Clinical Gastroenterology and Hepatology最新文献

{"title":"Reply to: Kang L, Ye T. Before Liver Stiffness Becomes the Single Early Prognostic Marker in MASLD, How Certain and How Additional Is the One-Year Change? Clin Gastroenterol Hepatol 2026 in press.","authors":"Gabriele Di Maria, Vincent Wai-Sun Wong, Salvatore Petta","doi":"10.1016/j.cgh.2026.10.006","DOIUrl":"https://doi.org/10.1016/j.cgh.2026.10.006","url":null,"abstract":"","PeriodicalId":10347,"journal":{"name":"Clinical Gastroenterology and Hepatology","volume":"56 1","pages":""},"PeriodicalIF":12.6,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149221681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimal Incidence Threshold for Cost-Effective Hepatocellular Carcinoma Surveillance in Alcohol-Associated Cirrhosis.","authors":"Ali Hajjar, Jovan Julien, Gizem Nemutlu, H Mert Sahinkoc, Mary Linton B Peters, Fasiha Kanwal, Jagpreet Chhatwal","doi":"10.1016/j.cgh.2026.09.035","DOIUrl":"https://doi.org/10.1016/j.cgh.2026.09.035","url":null,"abstract":"<p><strong>Background: </strong>Current guidelines recommend routine hepatocellular carcinoma (HCC) surveillance in patients with cirrhosis when annual HCC incidence exceeds 1 per 100 person-years, a threshold derived from older studies and not specific to alcohol-associated cirrhosis. However, contemporary data suggest that HCC incidence in this population is often below 1%, leaving the value of routine surveillance uncertain.</p><p><strong>Methods: </strong>We developed a Markov-based state-transition microsimulation model to simulate the natural history of HCC and subsequent treatment pathways in patients with alcohol-associated cirrhosis in the United States setting. The model compared biannual surveillance with ultrasound and alpha-fetoprotein (AFP) versus no surveillance separately for two distinct cohorts: patients who continued to actively consume alcohol and patients who had achieved sustained abstinence. Inputs included the natural history of alcohol-associated cirrhosis, HCC incidence, test performance, surveillance adherence, and contemporary treatment. Sensitivity analyses examined the robustness of model assumptions and findings.</p><p><strong>Results: </strong>Biannual surveillance becomes cost-effective when annual HCC incidence reached approximately 0.45 per 100 person-years using willingness-to-pay threshold of $100,000 per quality-adjusted life year (QALY). Among active drinkers, surveillance yielded an incremental cost-effectiveness ratio (ICER) of $18,952 per QALY; among abstinent patients, the ICER was $56,000 per QALY. Per 100,000 patients, routine surveillance generated an estimated 2,083 additional life-years and 992 QALYs in active drinkers and 3,357 life-years and 1,700 QALYs in abstinent patients.</p><p><strong>Conclusion: </strong>Routine biannual HCC surveillance with ultrasound and AFP is cost-effective for patients with alcohol-associated cirrhosis in the United States when HCC incidence exceeds 0.45 per 100 person-years, substantially below the historically cited 1 per 100 person-years threshold. Updating clinical guidelines to reflect these contemporary thresholds could improve early HCC detection in this high-risk population.</p>","PeriodicalId":10347,"journal":{"name":"Clinical Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":16.2,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early-life animal exposure was not associated with risk of inflammatory bowel disease: a nationwide birth cohort study.","authors":"Christina Balmer, Manasi Agrawal, Anne Vinkel Hansen, Joana Torres, Vivi Schlünssen, Tine Jess, Mette Julsgaard","doi":"10.1016/j.cgh.2026.09.049","DOIUrl":"https://doi.org/10.1016/j.cgh.2026.09.049","url":null,"abstract":"<p><strong>Background and aims: </strong>The incidence of inflammatory bowel disease (IBD) continues to rise globally. Early-life environmental exposures may influence immune development, but evidence regarding animal exposure remains inconsistent. We examined whether early-life exposure to pets or farm animals was associated with offspring risk of IBD in a prospective birth cohort.</p><p><strong>Methods: </strong>In this nationwide cohort study based on the Danish National Birth Cohort, prenatal offspring exposure to pets or farm animals, based on maternal reports, was used as the primary indicator of early-life animal exposure. Early-childhood exposure from birth to 18 months was examined in exposure-window analyses. Incident IBD, Crohn's disease (CD), and ulcerative colitis (UC) were identified through national registries. Associations were estimated using Cox proportional hazards models.</p><p><strong>Results: </strong>Among 90,306 offspring, 46% were prenatally exposed to pets and 7% to farm animals. During median follow-up of 24 years, 615 offspring developed IBD. Pet exposure was not associated with IBD risk (aHR 1.05, 95% CI 0.89-1.24), nor was farm animal exposure (aHR 1.00, 95% CI 0.73-1.37). Findings were consistent across specific animal categories and in analyses of CD and UC separately. In exposure-window analyses restricted to 63,958 offspring with maternal reports of both pre- and postnatal exposure, no associations were observed among offspring exposed only during pregnancy (aHR 1.10, 95% CI 0.75-1.63) or only during early childhood (aHR 0.73, 95% CI 0.46-1.15).</p><p><strong>Conclusions: </strong>Early-life exposure to pets or farm animals was not associated with offspring risk of IBD. These findings suggest that early-life animal exposure may not be a major determinant of disease development.</p>","PeriodicalId":10347,"journal":{"name":"Clinical Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":16.2,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diffuse esophageal eosinophilia is associated with increased endoscopic severity and topical steroid non-response in patients with eosinophilic esophagitis","authors":"Stefani Aleman MPH, Alexandra A. Weir MS, Sean S. LaFata BS, Timothy S. Gee BS, Angelica R. Mirzoca MPH, Arjun K. Juneja BS, Hannah L. Thel MD, Brenderia A. Cameron MD, Justin McCallen MD, Christopher J. Lee MD, Gustaf N. Hendrick MD, Jose C. Bermudez BS, Daniel Song MD, Walker D. Redd MD MSCR, Trevor S. Barlowe MD MSCR, Cary C. Cotton MD MPH, Craig C. Reed MD MSCR, Evan S. Dellon MD MPH","doi":"10.1016/j.cgh.2026.09.048","DOIUrl":"https://doi.org/10.1016/j.cgh.2026.09.048","url":null,"abstract":"Variability of esophageal eosinophil distributions and its impact on disease presentation and treatment outcomes in eosinophilic esophagitis (EoE) is unclear. We aimed to determine whether isolated proximal or distal involvement differs from diffuse involvement in EoE presentation and treatment outcomes.","PeriodicalId":10347,"journal":{"name":"Clinical Gastroenterology and Hepatology","volume":"59 1","pages":""},"PeriodicalIF":12.6,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149152561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alcohol-associated liver disease","authors":"Brian P. Lee MD, Haripriya Maddur MD, Juan Pablo Arab MD, Alexandre Louvet","doi":"10.1016/j.cgh.2026.10.003","DOIUrl":"https://doi.org/10.1016/j.cgh.2026.10.003","url":null,"abstract":"Alcohol-associated liver disease (ALD) is the leading cause of liver-related mortality in Western countries. The assessment of histological severity in ALD now relies predominantly on non-invasive methods, particularly elastography and blood-based tests, commercially available or laboratory-developed. These non-invasive approaches have largely replaced the need for liver biopsy. Management of ALD is based primarily on the treatment of alcohol use disorder, and access to pharmacological therapies and addiction specialists should be improved. At present, there is no specific treatment for ALD, with the exception of corticosteroid therapy for severe alcohol-associated hepatitis (AH), a distinct clinical entity associated with a poor prognosis that requires specialized management. In patients with advanced ALD who fail to improve despite sustained alcohol abstinence, liver transplantation remains the only effective therapeutic option. In this setting, a dedicated and multidisciplinary care pathway should be established to optimize patient selection, management, and long-term outcomes.","PeriodicalId":10347,"journal":{"name":"Clinical Gastroenterology and Hepatology","volume":"21 1","pages":""},"PeriodicalIF":12.6,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149152560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Weight changes differentially impact MASLD incidence, progression and outcomes based on genetic and metabolic risk profiles.","authors":"Lanlan Chen, Alfred Wei Chieh Kow, Guoyue Lv, Adrien Guillot, Frank Tacke","doi":"10.1016/j.cgh.2026.07.019","DOIUrl":"https://doi.org/10.1016/j.cgh.2026.07.019","url":null,"abstract":"<p><strong>Background & aims: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) comprises heterogeneous subgroups with liver- vs. cardiovascular-related adverse outcomes. Weight management is crucial in MASLD prevention and treatment, but its effect on MASLD subgroups is unclear.</p><p><strong>Methods: </strong>We assessed the impact of body weight dynamics on incident MASLD, steatosis resolution, fibrosis risk regression and related cardiovascular diseases (CVD) from the UK biobank. Genetic subgroups (i.e., hepatic and systemic) were defined by polygenic risk scores, a metabolic risk group by lipid accumulation product. A Cox proportional model evaluated impacts across the general population and sex-stratified subgroups.</p><p><strong>Results: </strong>Among 11,882 participants without MASLD, 1,350 developed MASLD during a median follow-up of 4 years. Each 1% reduction in body weight was associated with a 10% lower risk of MASLD (HR = 0.90 [0.89-0.91]). Among 6,013 participants with MASLD, 753 achieved MASLD resolution; each 1% weight reduction was associated with a 9% higher rate of resolution (HR = 1.09 [1.08-1.10]). Weight loss was also associated with a lower risk of MASLD-related CVD (HR = 0.98 [0.97-0.99]). Recommended weight loss for MASLD prevention (male/female) differed across hepatic (8.7%/13.1%), systemic (8.0%/11.8%), and metabolic-risk (10.9%/14.4%) groups. Estimated lower weight-loss thresholds associated with MASLD resolution were 5.3%/13.3% in hepatic-risk, 10.2%/10.7% in systemic-risk, and 5.7%/5.8% in metabolic-risk participants (male/female). For fibrosis-risk regression, no robust threshold was identified in hepatic-risk participants, but 7.7%/5.6% in metabolic-risk participants (male/female).</p><p><strong>Conclusion: </strong>Individualized weight management should be recommended according to the genetic and metabolic risk profiles of individuals.</p>","PeriodicalId":10347,"journal":{"name":"Clinical Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":16.2,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149148210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-world hepatic safety of the potassium-competitive acid blocker: A RUCAM-adjudicated multicenter cohort study.","authors":"Hye Yeon Chon, Hae-Ryong Yun, Da Hyun Jung, Jeonghyun Lim, So Hyeon Gwon, Nak-Hoon Son, Young Hoon Youn, Cheal Wung Huh","doi":"10.1016/j.cgh.2026.09.045","DOIUrl":"https://doi.org/10.1016/j.cgh.2026.09.045","url":null,"abstract":"<p><strong>Background & aims: </strong>Early-generation potassium-competitive acid blockers (P-CABs) were withdrawn during clinical development because of hepatotoxicity, and long-term real-world hepatic safety data for newer P-CABs remain scarce. Drug-induced liver injury (DILI) ascertainment in observational studies is further limited by the reliance on nonspecific outcome definitions. We aimed to evaluate the hepatic safety of tegoprazan compared with proton pump inhibitors (PPIs) and histamine-2 receptor antagonists (H2RAs) using Roussel Uclaf Causality Assessment Method (RUCAM)-based adjudication.</p><p><strong>Methods: </strong>This large-scale, multicenter retrospective cohort study used a new-user, active-comparator design including users of tegoprazan, PPIs, or H2RAs with ≥30 cumulative defined daily doses (cDDDs). Propensity score matching (PSM) balanced demographics, comorbidities, hepatotoxic co-medications, and baseline liver biochemistry. The primary outcome was RUCAM-adjudicated DILI (score ≥3); hazard ratios (HRs) were estimated by Cox regression with Firth's penalized likelihood for rare events.</p><p><strong>Results: </strong>Of 363,340 screened patients, 11,190 were included; PSM yielded 5,586 (1,862/group). RUCAM-possible DILI was very rare, with 3, 2, and 3 events (0.17, 0.07, and 0.15 per 100 person-years) in the tegoprazan, PPI, and H2RA groups, respectively. No increased risk was detected for tegoprazan versus H2RAs (Firth-penalized HR 0.98; 95% CI, 0.20-4.95) or PPIs (HR 1.63; 95% CI, 0.28-9.56), with wide confidence intervals. No case exceeded the \"possible\" RUCAM threshold.</p><p><strong>Conclusions: </strong>No increased risk of RUCAM-possible DILI was detected for tegoprazan compared with PPIs or H2RAs, although the small number of events precludes a conclusion of equivalent safety. The rarity of RUCAM-possible events across all acid-suppressive drug classes raises the possibility that previously reported signals may partly reflect differences in outcome ascertainment.</p>","PeriodicalId":10347,"journal":{"name":"Clinical Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":16.2,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149147381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Avoidant/restrictive food intake across the gastrointestinal tract.","authors":"Karen Routhiaux, Karen Van den Houte, Lukas Balsiger, Karlien Raymenants, Cedric Van de Bruaene, Bert Broeders, Annelies Verheyden, Helen Burton-Murray, Michael P Jones, Tim Vanuytsel, Jan Tack","doi":"10.1016/j.cgh.2026.09.046","DOIUrl":"https://doi.org/10.1016/j.cgh.2026.09.046","url":null,"abstract":"<p><strong>Background: </strong>Avoidant/restrictive food intake disorder (ARFID) is characterized by reduced dietary intake leading to medical and/or psychosocial impairment, independent of body image concerns. We aim to assess ARFID screening and characteristics in patients with gastrointestinal disorders versus healthy volunteers (HV), and its associations with symptom severity, extraintestinal symptoms and depression scores.</p><p><strong>Methods: </strong>We analyzed 92 HV and 467 patients from seven tertiary cohorts: irritable bowel syndrome (IBS, n=88), functional dyspepsia (FD, n=83), constipation (n=59), reflux (n=107), globus (n=45), dysphagia (n=37), and achalasia (n=48), grouped into non-esophageal (IBS, FD, constipation) and esophageal disorders (reflux, globus, dysphagia and achalasia). Assessments included Rome IV criteria, extraintestinal symptoms and depression scores (PHQ-12/9), and ARFID screening. ARFID+ was defined as NIAS+ (≥1 subscale cutoff: picky eating ≥10, appetite ≥9, fear ≥10) plus DSM-5 impairment. Odds ratios were derived from multiple logistic regression with three-level hierarchical approach adjusted for symptom severity, extra-intestinal, and depression symptoms.</p><p><strong>Results: </strong>Compared to HV, IBS (OR=15.0), FD (OR=10.6), constipation (OR=18.2), reflux (OR=5.2) and dysphagia (OR=7.0) were associated with ARFID+, whereas globus or achalasia were not. A higher prevalence of ARFID+ was observed in non-esophageal versus esophageal disorders (24% vs. 11%; OR=2.7, p<0.001), remaining significant after adjustments. Within non-esophageal disorders, depressive symptoms (OR=1.1) and food-related abdominal pain (OR=1.2) were independently associated with ARFID+, with fear-based food avoidance emerging as primary contributor to pain-related restrictive eating (β=0.3, p<0.001).</p><p><strong>Conclusion: </strong>ARFID symptoms are more prevalent across non-esophageal disorders compared to esophageal disorders. Within non-esophageal disorders, symptoms severity and food-related abdominal pain are associated with ARFID+, and mostly characterized by fear of aversive consequences.</p>","PeriodicalId":10347,"journal":{"name":"Clinical Gastroenterology and Hepatology","volume":" ","pages":""},"PeriodicalIF":16.2,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149147569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Referent Choice and Dose–Response Modeling Behind Moderate, Unsweetened Coffee","authors":"Xingyong Huang, Tao Han, Kai Zhang","doi":"10.1016/j.cgh.2026.08.040","DOIUrl":"https://doi.org/10.1016/j.cgh.2026.08.040","url":null,"abstract":"","PeriodicalId":10347,"journal":{"name":"Clinical Gastroenterology and Hepatology","volume":"13 1","pages":""},"PeriodicalIF":12.6,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TREAT-TO-TARGET IN INFLAMMATORY BOWEL DISEASE: PROMISE, PERILS, AND THE PATH FORWARD","authors":"Siddharth Singh MD MS, Olga Maria Nardone MD PhD, Mariangela Allocca MD PhD, Yuhong Yuan MD PhD, Jakob Begun MD PhD, Jason K. Hou MD MS, Mohammad Shehab MD, Taku Kobayashi MD PhD, Vineet Ahuja MD DM, Axel Dignass, Vipul Jairath MBChB Dphil","doi":"10.1016/j.cgh.2026.09.033","DOIUrl":"https://doi.org/10.1016/j.cgh.2026.09.033","url":null,"abstract":"Treat-to-target has become the organising framework for contemporary inflammatory bowel disease (IBD) management, yet its evidence base is less robust than its widespread endorsement might suggest. The approach rests on two equally essential pillars: defining the right therapeutic target, and adjusting treatment iteratively until that target is achieved. Over the past decade, the first pillar has advanced substantially: targets have deepened from symptomatic remission through endoscopic and histologic healing toward transmural and emerging molecular endpoints, supported largely by association data linking deeper remission to better long-term outcomes. The second pillar has received considerably less scrutiny. Completed randomised trials of iterative treatment adjustment have yielded mixed results in unselected populations, real-world monitoring remains inconsistent, and the most clinically pressing question, whether asymptomatic patients with residual inflammation benefit from optimising or switching advanced therapies, remains unanswered. In this review, we critically examine both pillars: the evolution and evidence base for treatment targets in IBD, the ability of current therapies to achieve them, the lessons from pivotal treat-to-target trials, and the barriers to real-world implementation. We propose a framework for individualising treat-to-target decisions based on disease history, inflammatory trajectory, therapeutic options, and patient preferences. Ongoing trials including QUOTIENT, VERDICT, and VECTORS may define whether the second pillar can be placed on as firm a footing as the first.","PeriodicalId":10347,"journal":{"name":"Clinical Gastroenterology and Hepatology","volume":"7 1","pages":""},"PeriodicalIF":12.6,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}