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.

Background: Helicobacter pylori infection and premalignant gastric mucosa can be reliably identified using conventional narrow band imaging (C-NBI) gastroscopy. The aim of our study was to compare standard biopsy with site specific biopsy for diagnosis of H. pylori infection and premalignant gastric mucosa in daily clinical practice. Materials and Methods: Of a total of 500 patients who underwent gastroscopy for investigation of dyspeptic symptoms, 250 patients underwent site specific biopsy using C-NBI (Group 1) and 250 standard biopsy (Group 2). Sensitivity, specificity, and positive and negative predictive values were assessed. The efficacy of detecting H. pylori associated gastritis and premalignant gastric mucosa according to the updated Sydney classification was also compared. Results: In group 1 the sensitivity, specificity, positive and negative predictive values for predicting H. pylori positivity were 95.4%, 97.3%, 98.8% and 90.0% respectively, compared to 92.9%, 88.6%, 83.2% and 76.1% in group 2. Site specific biopsy was more effective than standard biopsy in terms of both H. pylori infection status and premalignant gastric mucosa detection (P<0.01). Conclusions: Site specific biopsy using C-NBI can improve detection of H. pylori infection and premalignant gastric mucosa in daily clinical practice.

Background: Colorectal polyps are common in Thailand, particularly in the northeastern region. The present study aimed to determine any correlation between Helicobacter pylori-associated gastritis and colorectal polyps in the Thai population. Materials and Methods: A total of 303 patients undergoing esophagogastroduodenoscopy with colonoscopy for investigation of chronic abdominal pain participated in this study from November 2014 to October 2015. A diagnosis of Helicobacter pylori associated gastritis was made if the bacteria were seen on histopathological examination and a rapid urease test was positive. Colorectal polyps were confirmed by histological examination of colorectal biopsies. Patient demographic data were analyzed for correlations. Results: The prevalence of colorectal polyps was 77 (25.4%), lesions being found more frequently in Helicobacter pylori infected patients than non-infected subjects [38.4% vs. 12.5%; Odds Ratio (OR) (95% CI): 2.26 (1.32 -3.86), p < 0.01]. Patients with Helicobacter pylori -associated gastritis were at high risk of having adenomas featuring dysplasia [OR (95% CI): 1.15 (1.16 -7.99); P = 0.02]. There was no varaition in location of polyps, age group, sex and gastric lesions with respect to Helicobacter pylori status. Conclusions: This study showed that Helicobacter pylori associated gastritis is associated with an increased risk of colorectal polyps, especially adenomas with dysplasia in the Thai population. Patients with Helicobacter pylori-associated gastritis may benefit from concurrent colonoscopy for diagnosis of colorectal polyps as a preventive and early treatment for colorectal cancer.

Background/Aims: Genetic polymorphisms in Toll-like receptors (TLRs) are important influence on gastric lesion development and Helicobacter pylori susceptibility. Materials and Methods: TLR2 rs3804099 and rs3804100 and TLR4 rs10759932 were determined in a total of 400 patients. The association among genotypes and the risk of gastric lesion development and H. pylori susceptibility were evaluated by the odds ratios (ORs) and 95% confidence intervals (95% CIs) from logistic regression analyses. Results: TLR4 rs10759932, C/C homozygous genotype was associated with an increased risk of premalignant/malignant (OR=2.48, 95% CI=1. 96-4.62, p=0.015). The recessive model of TLR4 rs10759932 showed a decreased risk of H. pylori susceptibility (adjusted OR=0.52, 95% CI=0.38-0.82, p=0.046). Meanwhile, the recessive model was associated with an increased risk of non-malignant (OR=3.46, 95% CI=2. 25-5.67, p=0.001). In subjects with H. pylori infection, the recessive model was associated with an increased risk of p=0.001) and premalignant/malignant (OR=1.83, p=0.027). Conclusion: TLR4 rs10759932, but not TLR2 rs3804099 and rs3804100, was associated with risk of premalignant and/or malignant and H. pylori susceptibility. H. pylori infection seems to contribute to chronic gastritis, and premalignant/malignant supported the development of the premalignant/malignant lesions involved in H. pylori infection that is critical to gastric cancer in Thai patients.

Background and Aim. Identifying specific gastric mucosal morphologic patterns useful for detecting Helicobacter pylori associated gastritis and correlation with histopathological severity. Methods. The endoscopists classified the C-NBI gastroscopic findings into 5 gastric mucosal morphologic patterns as follows: type 1: regular arrangement of collecting venules, type 2: cone-shaped gastric pits, type 3: rod-shaped gastric pits with prominent sulci, type 4: ground glass-like morphology, and type 5: dark brown patches with bluish margin and irregular border. Biopsies of all of the cases were then evaluated by 5 pathologists for definitive Helicobacter pylori diagnosis. Result. Type 1 and type 2 patterns were statistically significant in predicting Helicobacter pylori negative status (58/60, P < 0.01). Type 3, type 4, and type 5 patterns were statistically significant in predicting Helicobacter pylori positive status (132/140, P < 0.01). Furthermore, the sensitivity, specificity, and positive and negative predictive values of type 3, 4, or 5 morphologies for predicting Helicobacter pylori positive were 94.28%, 96.66%, 98.50%, and 87.87%, respectively, correlated well with inflammation grading according to the Sydney classification (P < 0.01). Conclusion. Our study suggests that gastric mucosal morphologic patterns in the Helicobacter pylori infected gastric mucosa can be reliably identified using C-NBI gastroscopy with good correlation with inflammation grading.

Objectives This study aimed to evaluate the effects of periodontal therapy on the efficacy of Helicobacter pylori eradication and on the recurrence of infection after eradication. Methods We conducted a prospective randomized trial on 698 gastric H. pylori-infected patients, of whom 347 received gastric H. pylori treatment alone and 342 received gastric H. pylori treatment plus periodontal therapy. The presence of H. pylori and associated virulence genes were detected by real-time polymerase chain reaction. Results After eradication of gastric H. pylori infection, the recurrence of gastric H. pylori was significantly lower in the gastric H. pylori treatment plus periodontal therapy group than in the group receiving gastric H. pylori treatment alone (OR 0.67; 95% CI 0.45 to 0.99), whereas the eradication rate was not significantly different (OR 0.87; 95% CI 0.68 to 0.98). There was a close relationship between the presence of H. pylori in saliva and its presence in the stomach. Conclusions The oral cavity is an important reservoir for gastric H. pylori infection. Adjunctive periodontal therapy could enhance the efficiency of H. pylori treatment and reduce the recurrence of gastric H. pylori infection.

Recently, infection with Helicobacter spp. plays a role in the development of various cancer have been reported including biliary tract carcinoma mainly cholangiocarcinoma (CCA). There has been a strong, positive correlation between opisthorchiasis-associated CCA and infection with Helicobacter. Infection with H. bilis and H. hepaticus species can cause biliary cancer (Chang and Parsonnet, 2010). Recently, Deenonpoe et al (2015) reported liver fluke O.

Metformin is an oral anti-hyperglycemic agent, which is the most commonly prescribed medication in the treatment of type-2 diabetes mellitus. It is purportedly associated with a reduced risk for various cancers, mainly exerting anti-proliferation effects on various human cancer cell types, such as pancreas, prostate, breast, stomach and liver. This mini-review highlights the risk and benefit of metformin used for cholangiocarcinoma (CCA) prevention and therapy. The results indicated metformin might be a quite promising strategy CCA prevention and treatment, one mechanism being inhibition of CCA tumor growth by cell cycle arrest in both in vitro and in vivo. The AMPK/mTORC1 pathway in intrahepatic CCA cells is targeted by metformin. Furthermore, metformin inhibited CCA tumor growth via the regulation of Drosha-mediated expression of multiple carcinogenic miRNAs. The use of metformin seems to be safe in patients with cirrhosis, and provides a survival benefit. Once hepatic malignancies are already established, metformin does not offer any therapeutic potential. Clinical trials and epidemiological studies of the benefit of metformin use for CCA should be conducted. To date, whether metformin as a prospective chemotherapeutic for CCA is still questionable and waits further atttention.