Song JJ, Li N, Yu YW, Liu S. Letter to the Editor: Helicobacter pylori eradication restores aspirin responsiveness - a thromboinflammatory interpretation. World J Gastroenterol 2026; 32(36): 120338 [DOI: 10.3748/wjg.120338]
Corresponding Author of This Article
Yong-Wei Yu, Academic Fellow, Department of Intensive Care Unit, The First Affiliated Hospital, Zhejiang University School of Medicine, No. 79 Qingchun Road, Shangcheng District, Hangzhou 310003, Zhejiang Province, China. yuyongwei@zju.edu.cn
Research Domain of This Article
Cardiac & Cardiovascular Systems
Article-Type of This Article
letter
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Share the Article
Song JJ, Li N, Yu YW, Liu S. Letter to the Editor: Helicobacter pylori eradication restores aspirin responsiveness - a thromboinflammatory interpretation. World J Gastroenterol 2026; 32(36): 120338 [DOI: 10.3748/wjg.120338]
World J Gastroenterol. Sep 28, 2026; 32(36): 120338 Published online Sep 28, 2026. doi: 10.3748/wjg.120338
Letter to the Editor: Helicobacter pylori eradication restores aspirin responsiveness - a thromboinflammatory interpretation
Jian-Jiang Song, Ning Li, Yong-Wei Yu, Shuai Liu
Jian-Jiang Song, Shuai Liu, Department of Cardiology, The First People’s Hospital of Jiashan, Jiaxing 314100, Zhejiang Province, China
Ning Li, Department of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China
Yong-Wei Yu, Department of Intensive Care Unit, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China
Co-corresponding authors: Yong-Wei Yu and Shuai Liu.
Author contributions: Song JJ and Li N wrote the manuscript and performed literature collection. Yu YY and Liu S conceptualized and designed the study framework, critically revised the manuscript, and supervised the overall scientific content. Yu YY focused on the mechanistic interpretation and integration of thromboinflammatory pathways, whereas Liu S supervised the clinical relevance and overall academic direction of the manuscript. Both corresponding authors played important and indispensable roles in study design, scientific interpretation, and manuscript revision, and therefore qualify as co-corresponding authors. All listed authors have read and approved the final manuscript and consented to the submission.
AI contribution statement: Google Translate was used during manuscript preparation solely for language translation assistance. ChatGPT (Open AI) was used for limited grammar refinement and structural optimization of the text. In addition, AI-assisted tools were used only for preliminary conceptual layout reference during figure preparation. The final figure was manually created and revised by the authors, including modifications based on reviewer comments. The manuscript subsequently underwent professional language editing by Editage. No AI tool was involved in study design, data generation, data analysis, interpretation of results, formulation of conclusions, or reference generation. All AI-assisted outputs were critically reviewed, manually revised, and verified by the authors, who take full responsibility for the accuracy, originality, and integrity of the manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Yong-Wei Yu, Academic Fellow, Department of Intensive Care Unit, The First Affiliated Hospital, Zhejiang University School of Medicine, No. 79 Qingchun Road, Shangcheng District, Hangzhou 310003, Zhejiang Province, China. yuyongwei@zju.edu.cn
Received: February 24, 2026 Revised: April 15, 2026 Accepted: May 26, 2026 Published online: September 28, 2026 Processing time: 178 Days and 23.6 Hours
Abstract
This letter comments on the recent prospective study by Semeya et al in the World Journal of Gastroenterology showing that Helicobacter pylori (H. pylori) eradication reduces peptic ulcer bleeding and cardiovascular progression in chronic aspirin users. While the original authors attributed the cardiovascular benefit mainly to attenuation of inflammation-driven atherosclerosis, the short follow-up period and event-based endpoints suggest an alternative interpretation. We propose that the observed benefit may instead reflect restoration of aspirin responsiveness through resolution of infection-driven thromboinflammation. Persistent H. pylori infection may promote systemic inflammatory signaling, accelerate platelet turnover, increase reticulated platelets, and amplify platelet activation, thereby weakening effective cyclooxygenase-1 inhibition and producing functional aspirin resistance. Eradication may therefore normalize platelet pharmacodynamics without requiring short-term structural plaque regression. This hypothesis-generating interpretation links infection biology with antiplatelet variability and may help explain the rapid divergence in cardiovascular outcomes observed after eradication.
Core Tip: Helicobacter pylori infection may influence cardiovascular outcomes beyond peptic ulcer disease, particularly in chronic aspirin users. Persistent infection can sustain a thromboinflammatory state that increases platelet turnover and reactivity, thereby weakening effective cyclooxygenase-1 inhibition and producing functional aspirin resistance. We propose that the apparent cardiovascular benefit after eradication may reflect pharmacologic resensitization rather than short-term vascular remodeling. This hypothesis-generating perspective links infection biology with antiplatelet pharmacodynamics and may help explain inter-individual variability in aspirin efficacy.
