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Background: The purpose of this analysis is to evaluate the antimicrobial susceptibility of eight drugs effective against Helicobacter pylori (H. pylori) strains and the genetic diversity of H. pylori virulence genes to foresee clinical outcomes in North India. Materials and Methods: Fifty‐eight H. pylori strains isolated from patients suffering from various gastrointestinal (GI) diseases were included in the study. MICs of various antibiotics were determined by the agar dilution method. The chi‐squared test and Fisher exact test were used to determine the p‐value, which was considered significant at p‐value ≤ 0.05. RStudio 4.0 was used to for the data visualization. Results: The prevalence of drug resistance was found to be: cefixime (CFM) (41.3%), furazolidone (FZD) (34.4%), amoxicillin (AMX) (20.7%), levofloxacin (LVFX) (70.7%), metronidazole (MTZ) (39.6%), tetracycline (TET) (20.7%), clarithromycin (CLA) (17.2%), and rifabutin (RIF) (17.2%). Out of 58 H. pylori strains, 3 were pan susceptible. There were H. pylori strains with single‐drug resistance (21.8%, 12/55), dual resistance (30.9%, 17/55), triple resistance (20%, 11/55), and multidrug resistance (27.3%, 15/55). The resistance rate in MTZ, CLA and RIF were found to be significantly higher in females as compared to males (p = 0.005, p = 0.002, and p = 0.02), respectively. The resistance to TET exhibited significantly higher levels in gastritis compared to GERD, DU, and other disease groups (p = 0.04) respectively. Conclusion: TET, AMX, CLA, and RIF were found to be more effective antibiotics against H. pylori infections, whereas more studies are required to provide evidence on increasing resistance rate of LVFX. [ABSTRACT FROM AUTHOR]

Background: The relationship between gastroesophageal reflux disease (GERD) and Helicobacter pylori infection is a complicated topic. This study aimed to evaluate the association between H. pylori infection and GERD and identify the associated risk factors in North India. Methods: All individuals who were referred for an endoscopy because they had dyspepsia were included in a cross-sectional study. Using endoscopic assessment, GERD was diagnosed. As a comparison group, patients with normal esophageal function were chosen. H. pylori was cultured and genotyped to assess the virulent genes such as cagA, vacA, and iceA. The relationship of H. pylori infection with GERD and its associated risk factors were estimated with Chi‑square analysis, odds ratios, and 95% confidence intervals using multiple logistic regression analysis. Results: In total, 420 patients were included in this study, of whom 335 (79.8%) had GERD. The mean age was 44.01 ± 16.52 years. Overall, 143 (34%) patients were positive for H. pylori infection. cagA-negative H. pylori isolates were significantly associated with the GERD group. Variables such as gender, age, alcohol, smoking, body mass index (BMI), smoking, and hiatus hernia in patients had no significant association with H. pylori infection. However, increased age, gender, Frequency Scale for the Symptoms of GERD (FSSG) score, BMI, and presence of hiatus hernia were significantly associated with the GERD group. Conclusion: In our results, there was no association between H. pylori infection and GERD. The risk factors for GERD were age, gender, FSSG score, BMI, and hiatus hernia. Further studies are recommended. [ABSTRACT FROM AUTHOR]

Background: Gastritis is one of the most prevalent disorders affecting individuals. Helicobacter pylori infection, along with other factors such as lifestyle, gender, alcohol drinking, and smoking are causes of gastritis. Northeast Indian population is geographically, ethnically, culturally, and linguistically a blend of its surrounding nations, being different from the North Indian population. The objective of the study was to predict the prevalence and risk factors of gastritis in Northeast India and compare it with North India. Methods: A total of 909 dyspeptic patients (Northeast India: 362 and North India: 547) were enrolled and had undergone endoscopy. H. pylori status was identified, determined, and genotyped. They were divided into gastritis and nongastritis samples based on the presence or absence of gastric ulcerations and erosion. The risk factors for gastritis in Northeast and North India were estimated with Chi-square analysis, odds ratios, and 95% confidence intervals using multiple logistic regression analysis. Results: The prevalence of gastritis and H. pylori infection was higher in Northeast India than North India. The risk factors significantly associated with gastritis in Northeast region were H. pylori infection, increased smoking, and alcohol drinking and in North region were smoking and body mass index. Conclusion: Although our study found the risk factors associated with gastritis in Northeast India, the available data do not provide sufficient evidence. Further studies are recommended. [ABSTRACT FROM AUTHOR]

Curcumin is a potential natural remedy for preventing Helicobacter pylori -associated gastric inflammation and cancer. Here, we analyzed the effect of a phospholipid formulation of curcumin on H. pylori growth, translocation and phosphorylation of the virulence factor CagA and host protein kinase Src in vitro and in an in vivo mouse model of H. pylori infection. Growth of H. pylori was inhibited dose-dependently by curcumin in vitro. H. pylori was unable to metabolically reduce curcumin, whereas two enterobacteria, E. coli and Citrobacter rodentium , which efficiently reduced curcumin to the tetra- and hexahydro metabolites, evaded growth inhibition. Oxidative metabolism of curcumin was required for the growth inhibition of H. pylori and the translocation and phosphorylation of CagA and cSrc, since acetal- and diacetal-curcumin that do not undergo oxidative transformation were ineffective. Curcumin attenuated mRNA expression of the H. pylori virulence genes cagE and cagF in a dose-dependent manner and inhibited translocation and phosphorylation of CagA in gastric epithelial cells. H. pylori strains isolated from dietary curcumin-treated mice showed attenuated ability to induce cSrc phosphorylation and the mRNA expression of the gene encoding for IL-8, suggesting long-lasting effects of curcumin on the virulence of H. pylori. Our work provides mechanistic evidence that encourages testing of curcumin as a dietary approach to inhibit the virulence of CagA. [ABSTRACT FROM AUTHOR]