gastric lesions. The aim was to bridge the gap between endoscopy and HP in detection of chronic gastritis, AG and IM. Patients and methods : a prospective single-center study involved 150 patients with endoscopic criteria of gastric lesions with upper gastrointestinal symptoms referred for upper GI endoscopy met the endoscopic criteria and classified according to HP of biopsies from targeted gastric lesions into chronic gastritis (GI), AG(GII) or IM(GIII). We correlated the endoscopic criteria of the 3 groups with the HP results. Results : (73males & 75 females) with ages ranged17-75 years and mean± SD was 41.96 ± 15.95. GI, GII &GIII were [42 patients (28%),82 patients (54.7%) and 26 patients (17.3%)], respectively. Diffuse gastric mottling was more common in GI (74.3%, P<0.001), visible submucosal vessels, gastric atrophy predominated in GII (75.6, 82.3 & 73.1% (P 0.005,0.4 & <0.01)), respectively. Whitish raised lesions were more specific in GIII (85.7%) (P<0.001). The sensitivity and specificity of endoscopic suspicion of chronic gastritis were (86&88% in GI), (87&85% in GII) and (54% &100% in GIII) (p-0.001). The logistic regression model for risk factors was χ2= 25.74 and 49.32, p < 0.001. Conclusion : Conventional endoscopy has high sensitivity and specificity for suspicion of chronic gastritis and AG, but low sensitivity and very high specificity for IM. Targeted biopsies may be valuable with image enhanced techniques.

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Eradication of Helicobacter pylori and Gastric Cancer: A Controversial Relationship

Frontiers in Microbiology ◽

10.3389/fmicb.2021.630852 ◽

2021 ◽

Vol 12 ◽

Author(s):

Mariagrazia Piscione ◽

Mariangela Mazzone ◽

Maria Carmela Di Marcantonio ◽

Raffaella Muraro ◽

Gabriella Mincione

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Atrophic Gastritis ◽

Precancerous Lesions ◽

Eradication Therapy ◽

Developed Countries ◽

Gastric Carcinogenesis ◽

Gastric Disease ◽

Type I ◽

H Pylori

Worldwide, gastric cancer (GC) represents the fifth cancer for incidence, and the third as cause of death in developed countries. Indeed, it resulted in more than 780,000 deaths in 2018. Helicobacter pylori appears to be responsible for the majority of these cancers. On the basis of recent studies, and either alone or combined with additional etiological factors, H. pylori is considered a “type I carcinogen.” Over recent decades, new insights have been obtained into the strategies that have been adopted by H. pylori to survive the acidic conditions of the gastric environment, and to result in persistent infection, and dysregulation of host functions. The multistep processes involved in the development of GC are initiated by transition of the mucosa into chronic non-atrophic gastritis, which is primarily triggered by infection with H. pylori. This gastritis then progresses into atrophic gastritis and intestinal metaplasia, and then to dysplasia, and following Correa’s cascade, to adenocarcinoma. The use of antibiotics for eradication of H. pylori can reduce the incidence of precancerous lesions only in the early stages of gastric carcinogenesis. Here, we first survey the etiology and risk factors of GC, and then we analyze the mechanisms underlying tumorigenesis induced by H. pylori, focusing attention on virulence factor CagA, inflammation, oxidative stress, and ErbB2 receptor tyrosine kinase. Moreover, we investigate the relationships between H. pylori eradication therapy and other diseases, considering not only cardia (upper stomach) cancers and Barrett’s esophagus, but also asthma and allergies, through discussion of the “hygiene hypothesis. ” This hypothesis suggests that improved hygiene and antibiotic use in early life reduces microbial exposure, such that the immune response does not become primed, and individuals are not protected against atopic disorders, asthma, and autoimmune diseases. Finally, we overview recent advances to uncover the complex interplay between H. pylori and the gut microbiota during gastric carcinogenesis, as characterized by reduced bacterial diversity and increased microbial dysbiosis. Indeed, it is of particular importance to identify the bacterial taxa of the stomach that might predict the outcome of gastric disease through the stages of Correa’s cascade, to improve prevention and therapy of gastric carcinoma.

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Precancerous Gastric Lesions with Helicobacter pylori vacA+/babA2+/oipA+ Genotype Increase the Risk of Gastric Cancer

BioMed Research International ◽

10.1155/2020/7243029 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8 ◽

Cited By ~ 1

Author(s):

Theeraya Simawaranon Bartpho ◽

Wareeporn Wattanawongdon ◽

Taweesak Tongtawee ◽

Chatchanok Paoin ◽

Kokiet Kangwantas ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Clinical Outcomes ◽

Chronic Gastritis ◽

Virulence Genes ◽

Gastric Lesions ◽

Precancerous Gastric Lesions ◽

Increased Risk ◽

H Pylori ◽

Gastric Cancer Patients

Objective. The clinical outcomes of gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer have been attributed to the interplay of virulence factors of Helicobacter pylori (H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of cagA, vacA, iceA2, babA2, and oipA genes and their association with clinical outcomes. Methods. Chronic gastritis, atrophic gastritis, and intestinal metaplasia specimens were obtained from patients who underwent endoscopy and surgical resection between January 2017 and December 2018; specimens from gastric cancer patients treated between January 2014 and December 2018 were also added. H. pylori infection and virulence genes (cagA, vacA, iceA2, babA2, and oipA) were determined using real-time PCR. The association between H. pylori genotypes and clinical outcomes were evaluated using multivariate regression model analysis. The overall survival of gastric cancer patients was compared between genotype combinations. Results. H. pylori was positive in 166 patients with chronic gastritis, precancerous gastric lesions, and gastric cancer. The genes vacA, babA2, and oipA were most prevalent in chronic gastritis (73%), precancerous gastric lesions (62%), and gastric cancer (91%), respectively. The vacA, babA2, and oipA genes were associated with increased risk of gastric cancer (OR = 1.23; 95% CI = 1.13–3.32; P=0.033, OR = 2.64; 95% CI = 1.44–4.82, P=0.024, and OR = 2.79; 95% CI = 1.58–5.41; P=0.031, respectively). Interestingly, H. pylori vacA+/babA2+/oipA+ genotype infection was associated with increased risk of gastric cancer (OR = 3.85, 95% CI = 1.67–5.77, P=0.014). Conclusion. In this present study, we reported on the virulence genes of H. pylori infection to reveal their association with increased risk of chronic gastritis, precancerous gastric lesions, and gastric cancer. Precancerous gastric lesions with H. pylori vacA+/babA2+/oipA+ genotype increased the risk of gastric cancer.

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Dynamics of Helicobacter pylori infection as a determinant of progression of gastric precancerous lesions: 16-year follow-up of an eradication trial

Gut ◽

10.1136/gutjnl-2016-311685 ◽

2017 ◽

Vol 67 (7) ◽

pp. 1239-1246 ◽

Cited By ~ 49

Author(s):

Robertino M Mera ◽

Luis E Bravo ◽

M Constanza Camargo ◽

Juan C Bravo ◽

Alberto G Delgado ◽

...

Keyword(s):

Helicobacter Pylori ◽

Linear Models ◽

Precancerous Lesions ◽

Gastric Lesions ◽

Logistic Regression Models ◽

Risk Of Progression ◽

H Pylori ◽

Cumulative Time

ObjectiveTo evaluate the long-term effect of cumulative time exposed to Helicobacter pylori infection on the progression of gastric lesions.Design795 adults with precancerous gastric lesions were randomised to receive anti-H. pylori treatment at baseline. Gastric biopsies were obtained at baseline and at 3, 6, 12 and 16 years. A total of 456 individuals attended the 16-year visit. Cumulative time of H. pylori exposure was calculated as the number of years infected during follow-up. Multivariable logistic regression models were used to estimate the risk of progression to a more advanced diagnosis (versus no change/regression) as well as gastric cancer risk by intestinal metaplasia (IM) subtype. For a more detailed analysis of progression, we also used a histopathology score assessing both severity and extension of the gastric lesions (range 1–6). The score difference between baseline and 16 years was modelled by generalised linear models.ResultsIndividuals who were continuously infected with H. pylori for 16 years had a higher probability of progression to a more advanced diagnosis than those who cleared the infection and remained negative after baseline (p=0.001). Incomplete-type IM was associated with higher risk of progression to cancer than complete-type (OR, 11.3; 95% CI 1.4 to 91.4). The average histopathology score increased by 0.20 units/year (95% CI 0.12 to 0.28) among individuals continuously infected with H. pylori. The effect of cumulative time of infection on progression in the histopathology score was significantly higher for individuals with atrophy (without IM) than for individuals with IM (p<0.001).ConclusionsLong-term exposure to H. pylori infection was associated with progression of precancerous lesions. Individuals infected with H. pylori with these lesions may benefit from eradication, particularly those with atrophic gastritis without IM. Incomplete-type IM may be a useful marker for the identification of individuals at higher risk for cancer.

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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.

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NTESTINAL METAPLASIA AND HELICOBACTER PYLORI INFECTION IN PATIENTS WITH CHRONIC GASTRITIS.

Journal of Medicine and Pharmacy ◽

10.34071/jmp.2011.3.9 ◽

2011 ◽

pp. 63-71

Author(s):

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Chronic Gastritis ◽

Significant Relationship ◽

Precancerous Lesion ◽

Chronic Atrophic Gastritis ◽

Helicobacter Pylori Infection ◽

Antral Gastritis

Background: Intestinal metaplasia is a precancerous lesion. Helicobacter pylori is identified as an important cause of gastric cancer. This study is aimed at assessing the intestinal metaplasia and Helicobacter pylori infection and their relation in patients with chronic gastritis. Patients and methods: Study includes 75 patients with chronic gastritis diagnosed by clinical, endoscopic and histopathological criteria. Intestinal metaplasia is diagnosed by HE stain. Hp infection is tested by CLO-test from Viet A Ltd. Results: Hp infecton rate in this study is 66.67% and is highest in patients with antral gastritis. Intestinal metaplasia is found in 29.33% of patients with chronic gastritis with the predominance of complete intestinal metaplasia. The rate of intestinal metaplasia is the highest in the group with chronic atrophic gastritis. There is a significant relationship between intestinal metaplasia and Hp ìnfection. Conclusion: Hp and intestinal metaplasia are found at significant rates in chronic gastritis. The rate of intestinal metaplasia is clearly higher in the group with Hp-positive chronic gastritis.

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