Journal of Gastroenterology最新文献

{"title":"Reply to \"Comment on \"Escherichia coli as a gut microbial marker of obesity and its reduction following bariatric treatment\": ecological and functional perspectives\".","authors":"Tomoyuki Hayashi, Noriho Iida","doi":"10.1007/s00535-026-02511-4","DOIUrl":"10.1007/s00535-026-02511-4","url":null,"abstract":"","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1514-1515"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818685","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":"Reply to \"Did the COVID-19 pandemic disrupt the continuity of post-SVR surveillance in HCV-cured patients?\"","authors":"Masatsugu Ohara, Ritsuzo Kozuka, Yoshihito Uchida, Chikara Iino, Ryo Sasaki, Hiroki Tojima, Kazuhito Kawata, Satoru Kakizaki, Yoshio Tokumoto, Mizuki Endo, Akira Asai, Jun Inoue, Kenji Nagata, Hirokazu Takahashi, Tetsuro Shimakami, Koji Ogawa, Masaru Enomoto, Tadashi Ikegami, Tatsuya Ide, Naoya Sakamoto, Masaaki Korenaga","doi":"10.1007/s00535-026-02510-5","DOIUrl":"10.1007/s00535-026-02510-5","url":null,"abstract":"","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1518-1519"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148880127","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":"IgG4-related disease in gastroenterology: from pathogenesis to clinical management and long-term outcomes.","authors":"Yifei Wang, Luyi Peng, Wen Zhang","doi":"10.1007/s00535-026-02424-2","DOIUrl":"10.1007/s00535-026-02424-2","url":null,"abstract":"<p><p>IgG4-related disease is a rare, immune-mediated, multisystem fibroinflammatory condition. It is characterized by elevated serum IgG4 concentrations and tissue infiltration of IgG4-positive plasma cells with distinctive histopathological features, including storiform fibrosis and obliterative phlebitis. Gastroenterological involvement is diverse and represents a critical diagnostic consideration, encompassing the pancreas, bile ducts, liver, esophagus, stomach, and intestine. In this review, we summarize the current understanding of genetic susceptibility and environmental risk factors underlying this disease, and systematically describe the clinical presentations, histopathological characteristics, imaging findings, and serological profiles of each major gastroenterological manifestation. We further review evidence-based treatment regimens ranging from glucocorticoids and conventional immunosuppressants to emerging biologic therapies, discuss organ-specific therapeutic responses, and identify predictors of disease relapse along with long-term surveillance strategies. From a gastroenterologist's perspective, this review aims to provide a practical and integrated framework to facilitate early recognition, accurate differentiation from mimicking conditions such as pancreaticobiliary malignancies, and optimized long-term management of this complex yet treatable disease.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1393-1407"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147816186","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}

{"title":"Clinical outcomes of lean metabolic dysfunction-associated steatotic liver disease by phenotypic subtypes.","authors":"Chia-Chih Kuo, Chi-Hsing Chen, Hsing-Tao Kuo, Chih-Cheng Lai","doi":"10.1007/s00535-026-02481-7","DOIUrl":"10.1007/s00535-026-02481-7","url":null,"abstract":"<p><strong>Aims: </strong>Lean metabolic dysfunction-associated steatotic liver disease (MASLD) is often treated as a single entity despite substantial heterogeneity. We assessed whether body mass index (BMI) strata, cardio-metabolic risk factor (CMRF) phenotype, and CMRF burden stratify the risk of clinical outcomes.</p><p><strong>Methods: </strong>Using the TriNetX Global Network, we identified adults with MASLD from 2005 to 2024. Lean MASLD was defined by BMI less than 25 kg/m² and stratified into underweight and normal-weight groups. Underweight and normal-weight MASLD were compared after 1:1 propensity score matching. Within normal-weight MASLD, phenotypes were defined as hypertension-only, type 2 diabetes (T2D)-only, dyslipidemia-only, and multi-factor burden, categorized as 2 CMRF or 3 CMRF. Outcomes were major adverse liver outcomes (MALO), major adverse cardiovascular events (MACE), extrahepatic cancer, and all-cause mortality.</p><p><strong>Results: </strong>We identified 40,456 patients with lean MASLD, including 2121 underweight and 38,335 normal weight. After matching, 2115 patients remained in each group. Underweight MASLD had higher risks of all-cause mortality (HR 2.03; 95% CI 1.68-2.44) and MALO (HR 2.01; 95% CI 1.49-2.70). MACE risk was higher (HR 1.30; 95% CI 1.02-1.66), while extrahepatic cancer was not significantly different (HR, 1.14; 95% CI 0.85-1.52). Among normal-weight MASLD, multi-factor burden showed graded increases in mortality, MALO, and MACE compared with hypertension-only. T2D-only was associated with higher MALO, while dyslipidemia-only was associated with lower risks of mortality, MALO, and MACE.</p><p><strong>Conclusions: </strong>Lean MASLD is prognostically heterogeneous. Underweight status and CMRF phenotype and burden identify clinically meaningful risk strata across hepatic and extrahepatic outcomes.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1471-1482"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497643","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":"Did the COVID-19 pandemic disrupt the continuity of post-SVR surveillance in HCV-cured patients?","authors":"Hidenori Toyoda, Masanori Atsukawa","doi":"10.1007/s00535-026-02426-0","DOIUrl":"10.1007/s00535-026-02426-0","url":null,"abstract":"","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1516-1517"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773614","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":"Alcohol involvement may modify the association between previous hepatitis B virus infection and hepatocellular carcinoma risk in steatotic liver disease.","authors":"Naohiro Yasuura, Goki Suda, Masatsugu Ohara, Daisuke Yokoyama, Takatsugu Tanaka, Akimitsu Meno, Takuya Sho, Risako Kohya, Ruixin Deng, Qingjie Fu, Zijian Yang, Osamu Maehara, Shunsuke Ohnishi, Takashi Kitagataya, Naoki Kawagishi, Masato Nakai, Tatsuhiko Kakisaka, Akinobu Taketomi, Naoya Sakamoto","doi":"10.1007/s00535-026-02473-7","DOIUrl":"10.1007/s00535-026-02473-7","url":null,"abstract":"<p><strong>Background/aims: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related liver disease (MetALD), and alcohol-related liver disease (ALD) are emerging hepatocellular carcinoma (HCC) etiologies. Prior-HBV-infection (pHBV) has been linked to HCC in HBsAg-negative populations, but phenotype-specific effects across steatotic liver disease (SLD) remain unclear. We examined whether pHBV modifies 5-year HCC risk by SLD etiology.</p><p><strong>Methods: </strong>We analyzed 623 of 1116 patients with hepatic steatosis managed at a single center (2009-2024). pHBV was defined as HBsAg- and HBV DNA-negative status with anti-HBc and/or anti-HBs positivity. The primary endpoint was the 5-year cumulative HCC incidence. Kaplan-Meier, PSM, IPTW, and Cox interaction models were used.</p><p><strong>Results: </strong>pHBV was present in 152 patients (24.4%). Overall, pHBV was not associated with 5-year HCC after PSM (150 pairs; 6.58% vs. 5.60%; log-rank P = 0.701) or IPTW (3.80% vs. 4.27%; HR 0.97, 95% CI 0.37-2.54; P = 0.874). In MASLD/cryptogenic SLD, pHBV was associated with lower HCC incidence (PSM 1.32% vs. 9.53%, P = 0.027; IPTW 0.86% vs. 4.35%, P = 0.048). In ALD/MetALD, pHBV showed a borderline higher incidence (PSM 16.17% vs. 3.45%, P = 0.053; IPTW 12.78% vs. 3.99%, P = 0.073). Interaction analyses supported heterogeneity across etiologies (IPTW HR 12.96, P = 0.024; PSM HR 25.87, P = 0.034, Cox HR 7.83, P = 0.057).</p><p><strong>Conclusions: </strong>In HBsAg-negative SLD, the association between pHBV and HCC risk appears to differ according to alcohol involvement, with a potentially increased HCC risk in ALD/MetALD and a lower observed HCC incidence in MASLD/cryptogenic disease that requires cautious interpretation.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1460-1470"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338940","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":"Impact of 5-aminosalicylic acid intolerance on progression to difficult-to-treat ulcerative colitis: a retrospective cohort study.","authors":"Masashi Ohno, Atsushi Nishida, Shinya Yoshida, Yoshihiro Yokota, Takayuki Imai, Shigeki Bamba, Takuji Iwashita","doi":"10.1007/s00535-026-02486-2","DOIUrl":"10.1007/s00535-026-02486-2","url":null,"abstract":"<p><strong>Background: </strong>Intolerance to 5-aminosalicylic acid (5-ASA) is linked to poorer outcomes in ulcerative colitis (UC), but its impact on progression to difficult-to-treat (D2T) disease and the contribution of specific intolerance phenotypes remain uncertain. We evaluated the long-term prognostic impact of 5-ASA intolerance phenotypes and post-intolerance treatment status.</p><p><strong>Methods: </strong>This retrospective cohort study included 919 patients with UC. Cumulative incidence functions were compared using Gray's test, treating death and colectomy as competing events when assessing progression to D2T. Multivariable models were adjusted for baseline covariates and immunomodulator use. Landmark analyses and sensitivity analyses using secondary failure of ≥ 2 mechanisms of action after advanced therapy initiation were performed.</p><p><strong>Results: </strong>Among 919 patients, 145 (15.8%) were classified as 5-ASA intolerant, including 83 with acute intolerance syndrome (AIS) and 62 with non-AIS phenotypes. Overall intolerance was independently associated with an increased risk of D2T progression (subdistribution hazard ratio [sHR] 2.07, 95% confidence interval [CI] 1.14-3.75), but not with colectomy. The excess risk was largely driven by AIS (sHR: 3.25, 95% CI: 1.64-6.45). Landmark analyses showed that 5-ASA users at 90 or 365 days exhibited a lower cumulative incidence of D2T progression than non-users. Furthermore, following advanced therapy initiation, overall 5-ASA intolerance was not associated with secondary failure of ≥ 2 mechanisms of action, whereas AIS remained independently associated with this outcome.</p><p><strong>Conclusions: </strong>Progression to D2T UC among patients with 5-ASA intolerance is largely attributable to AIS. Careful characterization of 5-ASA phenotype may improve risk stratification and inform individualized therapeutic strategies in UC management.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1450-1459"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148604005","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":"Nationwide epidemiological survey of autoimmune pancreatitis in Japan in 2021.","authors":"Atsushi Masamune, Takanori Sano, Tetsuya Takikawa, Ryotaro Matsumoto, Shin Hamada, Toshiaki Abe, Yuichi Tanaka, Yoshifumi Takeyama, Kazuhiro Kikuta","doi":"10.1007/s00535-026-02438-w","DOIUrl":"10.1007/s00535-026-02438-w","url":null,"abstract":"<p><strong>Background: </strong>To update the clinic-epidemiological features of autoimmune pancreatitis (AIP) in Japan, we conducted the fifth nationwide survey.</p><p><strong>Methods: </strong>We performed a two-stage survey of patients with AIP who were treated at selected hospitals in 2021. The first-stage survey estimated the total number of patients with AIP, and the second-stage survey analyzed detailed clinical characteristics.</p><p><strong>Results: </strong>The estimated number of patients with AIP in 2021 was 16,750 (prevalence, 13.3 per 100,000 persons), representing a 25% increase from 2016. The number of newly diagnosed cases was 4210 (annual incidence, 3.4 per 100,000 persons). Clinical data were available for 2833 patients. The male-to-female ratio was 3.32:1, and the mean age in 2021 and the mean age at AIP diagnosis were 71.2 and 66.3 years, respectively. At diagnosis, 58.6% of patients were symptomatic, approximately half of whom presented with jaundice. Other organ involvement was observed in 67.8% of patients, most commonly sclerosing cholangitis. Histopathological examination was performed in 84.1% of cases, predominantly using endoscopic ultrasonography-guided tissue acquisition. Initial glucocorticoid therapy was administered to 84.2% of patients, and 93.8% received maintenance therapy. Kaplan-Meier analysis demonstrated a cumulative relapse incidence of 12.5%, 20.7%, 36.0%, 44.0%, 53.3%, and 68.9% at 3, 5, 10, 15, 20, and 25 years, respectively. Long-term overall survival was favorable; however, malignancies accounted for 40% of deaths.</p><p><strong>Conclusions: </strong>This nationwide survey updates the epidemiological and clinical characteristics of AIP in Japan. Patient numbers continue to rise, and the high cumulative risk of relapse underscores the need for second-line therapies beyond glucocorticoids.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1502-1511"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973034","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}

{"title":"RNF207 promotes colorectal cancer growth by regulating the Hippo-YAP pathway via enhanced MST1 ubiquitination and degradation.","authors":"Meng Wang, Xing Wen, Mei Yang, Jie Zhang, Jianhui Gu, Tianqi Lu","doi":"10.1007/s00535-026-02440-2","DOIUrl":"10.1007/s00535-026-02440-2","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer ranks second in global mortality rates, yet its molecular pathogenesis remains incompletely understood. Accumulating evidence indicates that E3 ubiquitin ligases modulate the activity and stability of critical oncoproteins via ubiquitination, positioning these enzymes as promising therapeutic targets for cancer intervention. The E3 ligase Ring finger protein 207 (RNF207), characterized as a regulator involved in heart disease, has not been investigated in colorectal cancer.</p><p><strong>Methods: </strong>We constructed RNF207 overexpression and knockdown colorectal cancer cell lines, and investigated the effects of RNF207 on the proliferation and migration of colorectal cancer cells through experiments such as CCK8, colony formation, migration, and invasion assays. In colorectal cancer cell lines and human colorectal cancer tissues, the influence of RNF207 on the Hippo-YAP signaling pathway was extensively investigated. The mechanism by which RNF207 regulates P-YAP and MST1 was explored through Co-IP and ubiquitination experiments. Finally, the effect of RNF207 on the growth of colorectal cancer was investigated in nude mice.</p><p><strong>Results: </strong>Here, we demonstrate that elevated RNF207 expression in colorectal tumors correlates with poor prognosis. Functional studies revealed that RNF207 enhances colorectal cancer cell proliferation, migration. Mechanistically, we identified that RNF207 promotes colorectal cancer progression through MST1-dependent regulation of Hippo-YAP signaling. Specifically, RNF207 interacts with MST1 and induces its proteasomal degradation via K48-linked ubiquitination dependent on the activity of E3 ligase, thereby attenuating YAP phosphorylation and activating YAP-driven transcription. Furthermore, the protein level of RNF207 was significantly negatively correlated with the protein levels of MST1 and P-YAP in colorectal tumors, and reducing the expression of RNF207 can effectively inhibit the growth of colorectal cancer.</p><p><strong>Conclusions: </strong>Collectively, our findings uncover a novel oncogenic function of RNF207 in colorectal cancer, whereby it facilitates MST1 degradation through K48 ubiquitination, leading to YAP hyper-activation. Targeting RNF207-MST1-YAP axis may represent a potential therapeutic for colorectal cancer treatment.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1431-1449"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148042453","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}

{"title":"Natural history of Barrett's esophagus over a 10-year period: a longitudinal endoscopic study in a Japanese population.","authors":"Kenta Watanabe, Sho Fukuda, Yasutaka Takahashi, So Kodama, Tatsuki Yoshida, Yohei Saruta, Ryo Okubo, Ryo Abe, So Takahashi, Kengo Onochi, Shuichi Ito, Kazuya Kimura, Toshiaki Suzuki, Tamotsu Matsuhashi, Katsunori Iijima","doi":"10.1007/s00535-026-02495-1","DOIUrl":"10.1007/s00535-026-02495-1","url":null,"abstract":"<p><strong>Background: </strong>Since Barrett's esophagus (BE) is an established precancerous condition for esophageal adenocarcinoma, understanding the natural history of BE is crucial for effective endoscopic surveillance. We aimed to elucidate temporal changes in BE status over a 10-year period using a database derived from repeated endoscopies.</p><p><strong>Methods: </strong>A total of 9,741 subjects who underwent screening esophagogastroduodenoscopy in 2014 and at least one follow-up examination by December 2025 were included. Transitions in BE status between the index and final examinations were classified as progression, regression, or no change based on differences in BE length. Logistic regression analyses were performed to investigate factors associated with BE progression.</p><p><strong>Results: </strong>The median follow-up period from the index to final examination was 8.8 years. Overall, BE ≥ 1 cm or BE ≥ 2 cm was newly identified at the final examination in 4.87% and 0.82%, respectively. Progression rates toward longer BE segments remained relatively constant across age groups, ranging from the 30 s to ≥ 70 years. Multivariable regression analyses revealed significant associations between reflux esophagitis and BE progression, with higher risks observed for both Los Angeles grade A and grade B or higher esophagitis.</p><p><strong>Conclusion: </strong>BE status remained stable in the majority of subjects during approximately nine years of follow-up; however, new BE ≥ 1 cm and ≥ 2 cm developed in 4.87% and 0.82% of subjects, respectively. Such progression occurred irrespective of age at baseline, providing evidence supporting flexible, adaptive surveillance strategies for BE.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"1408-1418"},"PeriodicalIF":5.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615931/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673923","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}