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Helicobacter pylori is main causative agent of acute gastritis and peptic ulcer disease. In certain population, this infection leads to gastric cancers viz., adenocarcinoma, and mucosal-associated lymphoid tissue (MALT) lymphoma. The objective of this study was to comparatively evaluate invasive (RUT) and non-invasive (IgM and IgG ELISA) methods for detection of H. pylori infection among patients visiting a tertiary care hospital. A total of 285 dyspeptic patients undergoing endoscopic examination were included in this study. From each patient one biopsy specimen and serum samples were collected. Biopsy specimen was subjected to RUT and IgM & IgG ELISA tests were performed using serum samples. H. pylori was detected in 127 (44.6%) and 126 (44.2%) cases by RUT and IgM ELISA, respectively. H. pylori were detected in 85 (29.8%) samples by IgG ELISA. Based on the combination of RUT and IgM ELISA test, total 128 (44.9%) patients were positive for H. pylori infection. Most of the positive cases belonged to 21-40 years age group (60 of 128) followed by 41-60 years age group (31 0f 128). All the three diagnostic methods viz., RUT, IgM ELISA and IgG ELISA used in this study showed a greater prevalence of H. pylori infection in female gender compared to male gender. In this study, sensitivity of both RUT and IgM ELISA was similar across different age groups and gender. The advantage of IgM ELISA over RUT is that it does not require endoscopy. Therefore, IgM ELISA could be considered as safe and an alternative method for detection of this pathogen. [ABSTRACT FROM AUTHOR]

Aim: The aim of the study was to find the role of Helicobacter pylori infection in the pathogenesis of minimal hepatic encephalopathy and effect of its eradication. Methods: A prospective study was conducted in the Department of Medicine, Nalanda Medical College and Hospital, Patna, Bihar, India, for 1 year. In patients of suspected cirrhosis of liver ultrasound and endoscopic examination were performed. Those with ultrasonographic findings of chronic liver disease and esophageal varices on endoscopic examination were included in this study. Of the 165 patients with liver cirrhosis screened, 65 had one or more exclusion criterion; the study thus included 100 patients. Biochemical tests and psychometric tests were performed initially on all patients included in the study. Results: Based on results of the psychometric tests, 35 (53.8%) of the 65 patients with liver cirrhosis had MHE. Clinical and demographic characteristics of the study patients are shown in Table 2. Hepatitis B virus infection was the most common (36%) cause of cirrhosis. In the study group, most patients were in Child-Pugh class A (25%) or B (58%); most patients in Child-Pugh class C who were screened fulfilled one or more exclusion criteria. Presence of MHE had no significant relationship with age, sex, Child-Pugh grade, and cause of cirrhosis. H. Pylori infection was found in 42 (64.6%) of 65 patients with MHE and 13 (37.1%) of 35 patients without MHE (p< 0.001). Fasting blood ammonia level were significantly higher in patients with MHE (1.65 [0.34] µg/mL) than in those without (1.06 [0.25] µg/mL; p <0.001). Among patients with MHE, fasting blood ammonia levels were significantly higher in patients who tested positive for H. Pylori (1.81 [0.33] µg/mL) than in those who tested negative (1.38 [0.13] µg/mL; p <0.001). Conclusion: H. Pylori infection plays a role in the causation of MHE in patients with liver cirrhosis. H. Eradication of H. Pylori in cirrhotic patients may prevent hepatic encephalopathy(HE). [ABSTRACT FROM AUTHOR]

Helicobacter pylori infection in stomach leads to gastric cancer, gastric ulcer, and duodenal ulcer. More than 1 million people die each year due to these diseases, but why most H. pylori -infected individuals remain asymptomatic while a certain proportion develops such severe gastric diseases remained an enigma. Several studies indicated that gastric and intestinal microbiota may play a critical role in the development of the H. pylori -associated diseases. However, no specific microbe in the gastric or intestinal microbiota has been clearly linked to H. pylori infection and related gastric diseases. Here, we studied H. pylori infection, its virulence genes, the intestinal microbiota, and the clinical status of Trivandrum residents (N = 375) in southwestern India by standard H. pylori culture, PCR genotype, Sanger sequencing, and microbiome analyses using Illumina Miseq and Nanopore GridION. Our analyses revealed that gastric colonization by virulent H. pylori strains (vacAs1i1m1cagA +) is necessary but not sufficient for developing these diseases. Conversely, distinct microbial pools exist in the lower gut of the H. pylori -infected vs. H. pylori -non-infected individuals. Bifidobacterium (belonging to the phylum Actinobacteria) and Bacteroides (belonging to the phylum Bacteroidetes) were present in lower relative abundance for the H. pylori + group than the H. pylori - group (p < 0.05). On the contrary, for the H. pylori + group, genus Dialister (bacteria belonging to the phylum Firmicutes) and genus Prevotella (bacteria belonging to the phylum Bacteroidetes) were present in higher abundance compared to the H. pylori- group (p < 0.05). Notably, those who carried H. pylori in the stomach and had developed aggressive gastric diseases also had extremely low relative abundance (p < 0.05) of several Bifidobacterium species (e.g., B. adolescentis , B. longum) in the lower gut suggesting a protective role of Bifidobacterium. Our results show the link between lower gastrointestinal microbes and upper gastrointestinal diseases. Moreover, the results are important for developing effective probiotic and early prognosis of severe gastric diseases. [ABSTRACT FROM AUTHOR]

• Antimicrobial resistance attributes are increasingly enriching in the genome of Helicobacter pylori. • Genome sequence and resistance traits are very heterogenous in H. pylori. • Comparative analysis of 143 whole-genome sequences of H. pylori identified multiple antibiotic resistance and virulence factors. • Current findings reveal the differential distribution of antibiotic resistance genes in the H. pylori strains. Helicobacter pylori is a ubiquitous bacterium and contributes significantly to the burden of chronic gastritis, peptic ulcers, and gastric cancer across the world. Adaptive phenotypes and virulence factors in H. pylori are heterogeneous and dynamic. However, limited information is available about the molecular nature of antimicrobial resistance phenotypes and virulence factors of H. pylori strains circulating in India. In the present study, we analyzed the whole genome sequences of 143 H. pylori strains, of which 32 are isolated from two different regions (eastern and southern) of India. Genomic repertoires of individual strains show distinct region-specific signatures. We observed lower resistance phenotypes and genotypes in the East Indian (Kolkata) H. pylori isolates against amoxicillin and furazolidone antibiotics, whereas higher resistance phenotypes to metronidazole and clarithromycin. Also, at molecular level, a greater number of AMR genes were observed in the east Indian H. pylori isolates as compared to the southern Indian isolates. From our findings, we suggest that metronidazole and clarithromycin antibiotics should be used judicially in the eastern India. However, no horizontally acquired antimicrobial resistance gene was observed in the current H. pylori strains. The comparative genome analysis shows that the number of genes involved in virulence, disease and resistance of H. pylori isolated from two different regions of India is significantly different. Single-nucleotide polymorphisms (SNPs) based phylogenetic analysis distinguished H. pylori strains into different clades according to their geographical locations. Conditionally beneficial functions including antibiotic resistance phenotypes that are linked with faster evolution rates in the Indian isolates. [ABSTRACT FROM AUTHOR]

Background/Aim: Collective evidences suggest the causal association of Helicobacter pylori infection with iron deficiency anemia. Generation of free radicals against this bacterium can lead to turbulence in oxidative-antioxidative system. This study was undertaken to evaluate the marker of oxidative protein injury, protein carbonylation, and total antioxidant status in anemic H. pylori-infected patients and to observe the alteration in them after treatment for 1 month with oral ferrous sulfate and anti-H. pylori therapy. Twenty anemic H. pylori-infected patients were randomly divided into 2 groups. The H. pylori-infected patients in Group I received both iron supplementation and anti-H pylori therapy, whereas patients in Group II received only the iron supplementation. Fifteen healthy volunteers served as controls. All the study parameters were estimated after 1 month of the treatment. Materials and Methods: Protein carbonylation and total antioxidant status were estimated using colorimetric method. Hematologic parameters were evaluated using Sysmex-K-100 automated cell counter. Results: In anemic H. pylori-infected patients, the protein carbonyls (PCOs) were significantly increased, whereas the total antioxidant status, iron, hemoglobin, and ferritin levels were significantly decreased compared with the controls. In Group I, while the PCOs level decreased significantly, there was a significant increase in the total antioxidant status, iron, hemoglobin, and ferritin levels after 1 month. No significant alterations were noted in the levels of PCOs, total antioxidant status, iron, hemoglobin, or ferritin in Group II patients after 1 month of the treatment. Conclusions: The findings from this study indicate that treatment for both anemia and H. pylori infections is required for lowering the oxidative stress markers, which synergistically bring about an appropriate correction of anemia soon in these patients. [ABSTRACT FROM AUTHOR]

The incidence of Helicobacter pylori gastritis is high in India and the number of individuals with vitamin B12 deficiency is also large. An association has been found between these two factors. It is necessary to determine whether H. pylori infection may be a factor in the causation of B12 deficiency and whether it is associated with any morphological changes on ultrastructural examination. A cohort-based study has been performed, which includes 505 young asymptomatic males. These cases have been investigated for presence of H. pylori and macrocytosis. The study confirms an association between H. pylori infection and B12 deficiency. It is recommended that H. pylori infection be looked for in subjects having macrocytosis of unknown etiology. [ABSTRACT FROM AUTHOR]

H. pylori have gradually acquired resistance to the commonly used antibiotics because of their use in many parasitic and anaerobic infections, which leads to treatment failure of various gastric and duodenal diseases associated with H. pylori infection. The present research work aimed to isolate and characterize the bioactive compound from the methanol extract of stem of Berberis aristata DC. This is traditionally used for the treatment of dyspepsia, dysentery and diarrhea against antibiotic-resistant gastric pathogen H. pylori. The in vitro antimicrobial activity of Berberine an active isolated compound from methanol extract of stem of Berberis aristata DC against drug-resistant H. pylori strain isolated from North Indian GERD patients. The H. pylori strain was only collected from those, who were devoid of any kind of anti -H. Pylori therapy. The methodology was in determining the Minimum inhibition concentration (MIC) using the microdilution method and disk diffusion method. H. pylori isolate was included in this study. Berberine from methanol extract of stem of Berberis aristata DC showed its potency on H. pylori -infected isolated from GERD patients with a maximum inhibition at 0.000075 μg/ml. Prevalence of metronidazole resistance ranges between 50 and 90% in developing countries including India. The emergence of dual drug resistance was reported in various studies. This study suggests that Berberine an isolated compound from methanol extract of stem of Berberis aristata DC used commonly known as Daru Haldi potentially active for the treatment of drug-resistant H. pylori infection. Berberine from methanol extract of stem of Berberis aristata DC with a concentration of 0.000075 μg/ml shows a positive effect safely and effectively. Image 1 [ABSTRACT FROM AUTHOR]

Interleukin 1 beta (IL-1β) and Tumor necrosis factor alpha (TNF-α) are key inflammatory cytokines whose polymorphisms have been correlated with increased susceptibility to gastric cancer (GC). Since geographical and racial differences exist in cancer rates, our study was aimed to evaluate the first possible association of polymorphisms in these genes with GC risk in West Bengal, India. Polymorphisms in IL-1β and TNF-α genes were genotyped in 120 GC patients and 135 healthy individuals. Combined effect of the SNPs in both genes with GC risk was determined through allele dosage analysis (ADA) and the survival data were analyzed by Log Rank Test. The study results revealed that IL-1β rs1143627: T > C, rs16944: C > T (p = 0.001;OR = 1.85; 95% CI 1.30-2.63) and rs1143633: G > A (p < 0.0001; OR = 2.53; 95% CI 1.67-3.83) and TNF-α rs1800630: C > A, rs1799964: T > C (p < 0.0001; OR = 2.31; 95% CI 1.54-3.46) polymorphisms significantly contributed toward GC risk. Moreover, ADA showed that carriage of 7 "effective" risk alleles conferred a risk of almost 10-fold in comparison to individuals carrying less than 3 "effective" risk alleles. Our survival analysis also indicated a significant association between IL-1β rs1143627: T > C and rs16944: C > T and patient survivability. The presence of H. pylori enhanced the risk in individuals with IL-1β rs1143627:CC and rs16944:TT genotypes. Further, meta-analysis revealed significant association of IL-1β rs1143627: T > C (p = 0.026; OR = 4.165; 95% CI 1.18-14.65) and rs16944: C > T (p = 0.01; OR = 5.49; 95% CI 1.48-20.37) in presence of H. pylori with gastric cancer in Asian population though no significant difference (p > 0.05) was found when compared to absence of H. pylori Environ. Mol. Mutagen. 59:653-667, 2018. © 2018 Wiley Periodicals, Inc., (© 2018 Wiley Periodicals, Inc.)