{"title":"A Bidirectional Association Between Helicobacter pylori Infection and Hyperlipidemia: Clinical Evidence and Mechanistic Insights.","authors":"Yan'an Zhou, Yuchen Zhu, Shuai Li, Zekun He, Yao Zhang, Zonglei Wang, Cong He, Hongtao Zhu, Nianshuang Li, Junming Li, Junyun Feng, Xiao Fei, Xingxing He, Huan Wang, Da Gan, Xia Huang, Nonghua Lv, Yuhui Wang, Wenhua He, Xidong Wu, Yin Zhu, Jianping Liu","doi":"10.1111/hel.70135","DOIUrl":"10.1111/hel.70135","url":null,"abstract":"<p><strong>Background and aims: </strong>Helicobacter pylori is a persistent gastric microbe with systemic consequences beyond the stomach, yet its contribution to host lipid dysregulation remains unclear.</p><p><strong>Methods: </strong>We analyzed clinical data from 57,295 adults with documented H. pylori status and detailed lipid profiles, including the non-HDL-C to HDL-C ratio (NHHR). Mechanistic validation was performed using in vitro and in vivo H. pylori PMSS1 infection models, combined with single-cell RNA sequencing, molecular analyses, histopathology, and lipidomics.</p><p><strong>Results: </strong>Helicobacter pylori infection was associated with increased LDL cholesterol and triglycerides, reduced HDL cholesterol, and elevated NHHR, which independently predicted hyperlipidemia risk. At the mechanistic level, H. pylori infection consistently suppressed gastric expression of Gpihbp1, a key mediator of lipoprotein lipase-dependent lipid transport. Infected mice developed systemic hyperlipidemia and exhibited lipidomic remodeling characterized by glycerolipid accumulation and reduced phosphatidylcholine species. Importantly, genetic deficiency of Gpihbp1 promoted gastric H. pylori colonization and exacerbated mucosal inflammation, revealing a reciprocal interaction between host lipid metabolism and bacterial persistence.</p><p><strong>Conclusion: </strong>These findings define a microbiota-host lipid transport axis linking chronic H. pylori infection to dyslipidemia and suggest that integrated targeting of microbial infection and metabolic dysfunction may offer therapeutic benefit.</p>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"31 3","pages":"e70135"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147947953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HelicobacterPub Date : 2026-05-01DOI: 10.1111/hel.70130
Xujin Chen, Dehua Tang, Ningjing Gao, Muhan Ni, Peng Yan, Zhanwen Ji, Xiang Xin, Cheng Yang, Lei Wang, Qiang Zhan
{"title":"Incorporating Helicobacter pylori Infection: A Novel Model for Predicting Advanced Colorectal Neoplasia.","authors":"Xujin Chen, Dehua Tang, Ningjing Gao, Muhan Ni, Peng Yan, Zhanwen Ji, Xiang Xin, Cheng Yang, Lei Wang, Qiang Zhan","doi":"10.1111/hel.70130","DOIUrl":"10.1111/hel.70130","url":null,"abstract":"<p><strong>Background and aims: </strong>Early detection of advanced colorectal neoplasia (ACN) is critical for reducing colorectal cancer (CRC) incidence and mortality. Existing prediction models exhibit limited discriminative power. This study aimed to develop and internally validate a novel risk prediction model for ACN, with particular emphasis on incorporating gastric-related indicators to enable integrated gastrointestinal tumor screening.</p><p><strong>Methods: </strong>Consecutive patients who underwent concurrent gastroscopy and colonoscopy for screening, symptomatic assessment, or surveillance purposes were recruited from the endoscopy center between January 1, 2021, and December 31, 2023. Comprehensive data including demographic characteristics, family history, Helicobacter pylori (H. pylori) infection status, and gastric histopathological results were collected. Patients with incomplete data were excluded a priori with no imputation. Candidate variables were selected using Elastic Net and LASSO regression to develop the prediction model. The model was trained on 80% of the data (n = 2045) and internally validated on the remaining 20% (n = 495).</p><p><strong>Results: </strong>Among 2540 participants [mean age 59.0 years; 1269 males (50.0%)], the overall prevalence of ACN was 13.1% (333/2540). The final Elastic Net model incorporated eight variables, with H. pylori infection as the strongest predictor. In the internal validation cohort, the model achieved an area under the curve (AUC) of 0.837 (95% CI: 0.781-0.892), with 75.8% sensitivity, 82.2% specificity, and 81.4% accuracy. Calibration metrics showed good agreement between predicted and observed ACN risks (Brier score = 0.103; calibration plots showed non-significant deviation from perfect calibration). It significantly outperformed the Asia-Pacific Colorectal Screening (APCS) score (AUC = 0.622), its revised edition (AUC = 0.589), and the Colorectal Tumor Prediction Score (AUC = 0.570) (all p < 0.001, DeLong's test). Using the model's optimal cutoff, 25.1% (124/495) of the internal validation cohort were stratified as high-risk, with an ACN detection rate of 37.9%. The number of participants needed to screen (PNS) to detect one ACN case was only 3 in the high-risk group, compared with 25 in the low-risk group, thus demonstrating markedly improved screening efficiency.</p><p><strong>Conclusions: </strong>This study develops and internally validates a risk prediction model for ACN that integrates gastric-related indicators, with H. pylori infection as the key predictor. The model exhibits promising retrospective risk stratification performance in patients undergoing concurrent gastroscopy and colonoscopy for screening, symptomatic assessment, or surveillance. It enables retrospective risk assessment during routine endoscopy, but its clinical utility for guiding prospective colonoscopy referral decisions requires further validation in prospective cohorts.</p>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"31 3","pages":"e70130"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13173598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147941313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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