Evidence map›Paper›PMID 40455334›Full record

ArticleJournal of molecular histology2025

Helicobacter pylori VacA-induced gastric mucosal atrophy: a comparative analysis with other forms of atrophic gastritis.

Yang-Kun Wang, Wen-Rui Chen, Ling-Yan Lu, Ying-Ying Li, Rui-Kun Qiu, Chao-Ya Zhu, Fa-Shun Zhang, Su-Nan Wang, Si-Liang Xu

Abstract readComparative Study
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In one paragraph

Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Yang-Kun Wang *Department of Pathology, The Fourth People's Hospital of Longgang District, Shenzhen, 518123, China.
Wen-Rui Chen *Department of Pathology, The Fourth People's Hospital of Longgang District, Shenzhen, 518123, China.
Ling-Yan LuDepartment of Pathology, The Fourth People's Hospital of Longgang District, Shenzhen, 518123, China.
Ying-Ying LiShenzhen Polytechnic University, Xili Lake, Xilihu Town, Nanshan District, Shenzhen, 518055, China.
Rui-Kun QiuDongshan Hospital, Meizhou , 514021, Guangdong Province, China.
Chao-Ya ZhuDepartment of Pathology, Third Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Fa-Shun ZhangDepartment of Pathology, Xuchang Central Hospital, Xuchang, 461000, Henan Province, China.
Su-Nan WangShenzhen Polytechnic University, Xili Lake, Xilihu Town, Nanshan District, Shenzhen, 518055, China. mwangsunan@163.com.
Si-Liang XuDepartment of Pathology, The Fourth People's Hospital of Longgang District, Shenzhen, 518123, China. siliangxu_xu@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to evaluate the atrophic changes induced by Helicobacter pylori VacA and compare them with other forms of atrophic gastritis.A comprehensive histomorphological analysis and immunohistochemical evaluation were performed on 984 endoscopic gastric mucosal biopsy samples from patients with endoscopically confirmed atrophic gastritis. H. pylori primarily adheres to surface mucus cells, where it proliferates and produces the vacuolating cytotoxin VacA. The underlying mechanism involves VacA inducing the upward migration and compensatory proliferation of cells located in the deeper regions of gastric pits, the isthmus of gastric glands, and the neck mucous cells, ultimately leading to gastric atrophy. In this study, a comparative analysis was performed with autoimmune atrophy, degenerative denaturation atrophy, drug-induced atrophy, and non-specific atrophy. Both clinical and histological characteristics were evaluated, and pathological diagnostic criteria for mucosal atrophy were proposed for the first time. Of the 984 cases examined, H. pylori-induced atrophic gastritis was identified in 648 cases, accounting for 65.9% (648/984); autoimmune atrophy in 34 cases, representing 3.5% (34/984); degenerative denaturation atrophy in 59 cases, representing 6.0% (59/984); drug-induced atrophy in 72 cases, making up 7.3% (72/984); and non-specific atrophy in 171 cases, accounting for 17.4% (171/984). H. pylori infection was found to be associated with a high prevalence of infectious atrophy, accompanied by active epithelial cell proliferation, intraepithelial neoplasia, early changes in mucosa-associated lymphoid tissue lymphoma, and cell proliferation outside the lymphatic follicular mantle. The comparative analysis of gastric mucosal atrophy induced by H. pylori VacA, in comparison to other forms of atrophic gastritis, is crucial for understanding the pathogenesis of gastric cancer and improving management strategies for its prevention and progression.

Indexed as

Bacterial ProteinsGastric MucosaGastritis, AtrophicHelicobacter InfectionsHelicobacter pyloriAdultAgedAtrophyFemaleHumansMaleMiddle AgedBacterial ProteinsVacA protein, Helicobacter pyloriGastric tumorHistologyImmunohistochemistryMucosal atrophyPathological diagnosis

Identifiers

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.