Current Perspectives in Atrophic Gastritis

Lahner, Edith; Conti, Laura; Annibale, Bruno; Corleto, Vito D.

doi:10.1007/s11894-020-00775-1

Cited by 38 publications

(30 citation statements)

References 86 publications

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“…Atrophic gastritis is the first step in Correa's cascade [36]. Pathologically, original gastric glands are replaced by intestinal metaplasia and pseudopyloric metaplasia, with or without fibrosis [37]. Li et al [27] demonstrated that intestinal metaplasia was most prevalent among patients with H. pylori infection and a high bile acid concentration in the gastric juice.…”

Section: Discussionmentioning

confidence: 99%

Pyloric Incompetence Associated with Helicobactor pylori Infection and Correlated to the Severity of Atrophic Gastritis

et al. 2022

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Duodenogastric reflux (DGR) causes bile reflux gastritis (BRG) and may develop into gastric cancer. DGR is classified as primary in non-operated stomachs or secondary to surgical intervention. Primary DGR and Helicobacter pylori (H. pylori) infection are reportedly related. However, the mechanism is not fully understood. This study aimed to elucidate the relationship between H. pylori infection and pyloric incompetence in a non-operated stomach. A total of 502 non-operated participants who underwent an upper intestinal endoscopy were prospectively enrolled. Endoscopic findings (EAC, endoscopic atrophy classification; nodular gastritis; xanthoma; fundic gland polyp; and incompetence of pylorus), sex, age, gastrin, pepsinogen (PG) I and PG II levels were evaluated. PG I/PG II ratio, anti-H. pylori-Ab positivity, and atrophic gastritis status were significantly different between the normal and incompetent pylori (p = 0.043, <0.001, and 0.001, respectively). Open-type atrophic gastritis was significantly higher in the incompetent pylori. Incompetence of the pylorus and EAC were moderately correlated (Cramer’s V = 0.25). Multivariate analysis revealed that the presence of anti-H. pylori-Ab was the only independent factor associated with the incompetence of the pylorus, with an adjusted odds ratio of 2.70 (95% CI: 1.47–4.94, p = 0.001). In conclusion, pyloric incompetence was associated with H. pylori infection and moderately correlated to the severity of atrophic gastritis in non-operated stomachs.

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Section: Discussionmentioning

confidence: 99%

Pyloric Incompetence Associated with Helicobactor pylori Infection and Correlated to the Severity of Atrophic Gastritis

et al. 2022

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“…In the general population, there is an age-related increase in the prevalence of PCA, from 2.5% in the third decade to 12% in the eighth decade (6,7). The prevalence is markedly higher in those affected by other autoimmune disorders, frequently accompanied by pernicious anemia (PA) (8)(9)(10). Thus, in patients with type 1 diabetes mellitus (DM1), PCAs are found in 10-15% of children and in 15-25% of adults (11)(12)(13).…”

Section: Abstract Background/aim: To Estimate the Prevalence Of Autoi...mentioning

confidence: 99%

Non-invasive Screening of Autoimmune Atrophic Gastritis in Asymptomatic Subjects by Serological Biomarker Test (GastroPanel^®)

et al. 2022

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“…Changes in the microbiome in response to H. pylori infection are responsible for various gastric pathologies as bacterial overgrowth is closely associated with the changes in gastric atrophy and decreased gastric acidity (Huang et al, 2020;Lahner et al, 2020;Stewart et al, 2020;Ye et al, 2020). Although not clearly defined, overt changes in the intestinal microbiota do occur as the gastric pathology progresses toward atrophic gastritis.…”

Section: Changes In the Microbiome Reflect The Rejuvenation Of H Pylori-associated Atrophic Gastritis In Response To Pd-msc Treatmentmentioning

confidence: 99%

Rejuvenation of Helicobacter pylori–Associated Atrophic Gastritis Through Concerted Actions of Placenta-Derived Mesenchymal Stem Cells Prevented Gastric Cancer

2021

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Chronic Helicobacter pylori infection causes gastric cancer via the progression of precancerous chronic atrophic gastritis (CAG). Therefore, repairing gastric atrophy could be a useful strategy in preventing H. pylori–associated gastric carcinogenesis. Although eradication of the bacterial pathogen offers one solution to this association, this study was designed to evaluate an alternative approach using mesenchymal stem cells to treat CAG and prevent carcinogenesis. Here, we used human placenta-derived mesenchymal stem cells (PD-MSCs) and their conditioned medium (CM) to treat H. pylori–associated CAG in a mice/cell model to explore their therapeutic effects and elucidate their molecular mechanisms. We compared the changes in the fecal microbiomes in response to PD-MSC treatments, and chronic H. pylori–infected mice were given ten treatments with PD-MSCs before being sacrificed for end point assays at around 36 weeks of age. These animals presented with significant reductions in the mean body weights of the control group, which were eradicated following PD-MSC treatment (p < 0.01). Significant changes in various pathological parameters including inflammation, gastric atrophy, erosions/ulcers, and dysplastic changes were noted in the control group (p < 0.01), but these were all significantly reduced in the PD-MSC/CM-treated groups. Lgr5+, Ki-67, H+/K+-ATPase, and Musashi-1 expressions were all significantly increased in the treated animals, while inflammatory mediators, MMP, and apoptotic executors were significantly decreased in the PD-MSC group compared to the control group (p < 0.001). Our model showed that H. pylori–initiated, high-salt diet–promoted gastric atrophic gastritis resulted in significant changes in the fecal microbiome at the phylum/genus level and that PD-MSC/CM interventions facilitated a return to more normal microbial communities. In conclusion, administration of PD-MSCs or their conditioned medium may present a novel rejuvenating agent in preventing the progression of H. pylori–associated premalignant lesions.

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Current Perspectives in Atrophic Gastritis

Cited by 38 publications

References 86 publications

Pyloric Incompetence Associated with Helicobactor pylori Infection and Correlated to the Severity of Atrophic Gastritis

Pyloric Incompetence Associated with Helicobactor pylori Infection and Correlated to the Severity of Atrophic Gastritis

Non-invasive Screening of Autoimmune Atrophic Gastritis in Asymptomatic Subjects by Serological Biomarker Test (GastroPanel^®)

Rejuvenation of Helicobacter pylori–Associated Atrophic Gastritis Through Concerted Actions of Placenta-Derived Mesenchymal Stem Cells Prevented Gastric Cancer

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Current Perspectives in Atrophic Gastritis

Cited by 38 publications

References 86 publications

Pyloric Incompetence Associated with Helicobactor pylori Infection and Correlated to the Severity of Atrophic Gastritis

Pyloric Incompetence Associated with Helicobactor pylori Infection and Correlated to the Severity of Atrophic Gastritis

Non-invasive Screening of Autoimmune Atrophic Gastritis in Asymptomatic Subjects by Serological Biomarker Test (GastroPanel®)

Rejuvenation of Helicobacter pylori–Associated Atrophic Gastritis Through Concerted Actions of Placenta-Derived Mesenchymal Stem Cells Prevented Gastric Cancer

Contact Info

Product

Resources

About

Non-invasive Screening of Autoimmune Atrophic Gastritis in Asymptomatic Subjects by Serological Biomarker Test (GastroPanel^®)