Pylori-associated Gastric Ulcer Research Articles

Time trends in the prevalence of Helicobacter pylori infection in patients with peptic ulcer disease: a single-center retrospective study in Shanghai.

ObjectiveThe present study aimed to investigate the recent trends in Helicobacter pylori infection associated with peptic ulcer disease in a large population in Shanghai.MethodsWe analyzed the medical records of all patients who had undergone upper gastrointestinal endoscopy (EGD) for uninvestigated dyspepsia at Ren Ji Hospital between 2013 and 2019 to determine the prevalence of H. pylori infection in patients with peptic ulcers.ResultsPeptic ulcers were found in 40,385 of the 383,413 patients who underwent EGD during the study period. Over the 7-year study period, the annual prevalence of H. pylori among patients receiving EGD declined from 32.2% to 26.5%. H. pylori was present in 60% of ulcers and the incidence was higher (66.9%) in duodenal compared with gastric ulcers (48.5%). The proportion of H. pylori-associated gastric ulcers declined from 52.2% to 49.3% and that of H. pylori-positive duodenal ulcers declined from 70.0% to 63.9%.ConclusionThe prevalence of H. pylori-positive peptic ulcers, mainly duodenal ulcers, fell from 2013 to 2019. However, the proportion of non-H. pylori-associated peptic ulcer disease increased, especially in elderly people, possibly due to the use of nonsteroidal anti-inflammatory drugs. Further research is needed to confirm this hypothesis.

Diagnosis and treatment of Helicobacter pylori infection with gastric ulceration: a case report

Helicobacter pylori bacteria can infect the gastrointestinal tract, with the potential to cause causing gastritis, peptic ulcer disease and/or gastric cancer. There are various diagnostic tools for H. pylori, with invasive gastroscopic biopsy as the gold standard. Infection can be eradicated with a combination of omeprazole, amoxicillin and clarithromycin. This article presents a case study of a 56-year-old woman who was diagnosed with an H. pylori-associated gastric ulcer and successfully treated with triple eradication therapy. It also explores the pathophysiology of H. pylori, covering its mechanisms of mobility, pH regulation and adhesion, as well as its virulence, expression of cytotoxins and potential progression to cancer.

Перспективы применения препаратов висмута в терапии H. pylori-ассоциированной язвенной болезни желудка у лиц, получающих цитостатическую терапию

Перспективы применения препаратов висмута в терапии H. pylori-ассоциированной язвенной болезни желудка у лиц, получающих цитостатическую терапию

Engineering bioinspired bacteria-adhesive clay nanoparticles with a membrane-disruptive property for the treatment of Helicobacter pylori infection.

We present a bioinspired design strategy to engineer bacteria-targeting and membrane-disruptive nanoparticles for the effective antibiotic therapy of Helicobacter pylori (H. pylori) infection. Antibacterial nanoparticles were self-assembled from highly exfoliated montmorillonite (eMMT) and cationic linear polyethyleneimine (lPEI) via electrostatic interactions. eMMT functions as a bioinspired 'sticky' building block for anchoring antibacterial nanoparticles onto the bacterial cell surface via bacteria-secreted extracellular polymeric substances (EPS), whereas membrane-disruptive lPEI is able to efficiently lyse the bacterial outer membrane to allow topical transmembrane delivery of antibiotics into the intracellular cytoplasm. As a result, eMMT-lPEI nanoparticles intercalated with the antibiotic metronidazole (MTZ) not only efficiently target bacteria via EPS-mediated adhesion and kill bacteria in vitro, but also can effectively remain in the stomach where H. pylori reside, thereby serving as an efficient drug carrier for the direct on-site release of MTZ into the bacterial cytoplasm. Importantly, MTZ-intercalated eMMT-lPEI nanoparticles were able to efficiently eradicate H. pylori in vivo and to significantly improve H. pylori-associated gastric ulcers and the inflammatory response in a mouse model, and also showed superior therapeutic efficacy as compared to standard triple therapy. Our findings reveal that bacterial adhesion plays a critical role in promoting efficient antimicrobial delivery and also represent an original bioinspired targeting strategy via specific EPS-mediated adsorption. The bacteria-adhesive eMMT-lPEI nanoparticles with membrane-disruptive ability may constitute a promising drug carrier system for the efficacious targeted delivery of antibiotics in the treatment of bacterial infections.

The role apoptosis in dysregulations of lokal and system immunitet at the Helicobacter pilory-infection

The level of intracellular apoptosis regulators (cell death antagonists (Bcl-2) and agonists (CPP-32)), proliferation antigen Ki67 in lymphocytes of biopsy materials of the mucous coat of stomach at Helicobacter pylori-associated gastric ulcer and chronic gastritis in Khakassian aboriginal population and newcomers have been studied. The lymphocyte apoptosis in peripheral blood in aboriginal population was assessed. Changes in immunological indices were revealed in patients infected with Helicobacter pylori compared to healthy donors and newcomers. These changes were characterized by the more intense apoptotic lymphocyte death compared to the number of such cells in patients with chronic gastritis and in the control group. The role of apoptosis disfunctions in the regulation of local and system immunity at Helicobacter pylori infection is discussed.

DEVELOPMENT OF SPORADIC GASTRIC FUNDIC GLAND POLYP AFTER ERADICATION OF HELICOBACTER PYLORI

The pathogenesis of sporadic gastric fundic gland polyps (FGP) without familial adenomatous polyposis remains unclear. However, development of FGP is associated with normal gastric mucosa without Helicobacter pylori infection. We report two cases of FGP newly developed after successful eradication therapy of H. pylori infection. H. pylori-associated gastric ulcers occurred in the two patients; H. pylori eradication was performed in the patients and was successful. The patients have not received medication of long-term proton pump inhibitors. Follow-up gastrointestinal endoscopy demonstrated a FGP in the fundus of the stomach of each patient after eradication therapy. Regression of sporadic FGP can be observed to coincide with the acquisition of H. pylori infection. Conversely, the present cases demonstrated that the curing of H. pylori infection could lead to the development of FGP.

Helicobacter pylori Infection with a Duodenal Ulcer in a 6-year-old Boy

A 6-year-old boy was hospitalized because of dark feces and facial pallor of 1 weeks duration. Other gastrointestinal symptoms, including vomiting and abdominal pain, were absent, but he felt dizziness when standing and fatigue on effort. Hematologic studies revealed iron-deficiency anemia, and endoscopy showed gastric erosions and a duodenal ulcer. All test results for Helicobacter pylori infection, including H. pylori antigen in stool, anti-H. pylori IgG immunoassay in serum, and the (13)C-urea breath test, were positive. Because an H. pylori-associated gastric ulcer had been diagnosed with endoscopy in the patients father 3 years earlier, father-son transmission was suspected. The patient was treated with triple-agent eradication therapy (proton pump inhibitor [lansoprazol], amoxicillin, and clarithromycin) for 2 weeks. One month after therapy was completed, eradication of H. pylori was confirmed by negative results on the stool antigen test. Peptic ulcer disease can occur in young children, as in this case. The stool antigen test kit is a useful and reliable method that can be used even in preschool children to diagnose H. pylori infection.

Helicobacter pylori-Associated Gastric Ulcer Exhibits Enhanced Mucosal Chemokine Activity at the Ulcer Site

Background and Aim: Although mucosal α- and β-chemokines are considered to be involved in the pathogenesis of Helicobacter pylori-associated gastritis, little is known how these chemokines are related to the ulcerogenesis in peptic ulcer patients. We examined the levels of interleukin (IL)-8 and macrophage inflammatory protein-1α (MIP-1α) in organ cultures and the numbers of inflammatory cells infiltrating the lamina propria by using the mucosal tissues obtained from gastric ulcer (GU) patients with and without H. pylori infection. Methods: Levels of IL-8 and MIP-1α secreted in organ cultures were measured by an enzyme-linked immunosorbent assay. Numbers of myeloperoxidase-positive neutrophils, CD68-positive macrophages, and mononuclear cells were determined in tissue sections. Results: The mucosal tissues of both the gastric antrum and the ulcer site obtained from patients with H. pylori-positive GU showed significantly higher levels of IL-8 and MIP-1α and increased numbers of inflammatory cells compared with the corresponding mucosal tissues from those with H. pylori-negative GU or the antral mucosal tissues from H. pylori-negative controls. When the values were compared between the mucosal tissues from the gastric antrum and those from the ulcer site, the latter group of tissues showed significantly higher levels of IL-8 and MIP-1α and increased numbers of neutrophils and macrophages than the former group regardless of its healing process in patients with H. pylori-positive GU. Conclusion: Mucosal α- and β-chemokines may be important to the ulcerogenesis in H. pylori-associated GU disease.

The evaluation of tissue kallikrein in Helicobacter pylori-associated gastric ulcer disease

Helicobacter pylori (Hp) associated ulcer disease is a common form of gastric disorder involving mucosal damage and invasion of the mucosa by polymorphic inflammatory cells with concomitant changes in the epithelial cell structure. The bacteria are thought to adhere by specific junction zones to the epithelial cell surface resulting in the degeneration of the mucosal layer. Our study was undertaken to examine the relative status of tissue kallikrein (TK) in antral and fundic biopsies, endoscopically obtained from 10 patients suspected of having gastric disorders. For histological evidence of inflammation the tissue was stained with hematoxylin and eosin and classified as mild, active, chronic and chronic active gastritis. Hp infection was determined by Giemsa staining. For localisation of TK, slide-mounted tissue sections were subjected to PAP and immunofluorescent staining using a goat anti-human TK IgG antibody. The results revealed that in the antral control tissue, removed during partial antractomy, TK was immunovisualised along the luminal border of the deep pyloric glands. The surface epithelia and superficial glands showed no labelling. The fundic control tissue revealed an absence of TK in the superficial and surface epithelial glands, but was positive in the parietal cells. The fundic biopsy specimens showed similar immunoreactivity in these areas. By contrast, in the inflammed pyloric mucosa, there was a shift of TK localisation to the basal part of the glandular cells and there was also expression of TK in the superficial glands that showed histological evidence of regeneration. In the fundic biopsies there was no change observed in the sites of TK localisation (similar to control tissue). It was observed, that even though 8 of the 10 subjects exhibited Hp infection, the inflamed mucosa showed no discernable difference in the staining patterns between the infected and non-infected tissue sections. Our findings suggest an important role for a B1/B2 kinin antagonist in patients with gastritis.

One week??s antibacterial therapy heals H. pylori-associated gastric ulcers

One week??s antibacterial therapy heals H. pylori-associated gastric ulcers

Long-Term Consequences ofHelicobacter pyloriEradication

Long-term infection with Helicobacter pylori could potentially lead to asymptomatic chronic gastritis, chronic dyspepsia, duodenal ulcer disease, gastric ulcer disease, or gastric malignancy, including both adenocarcinoma and B-cell lymphoma. Currently, the two most important indications for eradication of this bacterium are proven H. pylori-associated duodenal or gastric ulcer disease. Many studies have shown that successful eradication of H. pylori dramatically reduces the rate of duodenal ulcer relapse, and long-term follow-up data appear to support the claim 'no H. pylori, no gastritis; no gastritis, no ulcer', which follows on from the old, but certainly valid, dictum 'no acid, no ulcer'. Furthermore, absence of relapse parallels the marked improvement in gastric histology (e.g. regression of gastritis). Whether there is concomitant regression of gastric metaplasia in the duodenal bulb is, however, controversial. Despite the rather limited data for H. pylori-associated gastric ulcer, successful eradication of the organism has been equated with cure of peptic ulcer disease. Again, eradication parallels a substantial improvement in gastric histology. Although eradication of H. pylori is not currently recommended in asymptomatic individuals or dyspeptics, it has been well documented in previous studies that successful eradication improves the gastric histology in patients with H. pylori-associated dyspepsia. From these studies, it appears that the disappearance of polymorphs from the inflammatory infiltrate occurs rather rapidly after eradication, although regression of the mononuclear component of the inflammatory reaction is more prolonged.