Helicobacter Pylori Infection Of Stomach Research Articles

Association of Chronic Periodontitis with Helicobacter pylori Infection in Stomach or Mouth: A Systematic Review and Meta-Analysis.

Helicobacter pylori (H. pylori) infection and periodontitis are both inflammatory conditions associated with systemic diseases. Researchers have attempted to investigate the correlation between them. This systematic review and meta-analyses were conducted to investigate the association of H. pylori infection in the stomach and/or in subgingival plaque and gingival crevicular fluid with chronic periodontitis. The protocol was created according to the Preferred Reporting Items for Systematic review and Meta-Analysis Protocols (PRISMA-P) statement. The study was designed according to the Cochrane criteria. A comprehensive literature search was performed in MEDLINE, Scopus, and CENTRAL, combined with hand-searching and assessment of gray literature. The meta-analysis of the included studies was made by the Review Manager (RevMan) 5.4 software. The effect measure of the outcome was odds ratios with 95% confidence intervals. Heterogeneity was assessed by chi-square and I2. Four observational studies involving 818 subjects were included in this meta-analysis. The odds of oral H. pylori presence were higher in patients with chronic periodontitis, compared to healthy controls, with an odds ratio of 1.87 (95% confidence interval 0.85-4.10; p = 0.12). The odds of the presence of H. pylori in the stomach also were higher in patients with chronic periodontitis, with an odds ratio of 1.80 (95% confidence interval 0.82-3.95; p = 0.15). There is no evidence for an association between chronic periodontitis and the prevalence of H. pylori, detected either in subgingival plaque and gingival crevicular fluid or in the stomach.

Low Bifidobacterium Abundance in the Lower Gut Microbiota Is Associated With Helicobacter pylori-Related Gastric Ulcer and Gastric Cancer.

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.

Kinetics of urease inhibition by different fractions of Cassia fistula

Urease serves as the basis for Helicobacter pylori infection of stomach as well as urinary tract infection by Proteus, Klebsiella, Pseudomonas and Staphylococus species. Ureolytic activity by these pathogens causes various gastric and urinary diseases. Urease inhibitors can be used as potential approach for treatment of these infections. Cassia fistula, an ayurvedic medicinal plant also named as Aragvadha (a disease killer), was explored as source of urease inhibitors. In the present study, we evaluated the five different extracts viz. aqueous, methanol, hexane, chloroform and ethyl acetate for their urease inhibition potential. Except chloroform extract, all four samples exhibited more than 50% urease inhibitory activity. The IC50 of ethyl acetate sample was 0.27 mg/ml lower than standard thiourea. The inhibition kinetics of all four samples was studied. Line weaver Burk plot and Dixon plots revealed the ethyl acetate sub fraction as most potent inhibitor as it exhibited competitive mode of inhibition with Ki of 280 μg/ml. All the other samples exhibited mixed and uncompetitive mode of inhibition. Further characterization of bioactive compounds in the ethyl acetate sample was performed using GC-MS. The analysis identified 26 compounds in the sample. Mome-inositol, a derived sugar was found to be major compound (80.83%). From the present observation it can be concluded that C. fistula plant needs to be explored further for identifying the lead molecule to treat various ureolysis based diseases.

Fermented Foods: Are They Tasty Medicines for Helicobacter pylori Associated Peptic Ulcer and Gastric Cancer?

More than a million people die every year due to gastric cancer and peptic ulcer. Helicobacter pylori infection in stomach is the most important reason for these diseases. Interestingly, only 10–20% of the H. pylori infected individuals suffer from these gastric diseases and rest of the infected individuals remain asymptomatic. The genotypes of H. pylori, host genetic background, lifestyle including smoking and diet may determine clinical outcomes. People from different geographical regions have different food habits, which also include several unique fermented products of plant and animal origins. When consumed raw, the fermented foods bring in fresh inocula of microbes to gastrointestinal tract and several strains of these microbes, like Lactobacillus and Saccharomyces are known probiotics. In vitro and in vivo experiments as well as clinical trials suggest that several probiotics have anti-H. pylori effects. Here we discuss the possibility of using natural probiotics present in traditional fermented food and beverages to obtain protection against H. pylori induced gastric diseases.

Helicobacter pylori infection and comorbidity: Our diagnostic and therapeutic modalities

The discovery of Helicobacter pylori (Hp) bacteria and causal relationship of Helicobacter pylori infection with the origin of chronic gastritis, stomach and duodenal ulcer and stomach cancer represents an epochal event of the new age. The goal of the study is to examine the incidence of Helicobacter pylori infection of stomach and prove the connection between Helicobacter pylori infection and stomach and duodenum diseases (non-ulcer gastropathy, stomach ulcer, and duodenal bulb ulcer and stomach cancer). The study encompassed 250 randomly selected examinees of both genders and different age categories. All the examinees were subjected to quick urease test (QUT) from antral bioptate and stomach corpus acquired by upper gastrointestinal endoscopy with standard forceps. Hp positive examinees were subjected to one of four therapy protocols for eradication of Hp. The acquired data were treated with application of descriptive statistical methods (SV, SD , Min, MAX) and analytical statistical methods (Student t test, Hi quadrat test, Kruskal-Walish test, Mann-Whitny U-test, Wilcoxon test, ANOVA variant analysis, Spearman and Pearson correlation). 250 examinees tested by quick urease test (QUT), 54% were positive and 46% were negative (p>0.05). The proportion by genders between QUT positives and QUT negatives was approximately the same (p>0.05). Non-ulcer gastropathy was a dominant finding with both QUT negatives (92.2%) and QUT positives (77%) (p<0.01). The highest rate of eradication of Helicobacter pylori infection was shown by protocols B and D (75%), then protocol A (71%) and protocol C (57.2%) (p>0.05). Quick urease test (QUT) which requires upper digestive endoscopy and biopsy of stomach epithelia samples represents a minimum of invasive diagnostics of Helicobacter pylori infection and a minimum of confirmation of eradication in our conditions. Therapeutic protocols B and D have shown the highest rate of success in eradication with our patients.

Effect of Concomitant18O in13C-Urea on the Urea breath test

Helicobacter pylori infection in stomach has been extensively assessed by the 13C-urea breath test (UBT) with infra-red or mass spectrometer. However, analyses of commercially available 13C-urea for UBT showed about 10 atom% of 18O abundance. It is therefore very important to investigate the 18O-isotope effect on UBT. Using a mass spectrometer, breath samples of UBT were analyzed to investigate the change of mass spectra by the isotopic exchange reaction between 18O of carbon dioxide and 16O of water. As the result, the 18O content of 13C, 18O-carbon dioxide exhaled in UBT reached its natural abundance level immediately after the administration of 13C, 18O-urea. It was concluded that the 18O content of 13C, 18O-urea has no effect on UBT using either infra-red or mass spectroscopy. Copyright © 2000 John Wiley & Sons, Ltd.