Limited research has explored the efficacy of reduced amoxicillin dosages in vonoprazan-amoxicillin (VA) dual therapy for Helicobacter pylori eradication in China, and this study aimed to assess the noninferiority of these lower dosages compared to the standard high dose (3 g/d).
Methods
This was a noninferiority study with a −10% margin. H. pylori-positive patients from 13 centers in Jiangsu Province, China, were randomly assigned in a 1:1:1 ratio to receive a 14-day treatment, consisting of vonoprazan (20 mg BID) and high-dose amoxicillin (1 g TID, HVA), medium-dose amoxicillin (1 g BID, MVA), or low-dose amoxicillin (0.5 g TID, LVA). The eradication rates, adverse events (AEs), and medication adherence were compared.
Results
From January 13, 2023 to July 6, 2024, a total of 900 patients were enrolled. According to the intention-to-treat (ITT) and per-protocol (PP) analyses, the eradication rates for HVA, MVA, and LVA groups were 93.2% and 93.2%, 91.6% and 91.5%, and 87.0% and 86.8%, respectively. The efficacy of MVA was noninferior to HVA in ITT analysis (difference: −1.6%, 97.5% CI: −7.0% to 3.8%, p < 0.001) and PP analysis (difference: −1.7%, 97.5% CI: −7.1% to 3.7%, p < 0.001); LVA's effectiveness was less than HVA in ITT analysis (difference: −6.2%, 97.5% CI: −12.2% to −0.2%, p = 0.076) and PP analysis (difference:-6.4%, 97.5% CI: −12.4% to −0.3%, p = 0.089). The incidence of AEs and medication compliance among the three groups was similar.
Conclusions
A 14-day VA regimen requires ≥ 2 g/d amoxicillin to maintain noninferior eradication efficacy versus 3 g/d, supporting dose reduction without compromising effectiveness.
{"title":"Efficacy of Three Amoxicillin Doses in Vonoprazan Dual Therapy for Helicobacter pylori Eradication: A Randomized Noninferiority Trial","authors":"Ruolin Peng, Pengpeng Cai, Zhimei Zhang, Shengxiang Lv, Guangxia Chen, Yuling Xu, Bin He, Min Sun, Xiaorong Dai, Kunfeng Yan, Lu Shen, Jianrong Wang, Wei Li, Rui Yin, Jianxin Ge, Duanmin Hu, Kewei Hu, Xiaodan Xu, Hui Li, Chengyu Pan, Zhaotao Duan, Xuefeng Gao, Zhenyu Zhang, Wanli Liu","doi":"10.1111/hel.70050","DOIUrl":"https://doi.org/10.1111/hel.70050","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Limited research has explored the efficacy of reduced amoxicillin dosages in vonoprazan-amoxicillin (VA) dual therapy for <i>Helicobacter pylori</i> eradication in China, and this study aimed to assess the noninferiority of these lower dosages compared to the standard high dose (3 g/d).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This was a noninferiority study with a −10% margin. <i>H. pylori</i>-positive patients from 13 centers in Jiangsu Province, China, were randomly assigned in a 1:1:1 ratio to receive a 14-day treatment, consisting of vonoprazan (20 mg BID) and high-dose amoxicillin (1 g TID, HVA), medium-dose amoxicillin (1 g BID, MVA), or low-dose amoxicillin (0.5 g TID, LVA). The eradication rates, adverse events (AEs), and medication adherence were compared.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>From January 13, 2023 to July 6, 2024, a total of 900 patients were enrolled. According to the intention-to-treat (ITT) and per-protocol (PP) analyses, the eradication rates for HVA, MVA, and LVA groups were 93.2% and 93.2%, 91.6% and 91.5%, and 87.0% and 86.8%, respectively. The efficacy of MVA was noninferior to HVA in ITT analysis (difference: −1.6%, 97.5% CI: −7.0% to 3.8%, <i>p</i> < 0.001) and PP analysis (difference: −1.7%, 97.5% CI: −7.1% to 3.7%, <i>p</i> < 0.001); LVA's effectiveness was less than HVA in ITT analysis (difference: −6.2%, 97.5% CI: −12.2% to −0.2%, <i>p</i> = 0.076) and PP analysis (difference:-6.4%, 97.5% CI: −12.4% to −0.3%, <i>p</i> = 0.089). The incidence of AEs and medication compliance among the three groups was similar.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>A 14-day VA regimen requires ≥ 2 g/d amoxicillin to maintain noninferior eradication efficacy versus 3 g/d, supporting dose reduction without compromising effectiveness.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>ClinicalTrials.gov identifier: NCT05649540</p>\u0000 </section>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144232465","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}
Zhengchen Yu, Wenjuan Shen, Guochun Lou, Yan Li, Ziming Xie, Jun Ye
We appreciate the valuable comments and thoughtful critique offered by the reader regarding our study on tailored bismuth quadruple therapy based on fecal molecular susceptibility testing in first-line Helicobacter pylori eradication. In our response, we have sought to clarify the methodological rationale underlying our statistical analysis and terminology usage, particularly regarding superiority and non-inferiority testing. We have also addressed concerns regarding assessing prior macrolide exposure, outlining the practical considerations that informed our study design. We trust that our clarifications will help to elucidate the study's context and findings further, and we welcome continued academic dialogue on this important topic.
{"title":"Authors' Reply to the Letter on “Is Tailored Bismuth Quadruple Therapy (With Clarithromycin or Furazolidone) Based on Fecal Molecular Susceptibility Testing in First-Line Helicobacter pylori Eradication Treatment More Effective? A Three-Arm, Multicenter Randomized Clinical Trial”","authors":"Zhengchen Yu, Wenjuan Shen, Guochun Lou, Yan Li, Ziming Xie, Jun Ye","doi":"10.1111/hel.70049","DOIUrl":"https://doi.org/10.1111/hel.70049","url":null,"abstract":"<div>\u0000 \u0000 <p>We appreciate the valuable comments and thoughtful critique offered by the reader regarding our study on tailored bismuth quadruple therapy based on fecal molecular susceptibility testing in first-line <i>Helicobacter pylori</i> eradication. In our response, we have sought to clarify the methodological rationale underlying our statistical analysis and terminology usage, particularly regarding superiority and non-inferiority testing. We have also addressed concerns regarding assessing prior macrolide exposure, outlining the practical considerations that informed our study design. We trust that our clarifications will help to elucidate the study's context and findings further, and we welcome continued academic dialogue on this important topic.</p>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144220402","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}
Gastric Helicobacter species, including Helicobacter pylori and non-Helicobacter pylori Helicobacter (NHPH) species, are gram-negative fastidious bacteria that colonize the stomachs of both humans and animals such as pigs, dogs, cats, and monkeys. The H. pylori infection rate is decreasing due to improved living conditions and increased opportunities for H. pylori eradication therapy in developed countries. However, concerns about NHPH infection-induced gastric diseases are growing, especially low-grade gastric mucosa-associated lymphoid tissue lymphoma. Although NHPH infections have been reported for 30 years, especially H. suis infections, evidence of the correct infection rate, route of infection to humans, and direct and indirect associations with gastric diseases are insufficient. Presently, NHPH infection can be diagnosed using histopathological and immunohistochemical findings, polymerase chain reaction, culture tests, or enzyme-linked immunosorbent assays. Several basic and clinical studies have begun to report the bacteriologic characteristics and routes of NHPH infection. In addition, the high effectiveness of eradication therapy using a combination of an acid inhibitor and two types of antibiotics, which is the same eradication regimen for H. pylori infection, has been reported. However, evidence on antibiotic resistance, appropriate dosing dosage, or drug type provided by randomized control trials is lacking. Several issues regarding the etiology, virulence, diagnosis, and treatment of NHPH infections should be addressed in the future.
{"title":"Roles of Gastric Non-Helicobacter pylori Helicobacter Species in Gastric Disease Development: A Review","authors":"Mitsushige Sugimoto, Emiko Rimbara, Masaki Murata, Yoshio Yamaoka","doi":"10.1111/hel.70051","DOIUrl":"https://doi.org/10.1111/hel.70051","url":null,"abstract":"<div>\u0000 \u0000 <p>Gastric <i>Helicobacter</i> species, including <i>Helicobacter pylori</i> and non-<i>Helicobacter pylori Helicobacter</i> (NHPH) species, are gram-negative fastidious bacteria that colonize the stomachs of both humans and animals such as pigs, dogs, cats, and monkeys. The <i>H. pylori</i> infection rate is decreasing due to improved living conditions and increased opportunities for <i>H. pylori</i> eradication therapy in developed countries. However, concerns about NHPH infection-induced gastric diseases are growing, especially low-grade gastric mucosa-associated lymphoid tissue lymphoma. Although NHPH infections have been reported for 30 years, especially <i>H. suis</i> infections, evidence of the correct infection rate, route of infection to humans, and direct and indirect associations with gastric diseases are insufficient. Presently, NHPH infection can be diagnosed using histopathological and immunohistochemical findings, polymerase chain reaction, culture tests, or enzyme-linked immunosorbent assays. Several basic and clinical studies have begun to report the bacteriologic characteristics and routes of NHPH infection. In addition, the high effectiveness of eradication therapy using a combination of an acid inhibitor and two types of antibiotics, which is the same eradication regimen for <i>H. pylori</i> infection, has been reported. However, evidence on antibiotic resistance, appropriate dosing dosage, or drug type provided by randomized control trials is lacking. Several issues regarding the etiology, virulence, diagnosis, and treatment of NHPH infections should be addressed in the future.</p>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144206735","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}
<p>We read with great interest the article titled “Parietal Cell Antibody Levels Among Chronic Gastritis Patients in a Country with Low <i>Helicobacter pylori</i> Infection: Epidemiology, Histopathological Features, and <i>H. pylori</i> infection” by Amalia et al. [<span>1</span>]. In this study, the authors investigated the prevalence of autoimmune gastritis (AIG), and its association with <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection status and gastric histopathological features in the Indonesian population. Given the previously reported high incidence of gastritis and relatively low <i>H. pylori</i> infection rates in this region, exploring other causes of gastritis, such as AIG, is essential for improving diagnostic accuracy and guiding clinical risk management [<span>2</span>].</p><p>While the authors conducted a comprehensive analysis of parietal cell antibody (PCA) levels and its association with clinicopathological features, several aspects of the study's methodology and interpretation raise concerns and warrant further clarification. A key observation of this study is the reported 78.99% prevalence of PCA positivity among 113 Indonesian patients with chronic gastritis and 25 healthy controls, while only one patient was diagnosed with AIG. The authors suggest that this discrepancy might be due to <i>H. pylori</i>-associated immune activation. However, we think it may also reflect the combined impact of overly strict diagnostic criteria for AIG and the inappropriate interpretation of PCA results.</p><p>In the diagnostic methods, AIG was defined based on the PCA positivity, absence of <i>H. pylori</i> infection, histopathological features associated with AIG, and sparing of the antrum. We understand the concern that coexisting <i>H. pylori</i> infection may complicate the diagnosis of AIG, as it can cause histopathological changes that resemble AIG. But we note that neither antrum sparing nor negative <i>H. pylori</i>-negative status should be a required criterion for AIG diagnosis. Our previous findings have shown that AIG can coexist with <i>H. pylori</i> infection, and hence patients may present with antral inflammation or atrophy. Such patients still show characteristic serological features similar to AIG patients without <i>H. pylori</i> infection, including decreased pepsinogen (PG) I levels and elevated gastrin 17 [<span>3</span>]. Additionally, they may exhibit pathological findings such as enterochromaffin-like (ECL) cell hyperplasia [<span>4</span>], which was not investigated in the study by Amalia et al. Therefore, we think the criteria used may have led to underdiagnosis of AIG in the Indonesia cohort. Rather than excluding patients with <i>H. pylori</i> infection or antrum inflammation/atrophy, more specific diagnostic tests should be considered to improve the diagnosis of AIG, especially given this is the first study reporting AIG prevalence in this region.</p><p>Adding to these diagnostic challenges Beyond these di
我们饶有兴趣地阅读了Amalia等人的文章《幽门螺杆菌低感染率国家慢性胃炎患者的壁细胞抗体水平：流行病学、组织病理学特征和幽门螺杆菌感染》[b]。在这项研究中，作者调查了印尼人群中自身免疫性胃炎（AIG）的患病率及其与幽门螺杆菌（h.p ylori）感染状况和胃组织病理学特征的关系。鉴于先前报道的该地区胃炎发病率高，幽门螺杆菌感染率相对较低，探索其他胃炎原因，如AIG，对于提高诊断准确性和指导临床风险管理bbb至关重要。虽然作者对壁细胞抗体（PCA）水平及其与临床病理特征的关系进行了全面分析，但该研究方法和解释的几个方面引起了关注，需要进一步澄清。本研究的一个关键观察结果是，在113名印度尼西亚慢性胃炎患者和25名健康对照者中，PCA阳性率为78.99%，而只有1名患者被诊断为AIG。作者认为这种差异可能是由于幽门螺杆菌相关的免疫激活。然而，我们认为这也可能反映了AIG过于严格的诊断标准和对PCA结果的不适当解释的综合影响。在诊断方法中，AIG的定义是基于PCA阳性，没有幽门螺杆菌感染，AIG相关的组织病理学特征，以及保留上腔。我们了解并发幽门螺杆菌感染可能使AIG的诊断复杂化的担忧，因为它可以引起类似AIG的组织病理学改变。但我们注意到，无论是胃窦保留还是幽门螺杆菌阴性状态都不应作为AIG诊断的必要标准。我们之前的研究结果表明，AIG可以与幽门螺杆菌感染共存，因此患者可能出现胃窦炎症或萎缩。这类患者仍表现出与未感染幽门螺杆菌的AIG患者相似的血清学特征，包括胃蛋白酶原（PG） I水平降低和胃泌素水平升高。此外，它们还可能表现出肠色素样（ECL）细胞增生[4]等病理表现，Amalia等人并未对此进行研究。因此，我们认为所使用的标准可能导致印度尼西亚队列中AIG的诊断不足。而不是排除幽门螺杆菌感染或上腔炎症/萎缩的患者，更具体的诊断测试应考虑提高AIG的诊断，特别是考虑到这是第一个研究报告AIG在该地区的流行。除了这些诊断标准之外，本研究中用于检测PCA的方法也需要仔细考虑。Amalia等人使用间接免疫荧光抗体试验（IFT）检测PCA的存在，这是一种半定量方法，灵敏度高，但特异性有限。值得注意的是，近一半的患者具有临界PCA水平（10单位/mL，在检测范围从0到300单位/mL，其中10单位/mL是第一个离散值），这需要仔细解释。我们自己的研究表明，256例患者中有81例（31.6%）使用IFT检测为PCA阳性，但只有18%的患者通过H+/K+- atp酶特异性EliA（一种自动定量酶荧光免疫测定法）和病理bbb证实为阳性。此外，研究表明，在一般健康成人人群中，PCA的发生率较低，他们可能永远不会发生AIG或恶性贫血[3,5]。虽然Amalia等人显示了胃体炎症评分与PCA水平之间的相关性，但从他们的报告中尚不清楚对照组与胃炎患者相比是否表现出较低的PCA患病率。因此，可能需要额外的测试来证明PCA的存在。作者认为，在该队列中观察到的高PCA患病率与幽门螺杆菌感染之间存在潜在联系。虽然幽门螺杆菌可以通过分子模仿引发自身免疫反应的假设在生物学上是合理的，但本研究中提供的当前PCA数据可能在一定程度上限制了这一解释的可信度。为了进一步探讨这一点，我们检查了81例胃萎缩患者的数据，发现有幽门螺杆菌感染和没有幽门螺杆菌感染的患者的PCA水平（由EliA测定）没有显著差异（36.1比39.4,p = 0.24，图1A）。进一步的相关分析显示，在幽门螺杆菌感染患者中，血清PCA水平高度与幽门螺杆菌抗体滴度无关（r = 0.08, p = 0.66，图1B）。最后，作者检查了幽门螺杆菌抗体水平和PCA水平与临床病理特征（如炎症、萎缩和PG I/II比值）的关系。 他们的研究结果表明，幽门螺杆菌抗体和PCA水平在胃窦或身体炎症患者以及萎缩患者中较高。鉴于已知幽门螺杆菌感染和AIG会引起炎症和萎缩性粘膜改变，这似乎是意料之中的。然而，幽门螺杆菌感染患者和AIG患者的抗体滴度高度可能受到患者遗传、BMI、细菌负荷、免疫应答、抗体衰减和许多其他因素的影响。因此，目前尚不清楚IgG水平与萎缩阶段之间的相关性在生物学上意味着什么，并且在将幽门螺杆菌血清阴性和PCA阴性患者从线性回归分析中排除后，观察相关性是否仍然显著将是一件有趣的事情。我们自己的数据显示，至少在我们的胃癌前病变患者队列中，由OLGA评分确定的萎缩水平与抗h抗体IgG水平无关。螺杆菌抗体(r =−0.05,p = 0.70,图1 c)或PCA (r = 0.09, p = 0.69,图1 d)。总之，我们认为Amalia等人使用的诊断标准可能导致低估了印尼队列中AIG的患病率，而高估了PCA的患病率。更具体的血清学检测（如EliA、抗内因子抗体、胃蛋白酶原I和胃泌素-17）和其他组织学特征（如肠嗜铬细胞样（ECL）细胞增生）应结合，以提高PCA的检测和AIG的诊断。郭小培：构思，撰写原稿。Manon C . W . Spaander：概念化、审查和编辑。格温妮·M·富勒：概念化、写作和编辑。作者没有什么可报告的。该研究得到了Erasmus MC医学伦理审查委员会（MEC-2009-090）的批准，并获得了所有参与者的知情同意。
{"title":"Letter to the Editor: “Parietal Cell Antibody Levels Among Chronic Gastritis Patients in a Country With Low Helicobacter pylori Infection: Epidemiology, Histopathological Features, and H. pylori Infection”","authors":"Xiaopei Guo, Manon C W Spaander, Gwenny M Fuhler","doi":"10.1111/hel.70053","DOIUrl":"https://doi.org/10.1111/hel.70053","url":null,"abstract":"<p>We read with great interest the article titled “Parietal Cell Antibody Levels Among Chronic Gastritis Patients in a Country with Low <i>Helicobacter pylori</i> Infection: Epidemiology, Histopathological Features, and <i>H. pylori</i> infection” by Amalia et al. [<span>1</span>]. In this study, the authors investigated the prevalence of autoimmune gastritis (AIG), and its association with <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection status and gastric histopathological features in the Indonesian population. Given the previously reported high incidence of gastritis and relatively low <i>H. pylori</i> infection rates in this region, exploring other causes of gastritis, such as AIG, is essential for improving diagnostic accuracy and guiding clinical risk management [<span>2</span>].</p><p>While the authors conducted a comprehensive analysis of parietal cell antibody (PCA) levels and its association with clinicopathological features, several aspects of the study's methodology and interpretation raise concerns and warrant further clarification. A key observation of this study is the reported 78.99% prevalence of PCA positivity among 113 Indonesian patients with chronic gastritis and 25 healthy controls, while only one patient was diagnosed with AIG. The authors suggest that this discrepancy might be due to <i>H. pylori</i>-associated immune activation. However, we think it may also reflect the combined impact of overly strict diagnostic criteria for AIG and the inappropriate interpretation of PCA results.</p><p>In the diagnostic methods, AIG was defined based on the PCA positivity, absence of <i>H. pylori</i> infection, histopathological features associated with AIG, and sparing of the antrum. We understand the concern that coexisting <i>H. pylori</i> infection may complicate the diagnosis of AIG, as it can cause histopathological changes that resemble AIG. But we note that neither antrum sparing nor negative <i>H. pylori</i>-negative status should be a required criterion for AIG diagnosis. Our previous findings have shown that AIG can coexist with <i>H. pylori</i> infection, and hence patients may present with antral inflammation or atrophy. Such patients still show characteristic serological features similar to AIG patients without <i>H. pylori</i> infection, including decreased pepsinogen (PG) I levels and elevated gastrin 17 [<span>3</span>]. Additionally, they may exhibit pathological findings such as enterochromaffin-like (ECL) cell hyperplasia [<span>4</span>], which was not investigated in the study by Amalia et al. Therefore, we think the criteria used may have led to underdiagnosis of AIG in the Indonesia cohort. Rather than excluding patients with <i>H. pylori</i> infection or antrum inflammation/atrophy, more specific diagnostic tests should be considered to improve the diagnosis of AIG, especially given this is the first study reporting AIG prevalence in this region.</p><p>Adding to these diagnostic challenges Beyond these di","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.70053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144206830","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}
<div> <section> <h3> Background</h3> <p>Recent studies have found that in addition to directly impacting the gastric microbiome, <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection may cause intestinal microbial dysbiosis. However, most existing studies on the influence of <i>H. pylori</i> infection on the intestinal microbiome used fecal specimens with inconsistent conclusions. Only one limited study on 8 <i>H. pylori</i>-infected patients has previously assessed the impact of <i>H. pylori</i> infection on the microbiome of the entire gastrointestinal tract, finding no significant effect on the bacterial composition of the lower gastrointestinal tract.</p> </section> <section> <h3> Methods</h3> <p>This single-center cross-sectional study collected mucosa of the esophagus, stomach, small intestine, and colon, as well as gastric juice and feces from 120 participants of the <i>H. pylori-</i>infected group (HIG) and 30 of the healthy control group (HCG). 16S rRNA sequencing was applied to analyze the bacterial composition and functional pathways, and metagenomics was adopted to assess the composition of viruses, eukaryotes, and archaea in the feces, as well as the antibiotic resistance gene (ARG) and virulence factors of bacteria (VF).</p> </section> <section> <h3> Results</h3> <p>Compared with the HCG, the alpha and beta diversity of bacteria in the mucosa of the whole digestive tract and the gastric juice of the HIG showed significant changes, with increased microbial dysbiosis index and significantly different compositions at the phylum and genus levels. Functional pathway analysis revealed that the metabolic characteristics of the flora changed in the HIG, with site-specific differences. Fecal specimens demonstrated no significant differences in the above indicators between the two groups. In addition, feces-based metagenomic analysis revealed that only eukaryotes had higher diversity in the HIG, whereas viruses and archaea showed no significant changes; the Shannon index of ARG increased; and VF showed no significant change.</p> </section> <section> <h3> Conclusions</h3> <p>This study revealed that <i>H. pylori</i> infection significantly influenced the diversity, composition, and metabolic functional pathway of bacteria in different parts of the digestive tract and the gastric juice. Moreover, fecal microbial composition may not fully represent the mucosal microbial composition of the gastrointestinal tract.</p> </section> <section> <h3> Trial Registration</h3> <p>Chinese Clinical Trial Registry: ChiCTR2300073419</p> </section>
{"title":"The Systemic Impact of Helicobacter pylori Infection on the Microbiome of Whole Digestive Tract Based on Mucosal, Gastric Juice, and Fecal Specimens","authors":"Yuxin Wang, Kai Zhou, Yuexi Zhang, Cailing Li, Yuxin Zhang, Xinlu Ren, Changmin Mi, Lingling Ma, Yuqi Duan, Mengqi Liu, Guangjie Ping, Xueli Tian, Zhiqiang Song","doi":"10.1111/hel.70047","DOIUrl":"https://doi.org/10.1111/hel.70047","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Recent studies have found that in addition to directly impacting the gastric microbiome, <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection may cause intestinal microbial dysbiosis. However, most existing studies on the influence of <i>H. pylori</i> infection on the intestinal microbiome used fecal specimens with inconsistent conclusions. Only one limited study on 8 <i>H. pylori</i>-infected patients has previously assessed the impact of <i>H. pylori</i> infection on the microbiome of the entire gastrointestinal tract, finding no significant effect on the bacterial composition of the lower gastrointestinal tract.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This single-center cross-sectional study collected mucosa of the esophagus, stomach, small intestine, and colon, as well as gastric juice and feces from 120 participants of the <i>H. pylori-</i>infected group (HIG) and 30 of the healthy control group (HCG). 16S rRNA sequencing was applied to analyze the bacterial composition and functional pathways, and metagenomics was adopted to assess the composition of viruses, eukaryotes, and archaea in the feces, as well as the antibiotic resistance gene (ARG) and virulence factors of bacteria (VF).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Compared with the HCG, the alpha and beta diversity of bacteria in the mucosa of the whole digestive tract and the gastric juice of the HIG showed significant changes, with increased microbial dysbiosis index and significantly different compositions at the phylum and genus levels. Functional pathway analysis revealed that the metabolic characteristics of the flora changed in the HIG, with site-specific differences. Fecal specimens demonstrated no significant differences in the above indicators between the two groups. In addition, feces-based metagenomic analysis revealed that only eukaryotes had higher diversity in the HIG, whereas viruses and archaea showed no significant changes; the Shannon index of ARG increased; and VF showed no significant change.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study revealed that <i>H. pylori</i> infection significantly influenced the diversity, composition, and metabolic functional pathway of bacteria in different parts of the digestive tract and the gastric juice. Moreover, fecal microbial composition may not fully represent the mucosal microbial composition of the gastrointestinal tract.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>Chinese Clinical Trial Registry: ChiCTR2300073419</p>\u0000 </section>\u0000 ","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148629","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}
{"title":"Dr Martin Bingham Skirrow—A Passionate Microbiologist and Early Advocate for Helicobacter pylori","authors":"Cliodna McNulty","doi":"10.1111/hel.70048","DOIUrl":"https://doi.org/10.1111/hel.70048","url":null,"abstract":"","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148628","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}
Gastric cancer (GC) is a leading cause of cancer-related mortality worldwide, with Helicobacter pylori (H. pylori) infection recognized as a significant risk factor. H. pylori infects approximately 50% of the global population, contributing to chronic gastritis, peptic ulcers, and the development of GC. The oncoprotein Gankyrin (PSMD10) has been implicated in various human cancers, including hepatocellular carcinoma, gastric cancer, and lung cancer, by modulating autophagy and inflammatory pathways.
Methods
In this study, we explored the role of Gankyrin in H. pylori-induced gastric tumorigenesis via a Swiss albino mouse xenograft model. Mice were subcutaneously injected with H. pylori-infected AGS cells with or without Gankyrin knockdown.
Results
We assessed tumor growth and inflammatory markers (TNF-α and IL-6) levels and Gankyrin's downstream signaling molecules (p53, pRb, and NF-κB). Our results demonstrated that Gankyrin knockdown significantly decreased tumor formation in Swiss albino mice engrafted with H. Pylori-infected AGS cells. Notably, treatment with cyclosporine A significantly decreased the expression of TNF-α in all the AGS-engrafted mice except the PBS group. Moreover, our results show that the downregulation of Gankyrin significantly elevated the expression of NF-κB, pRb, and p53.
Conclusion
These findings suggest that Gankyrin plays a crucial role in H. pylori-mediated GC progression by modulating inflammatory and tumor suppressor pathways. Targeting Gankyrin could provide a therapeutic strategy to mitigate the development of GC associated with H. pylori infection.
{"title":"Gankyrin Inhibition Can Control Helicobacter pylori Generated Gastric Cancer Using In Vivo Xenograft Models","authors":"Dharmendra Kashyap, Pranit Hemant Bagde, Siddharth Singh, Nidhi Varshney, Tarun Prakash Verma, Anamika Singh, Hamendra Singh Parmar, Hem Chandra Jha","doi":"10.1111/hel.70046","DOIUrl":"https://doi.org/10.1111/hel.70046","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Gastric cancer (GC) is a leading cause of cancer-related mortality worldwide, with <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection recognized as a significant risk factor. <i>H. pylori</i> infects approximately 50% of the global population, contributing to chronic gastritis, peptic ulcers, and the development of GC. The oncoprotein Gankyrin (PSMD10) has been implicated in various human cancers, including hepatocellular carcinoma, gastric cancer, and lung cancer, by modulating autophagy and inflammatory pathways.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this study, we explored the role of Gankyrin in <i>H. pylori</i>-induced gastric tumorigenesis via a Swiss albino mouse xenograft model. Mice were subcutaneously injected with <i>H. pylori</i>-infected AGS cells with or without Gankyrin knockdown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We assessed tumor growth and inflammatory markers (TNF-α and IL-6) levels and Gankyrin's downstream signaling molecules (p53, pRb, and NF-κB). Our results demonstrated that Gankyrin knockdown significantly decreased tumor formation in Swiss albino mice engrafted with <i>H. Pylori</i>-infected AGS cells. Notably, treatment with cyclosporine A significantly decreased the expression of TNF-α in all the AGS-engrafted mice except the PBS group. Moreover, our results show that the downregulation of Gankyrin significantly elevated the expression of NF-κB, pRb, and p53.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings suggest that Gankyrin plays a crucial role in <i>H. pylori</i>-mediated GC progression by modulating inflammatory and tumor suppressor pathways. Targeting Gankyrin could provide a therapeutic strategy to mitigate the development of GC associated with <i>H. pylori</i> infection.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144135545","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}
Young Sin Cho, Sun Moon Kim, Sun Hyung Kang, Hee Seok Moon, Jae Kyu Sung, Ki Bae Bang, Sung Hyeok Ryou, Ki Bae Kim, Hae Joung Sul, Seung-Woo Lee
Background
The increasing trend of clarithromycin resistance in Helicobacter pylori (H. pylori) is the primary cause of failure of standard triple therapy. Concomitant therapy is recommended as an alternative in regions with high rates of clarithromycin resistance. Recently, tailored therapies based on resistance testing have emerged as viable treatment approaches. We aimed to compare the eradication rates and adverse effects of concomitant and tailored therapies.
Materials and Methods
We enrolled 319 patients diagnosed with H. pylori infection using dual-priming oligonucleotide (DPO) polymerase chain reaction (PCR) tests conducted in six hospitals across the Daejeon and Chungcheong regions of Korea. Based on DPO-PCR results, patients were randomly assigned to either the concomitant therapy group (non-bismuth quadruple therapy) or the tailored therapy group (standard triple therapy for clarithromycin-sensitive cases and bismuth quadruple therapy for clarithromycin-resistant cases). Demographics, eradication success rates, adverse effects, and patient compliance were assessed. Data were analyzed using modified intention-to-treat (mITT) and per-protocol (PP) analyses.
Results
The eradication rate was significantly higher in the tailored therapy group than in the concomitant therapy group in PP analysis (92.62% vs. 85.21%, p = 0.026). The severity of adverse effects was significantly greater in the concomitant therapy group than in the tailored therapy group (p = 0.025).
Conclusion
Considering the high eradication success rate and low severity of adverse effects, tailored therapy based on DPO-PCR is preferable to concomitant therapy without resistance testing for the treatment of H. pylori infection.
Trial Registration
Clinical Research Information Service (CRIS): KCT0004162
背景幽门螺杆菌（Helicobacter pylori， H. pylori）对克拉霉素耐药性的上升趋势是标准三联治疗失败的主要原因。在克拉霉素耐药率高的地区，建议采用联合治疗。最近，基于耐药性测试的量身定制疗法已成为可行的治疗方法。我们的目的是比较伴随治疗和定制治疗的根除率和不良反应。材料与方法采用双引物寡核苷酸（DPO）聚合酶链反应（PCR）方法，对大田和忠清地区6家医院诊断为幽门螺杆菌感染的319例患者进行了研究。根据DPO-PCR结果，患者被随机分配到合并治疗组（非铋四联治疗）或定制治疗组（克拉霉素敏感病例标准三联治疗，克拉霉素耐药病例铋四联治疗）。对人口统计学、根除成功率、不良反应和患者依从性进行了评估。使用改进的意向治疗（mITT）和方案分析（PP）对数据进行分析。结果在PP分析中，定制治疗组的根除率明显高于伴随治疗组（92.62% vs. 85.21%, p = 0.026）。合并治疗组不良反应严重程度显著高于定制治疗组（p = 0.025）。结论考虑到根除成功率高、不良反应严重程度低，基于DPO-PCR的个体化治疗比不进行耐药检测的联合治疗更适合幽门螺杆菌感染的治疗。临床研究信息服务中心（CRIS）： KCT0004162
{"title":"Comparison of Therapeutic Outcomes Between Concomitant Therapy and Tailored Therapy for Helicobacter pylori: A Multicenter, Prospective, and Randomized Study","authors":"Young Sin Cho, Sun Moon Kim, Sun Hyung Kang, Hee Seok Moon, Jae Kyu Sung, Ki Bae Bang, Sung Hyeok Ryou, Ki Bae Kim, Hae Joung Sul, Seung-Woo Lee","doi":"10.1111/hel.70040","DOIUrl":"https://doi.org/10.1111/hel.70040","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The increasing trend of clarithromycin resistance in <i>Helicobacter pylori</i> (<i>H. pylori</i>) is the primary cause of failure of standard triple therapy. Concomitant therapy is recommended as an alternative in regions with high rates of clarithromycin resistance. Recently, tailored therapies based on resistance testing have emerged as viable treatment approaches. We aimed to compare the eradication rates and adverse effects of concomitant and tailored therapies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>We enrolled 319 patients diagnosed with <i>H. pylori</i> infection using dual-priming oligonucleotide (DPO) polymerase chain reaction (PCR) tests conducted in six hospitals across the Daejeon and Chungcheong regions of Korea. Based on DPO-PCR results, patients were randomly assigned to either the concomitant therapy group (non-bismuth quadruple therapy) or the tailored therapy group (standard triple therapy for clarithromycin-sensitive cases and bismuth quadruple therapy for clarithromycin-resistant cases). Demographics, eradication success rates, adverse effects, and patient compliance were assessed. Data were analyzed using modified intention-to-treat (mITT) and per-protocol (PP) analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The eradication rate was significantly higher in the tailored therapy group than in the concomitant therapy group in PP analysis (92.62% vs. 85.21%, <i>p</i> = 0.026). The severity of adverse effects was significantly greater in the concomitant therapy group than in the tailored therapy group (<i>p</i> = 0.025).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Considering the high eradication success rate and low severity of adverse effects, tailored therapy based on DPO-PCR is preferable to concomitant therapy without resistance testing for the treatment of <i>H. pylori</i> infection.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>Clinical Research Information Service (CRIS): KCT0004162</p>\u0000 </section>\u0000 </div>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144108801","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}
V. Mishra, D. Dash, A. K. Panda, et al., “Efficacy of Lactobacillus spp. Supplementation in Helicobacter pylori Eradication: A Systematic Meta-Analysis of Randomized Controlled Trials With Trial Sequential Analysis,” Helicobacter 29, no. 6 (2024): e70006, doi: https://doi.org/10.1111/hel.70006.
In the Abstract, Results (Sections 3.3–3.4), and GRADE evidence profile (Table 1), the risk ratio (RR) 95% CI values were mistakenly reported from Egger's regression 95% CI values (Table S3). Below, we provide a table of actual 95% CI values for RR as reported in the Forest plots (Figures 1–4).
We apologize for this error.
V. Mishra， D. Dash， A. K. Panda等，“补充乳酸杆菌对根除幽门螺杆菌的功效：随机对照试验的系统荟萃分析与试验序列分析”，《幽门螺杆菌》，第29期。6 (2024): e70006, doi: https://doi.org/10.1111/hel.70006.In摘要，结果（3.3-3.4节）和GRADE证据概要（表1），风险比（RR） 95% CI值错误地报告了Egger's回归95% CI值（表S3）。下面，我们提供了Forest图中报告的RR的实际95% CI值的表格（图1-4）。我们为这个错误道歉。
{"title":"Correction to “Efficacy of Lactobacillus spp. Supplementation in Helicobacter pylori Eradication: A Systematic Meta-Analysis of Randomized Controlled Trials With Trial Sequential Analysis”","authors":"","doi":"10.1111/hel.70044","DOIUrl":"https://doi.org/10.1111/hel.70044","url":null,"abstract":"<p>V. Mishra, D. Dash, A. K. Panda, et al., “Efficacy of <i>Lactobacillus</i> spp. Supplementation in <i>Helicobacter pylori</i> Eradication: A Systematic Meta-Analysis of Randomized Controlled Trials With Trial Sequential Analysis,” Helicobacter 29, no. 6 (2024): e70006, doi: https://doi.org/10.1111/hel.70006.</p><p>In the Abstract, Results (Sections 3.3–3.4), and GRADE evidence profile (Table 1), the risk ratio (RR) 95% CI values were mistakenly reported from Egger's regression 95% CI values (Table S3). Below, we provide a table of actual 95% CI values for RR as reported in the Forest plots (Figures 1–4).</p><p>We apologize for this error.</p>","PeriodicalId":13223,"journal":{"name":"Helicobacter","volume":"30 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/hel.70044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144074359","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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