Lancet Gastroenterology & Hepatology柳叶刀胃肠病学与肝病学
Lancet Gastroenterology & Hepatology(英文缩写 LANCET GASTROENTEROL),ISSN 2468-1253,eISSN 2468-1253,中文译名:柳叶刀胃肠病学与肝病学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
Lancet Gastroenterology & Hepatology 最新收录文献
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1. Pain management in chronic pancreatitis: beyond opioids.
1. 慢性胰腺炎的疼痛管理：超越阿片类药物PMID:日期:2026-09-29Chronic pancreatitis is characterised by complex, multifactorial pain affecting 80-90% of patients. Pain arises from overlapping nociceptive and neuropathic mechanisms, often accompanied by CNS sensitisation and reorganisation that amplify symptoms (nociplastic pain). Opioid use is highly prevalent in chronic pancreatitis despite its many side-effects and addictive potential, and there is a need for alternative treatment strategies. Non-opioid pharmacological treatments, including neuromodulators, target specific pain mechanisms, with gabapentinoids showing the strongest evidence. Other interventions, such as cognitive behavioural therapy, antioxidants, dietary strategies, and lifestyle modification, might provide additional benefit, but high-quality evidence remains scarce. Endoscopic and surgical interventions relieve obstructive disease; however, the evidence base has a shortage of sham-controlled trials, complicating the interpretation of treatment effect. Emerging approaches, including novel neuromodulatory and anti-inflammatory therapies and integration of pharmacological and non-pharmacological treatments, hold promise for improving pain control. Multidimensional assessment, combining patient-reported outcomes, quantitative sensory testing, imaging, and emerging biomarkers, enables pain phenotyping and could support more individualised and more effective management, guiding multimodal strategies. Future research should prioritise mechanism-based trials, refined patient phenotyping, and predictive biomarkers to guide personalised therapies.
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2. Short-course prophylaxis with the Toronto HCV protocol for recipients of non-liver solid organ transplants from donors with hepatitis C viraemia: a retrospective, matched cohort study.
2. 非肝脏实体器官移植受者接受来自丙型肝炎病毒血症供体的多伦多HCV方案短程预防：一项回顾性匹配队列研究PMID:日期:2026-09-29Organs from donors positive for hepatitis C virus (HCV) nucleic acid testing (NAT-positive) expand the non-liver solid organ donor pool. Standard post-transplantation direct-acting antiviral therapy requires an 8-12-week course, which might add logistical, financial, and pharmacological complexity. We therefore aimed to evaluate long-term follow-up from an initial pilot trial and outcomes after adoption of the short-course Toronto HCV protocol as the institutional standard of care in HCV-negative recipients of organs from HCV viraemic donors. This retrospective, matched cohort study was conducted at a single transplant centre at Toronto General Hospital (Toronto, ON, Canada). Eligible patients were HCV NAT-negative recipients (aged ≥18 years) who received kidney, kidney-pancreas, pancreas, heart, or lung transplants from an HCV NAT-positive donor (aged <70 years). Recipients were categorised into the initial cohort (received treatment during the initial pilot study; n=30) and standard of care cohort (received treatment after institutional adoption of the Toronto HCV protocol on Jan 9, 2020; n=86). The Toronto HCV protocol consists of oral glecaprevir 300 mg/day and pibrentasvir 120 mg/day and oral ezetimibe 10 mg/day for 8 days. The first dose is administered 6-12 h before transplantation for 8 days (one pretransplantation dose and seven post-transplantation doses). Data were abstracted from electronic medical records. Each donor-positive, recipient-negative (D+R-) recipient of kidney, lung, and heart transplants was matched with up to four donor-negative, recipient-negative (D-R-) controls based on organ type, sex, age, transplantation date, and primary disease. The primary outcome was undetectable HCV RNA at 12 weeks post-transplantation or at the latest documented assessment for recipients who died before that timepoint. Secondary outcomes were 2-year overall survival, graft function at 1 year (mean estimated glomerular filtration rate [eGFR], mean forced expiratory volume in 1 s [FEV], and left ventricular ejection fraction <40%), and safety. Survival was compared between D+R- recipients and matched D-R- controls separately for each organ type using a Cox proportional hazards regression model stratified by matched set. Between Feb 4, 2019, and Dec 31, 2024, 116 D+R- non-liver solid organ transplantations were performed using organs from 72 unique HCV NAT-positive donors: 56 (48%) kidney, 34 (29%) lung, 16 (14%) heart, six (5%) kidney-pancreas, and four (3%) pancreas transplants. The mean recipient age was 54·6 years (SD 14·4). 79 (68%) recipients were male and 37 (32%) were female. The matched D-R- cohort consisted of 168 kidney, 103 lung, and 16 heart transplant recipients (matching was not done for other organs due to small numbers). All 116 (100%) D+R- recipients met the primary endpoint; 114 (98%) recipients had documented undetectable HCV RNA at 12 weeks post-transplantation and two (2%) recipients who died before 12 weeks had undetectable HCV RNA at the latest assessment before death. 25 (22%) deaths occurred during a median follow-up of 140 weeks (IQR 46-212). 2-year overall survival was 83·9% (95% CI 74·6-90·0) among the 106 kidney, lung, and heart recipients; no deaths occurred among the ten pancreas or kidney-pancreas recipients. Within each organ group, there was no difference in 2-year overall survival between D+R- and D-R- recipients for kidney (93·5% [95% CI 81·1-97·9] vs 94·8% [89·8-97·4]; hazard ratio [HR] 1·50 [95% CI 0·38-6·00], p=0·57), lung (70·6% [50·9-83·5] vs 78·7% [68·8-85·7]; HR 1·62 [0·70-3·73], p=0·26), or heart (81·3% [52·5-93·5] vs 81·3% [52·5-93·5]; HR 3·00 [0·31-28·84], p=0·34) transplants. Graft function at 1 year was similar between D+R- and D-R- recipients (mean eGFR 63·9 mL/min per 1·73m [SD 22·2] vs 57·4 mL/min per 1·73m [20·9], p=0·24; mean FEV 2·18 L [SD 0·87] vs 2·29 L [0·85], p=0·59; and left ventricular ejection fraction <40% in one [6%] vs three [19%], p=0·60). No HCV-related complications were reported and there were no treatment-related deaths, treatment discontinuations, dose modifications, or clinically significant drug-drug interactions. One (1%) grade 3 elevation in alanine aminotransferase in a kidney recipient was deemed possibly related to treatment. Laboratory tests for cause of liver injury in this patient were unrevealing and liver biopsy showed non-specific acute hepatitis with moderate steatosis and no fibrosis. The Toronto HCV protocol prevented or rapidly cleared HCV infection in D+R- recipients of non-liver solid organ transplants, with no difference in overall survival versus matched D-R- controls. This short-course approach offers a practical, lower cost alternative to standard post-transplantation antiviral regimens and supports routine use of organs from donors with HCV viraemia. None.
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3. Aspirin after curative-intent treatment of colorectal cancer liver metastases (ASAC): a multicentre, phase 3, randomised, double-blind, placebo-controlled trial.
3. 结直肠癌肝转移根治性治疗后使用阿司匹林（ASAC）：一项多中心、3期、随机、双盲、安慰剂对照试验PMID:日期:2026-09-23Colorectal cancer frequently metastasises to the liver. Recurrence after curative-intent treatment of colorectal cancer liver metastases is common. Aspirin has shown preventive and antitumour effects in colorectal cancer, but its role after treatment of metastatic disease is uncertain. We aimed to establish whether adjuvant aspirin improves disease-free survival after curative-intent treatment of colorectal cancer liver metastases. In this phase 3, randomised, double-blind, placebo-controlled trial conducted at 14 centres in Norway, Sweden, and Denmark, patients who had undergone curative-intent treatment for colorectal cancer liver metastases were randomly assigned (1:1), stratified by study site using a centrally generated computerised sequence with variable block sizes, to aspirin 160 mg per day or matching placebo for up to 3 years or until recurrence, death, or treatment discontinuation. The primary outcome was disease-free survival in the full analysis set, comprising all patients who initiated study treatment. The trial is completed and this is the final analysis. This trial is registered with ClinicalTrials.gov, NCT03326791, and EudraCT, 2014-003601-15. Between Dec 15, 2017, and Jan 27, 2022, 466 patients were randomly assigned, of whom 428 initiated study treatment and were included in the full analysis set (217 assigned aspirin and 211 assigned placebo); 272 (64%) were male, 156 (36%) were female, and the mean age was 62·2 years. 269 disease-free survival events occurred (138 in the aspirin group and 131 in the placebo group). Aspirin did not improve disease-free survival (hazard ratio [HR] for recurrence or death 1·08 [95·44% CI 0·85-1·38]; p=0·58). Median disease-free survival was 1·13 years (95·44% CI 0·92-1·44) with aspirin and 1·40 years (1·11-1·69) with placebo. Overall survival at 36 months was 76% (95% CI 69·4-82·7) with aspirin and 85% (79·5-90·8) with placebo (HR for death 1·64 [95% CI 1·01-2·65]; p=0·045). Time to recurrence did not differ between groups (adjusted cause-specific HR 1·06 [95% CI 0·83-1·35]; p=0·64). 24 serious adverse events occurred in 17 (8%) of 217 patients in the aspirin group and five serious adverse events occurred in four (2%) of 211 patients in the placebo group. Clinically relevant adverse events and serious adverse events that occurred more commonly in the aspirin group than in the placebo group were myocardial infarction (two vs 0), epistaxis (four vs 0), duodenal ulcer (two vs 0), and cerebral haemorrhage (two vs 0). There were no treatment-related deaths. Adjuvant aspirin did not improve disease-free survival and was associated with lower overall survival and more serious adverse events. These findings do not support routine use of aspirin after curative-intent treatment of colorectal cancer liver metastases. Research Council of Norway, Norwegian Cancer Society, Therapy Research in the Specialist Health Services Norway, and Oslo University Hospital Fondsstiftelsen.
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4. Lessons from the European LiverScreen and Chinese LiverHealth projects.
4. 欧洲肝筛项目和中国肝健康项目的经验教训PMID:日期:2026-09-22该文献暂无摘要。
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5. Prevalence of liver fibrosis and steatotic liver disease in community-dwelling adults in China (the CHESS-LiverHealth project): cross-sectional baseline data from a prospective cohort study.
5. 中国社区成年人肝纤维化和脂肪性肝病患病率（CHESS-LiverHealth项目）：一项前瞻性队列研究的横断面基线数据PMID:日期:2026-09-22Chronic liver disease is rapidly increasing worldwide, largely driven by the growing epidemics of overweight and obesity, diabetes, and harmful alcohol consumption. China has the world's largest population with these conditions, but has scarce prospective, community-based data to estimate the true burden of chronic liver disease. We aimed to estimate the prevalence of liver fibrosis and steatotic liver disease and identify their associated factors in community-dwelling adults in China. The CHESS-LiverHealth project was an investigator-initiated, prospective, community-based cohort study conducted at 18 sites corresponding to county-level units in 13 provincial-level administrative regions in China. Community-dwelling adults aged 18 years or older were enrolled and underwent vibration-controlled transient elastography (VCTE). We report cross-sectional baseline data from this study. The primary outcome was the prevalence of liver fibrosis, as estimated by a liver stiffness measurement (LSM) of 8 kPa or more. Secondary outcomes included the prevalence of liver fibrosis at higher LSM thresholds (≥10 kPa and ≥12 kPa), steatotic liver disease (controlled attenuation parameter ≥248 dB/m) and its severity categories, and steatotic liver disease subtypes-metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic and alcohol-associated liver disease (MetALD), and alcohol-associated liver disease (ALD)-together with factors associated with these outcomes. Between Sept 23, 2024, and Jan 23, 2026, 38 859 individuals entered the recruitment pathways, of whom 29 023 were enrolled. After exclusion of individuals with previous cirrhosis, liver cancer or other malignancies, those with missing or unreliable VCTE measurements, and those with incomplete baseline information, 25 736 individuals were included in this analysis. These individuals had a median age of 51·0 years (IQR 38·0-60·0); 11 548 (44·9%) were male and 14 188 (55·1%) were female. The prevalence of LSM of 8 kPa or more was 4·4% (95% CI 4·2-4·7; n=1136), LSM 10 kPa or more was 1·6% (1·5-1·8; n=421), and LSM 12 kPa or more was 0·8% (0·7-0·9; n=205). Steatotic liver disease was present in 43·7% (43·1-44·3; n=11 242) of participants, with MASLD in 39·5% (38·9-40·1; n=10 162), MetALD in 2·0% (1·8-2·2; n=516), and ALD in 1·6% (1·5-1·8; n=411) of participants. The highest prevalences of LSM of 8 kPa or more were observed in individuals with obesity (10·7% [9·8-11·6]; n=487 of 4560) and type 2 diabetes (10·7% [9·7-11·8]; n=365 of 3400). In multivariable analyses, male sex, older age, heavy alcohol consumption, an Alcohol Use Disorders Identification Test score of 16 or more, overweight or obesity, central obesity, prediabetes or type 2 diabetes, hypertension, dyslipidaemia, and an increasing number of cardiometabolic risk factors were independently associated with both LSM of 8 kPa or more and steatotic liver disease. Chronic viral hepatitis was also independently associated with LSM of 8 kPa or more. Liver fibrosis and steatotic liver disease are prevalent in community-dwelling Chinese adults, driven by metabolic factors and alcohol consumption. These findings identify chronic liver disease as a major public health challenge in China. Community-based, non-invasive screening integrated with metabolic and alcohol risk assessment might offer a crucial opportunity for early detection and targeted interventions to curb the progression to cirrhosis and hepatocellular carcinoma. Zhongda Hospital, School of Medicine, Southeast University.
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6. Genetic variants and the risk of renal impairment in decompensated cirrhosis: a multi-ancestry genome-wide association study.
6. 遗传变异与失代偿期肝硬化肾功能损害风险：一项多祖先全基因组关联研究PMID:日期:2026-09-18Renal impairment is a major complication of decompensated cirrhosis and a key driver of mortality. Despite its clinical significance, the genetic architecture of susceptibility to renal impairment in this context remains largely unexplored. We conducted a multi-ancestry genome-wide association study (GWAS) to identify genetic loci associated with renal impairment in decompensated cirrhosis. We performed a GWAS for serum creatinine levels in 3220 patients with decompensated cirrhosis across five cohorts (CANONIC [n=707], PREDICT [n=825], ACLARA [n=671], Bologna [n=272], and Brussels [n=745]); with 83% of patients having European and 17% having admixed American genetic ancestry. Findings were replicated in 1728 European patients with decompensated cirrhosis across four independent cohorts (Czech-Romanian [n=988], CirVir-CIRRAL [n=139], French-Belgian [n=294], and German [n=307]). Associations were evaluated in 3139 patients with compensated cirrhosis (EuroLiver [n=851], CirVir-CIRRAL [n=1142], and the UK Biobank [n=1146]) and 402 683 individuals from the UK Biobank with no history of cirrhosis, who served as a general population comparator. Single-cell and spatial transcriptomics mapped GWAS associations to cell types in the liver, blood, and kidney. We identified a genome-wide significant association at the SUSD1 locus (lead variant rs2099161[C→T]; trans-ancestry-discovery β=0·16 [95% CI 0·11 to 0·21], p=4·32 × 10; independent replication β=0·09 [0·03 to 0·16], p=5·34 × 10; combined meta-analysis β=0·13 [0·09 to 0·17], p=8·31 × 10; I=0%). The effect was specific to decompensated cirrhosis, with no association in compensated cirrhosis (β= -0·0003 [-0·0460 to 0·0454], p=0·99) or the general population (β= -0·005 [-0·009 to -0·002], p=3·78 × 10). Each additional copy of the rs2099161(C) risk allele was associated with a higher risk of kidney failure at inclusion in the ACLARA, CANONIC, PREDICT, Bologna, Brussels, Czech-Romanian, and French-Belgian cohorts (n=4390, p=6·34 × 10). The risk was highest in CC homozygotes compared with patients with the TT genotype (odds ratio 1·60 [95% CI 1·21 to 2·11]). A similar pattern was observed for incident kidney failure at 1 week (CANONIC cohort n=638, p=0·035, CC vs TT genotypes 2·00 [1·10 to 3·65]), and terlipressin requirement (PREDICT, ACLARA, and Brussels cohorts, n=2161, p=0·027, CC vs TT genotypes 2·06 [1·08 to 3·93]). Transcriptomic analyses identified plasmacytoid dendritic cells as the primary SUSD1-expressing cell-type with elevated expression in patients with renal impairment across compartments. Patients with renal impairment showed increased abundance of plasmacytoid dendritic cells and type-I-interferon signalling in liver and kidney tissues. SUSD1 is a risk locus for renal impairment in decompensated cirrhosis, with genetic effects that appear context-dependent across cirrhosis stages and the general population. Our findings implicate the plasmacytoid dendritic cell-interferon axis as a candidate mechanism linking liver dysfunction to kidney injury. European Foundation for the Study of Chronic Liver Failure and Horizon Europe.
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7. Decompensation unmasks renal susceptibility in cirrhosis.
7. 失代偿揭示了肝硬化患者的肾脏易感性PMID:日期:2026-09-18该文献暂无摘要。
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8. Long-term outcomes of top-down therapy versus a conventional step-up strategy in adults newly diagnosed with Crohn's disease: 5-year follow-up of the PROFILE trial.
PMID:日期:2026-09-10The PROFILE trial previously reported better 48-week outcomes for patients with Crohn's disease who received top-down anti-TNF treatment from diagnosis, compared with a conventional step-up strategy. Through subsequent follow-up of PROFILE participants, we aimed to assess whether the benefit of top-down treatment from diagnosis results in modification of the long-term disease course. PROFILE was a multicentre, open-label, randomised controlled trial completed in 40 hospitals in the UK, which included patients aged 16-80 years with newly diagnosed Crohn's disease. Eligible patients were randomly assigned via a secure online platform to a top-down (infliximab plus immunomodulator) or a step-up protocolised treatment strategy for 48 weeks, after which participants reverted to local standards of care. Objective outcome data were extracted for up to 5 years after the week 48 visit, including need for Crohn's-related abdominal surgery as the primary outcome. Data were analysed based on the original PROFILE randomisation and intention-to-treat population. Participants without long-term follow-up data were censored at the week 48 visit. Time-to-event analyses were performed using the Kaplan-Meier method and Cox proportional hazards model. The trial was registered with the ISRCTN registry, number 11808228 and is complete. Between Dec 29, 2017, and Jan 5, 2022, 483 patients were assessed for inclusion. 389 patients were enrolled and randomly assigned (three patients were excluded due to ineligibility), 193 to top-down treatment and 193 to step-up treatment. Of the 386 participants in the PROFILE primary trial, 358 (93%) had post-week 48 records available for review (182 [51%] top-down and 176 [49%] step-up). Median follow-up was approximately 5 years from randomisation (1809 days [IQR 1300-2101]), by which point 172 (89%) of 193 patients in the step-up group and 191 (99%) of 193 patients in the top-down group had received biological or immunomodulator therapy. Relating to the primary outcome, during follow-up there were 28 Crohn's disease-related abdominal surgeries in 26 patients treated with a step-up approach versus six surgeries in six patients treated with a top-down approach. Time to surgery was shorter in the step-up group than the top-down group (adjusted hazard ratio [aHR] 5·23 [95% CI 1·99-13·76]; p=0·0008). For the secondary outcomes, incidence of Crohn's disease-related hospital admissions was higher in patients originally managed with step-up treatment versus top-down treatment (41 [21%] of 193 patients vs 22 [11%] of 193 patients); and time to first hospital admission was shorter with step-up treatment than with top-down treatment (aHR 2·01 [95% CI 1·18-3·41], p=0·017). Progression to B2 or B3 complications was also more frequent in those originally managed with step-up treatment compared with top-down treatment (32 [17%] of 192 patients vs 13 [7%] of 193 patients); with time to disease progression being shorter in the step-up group than in the top-down group (aHR 2·46 [95% CI 1·25-4·86]; p=0·010). There was no difference in safety outcomes between groups for either serious infections (12 [6%] of 193 step-up patients and 14 [7%] of 193 top-down patients) or malignancies (five patients [3%] and three patients [2%] respectively). Early top-down anti-TNF treatment from diagnosis was associated with improved long-term outcomes at 5 years compared with step-up treatment and is suggestive of a disease-modifying effect in Crohn's disease. Wellcome and Celltrion.
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9. Germline multigene panel testing for colorectal cancer: a systematic review and meta-analysis.
9. 结直肠癌胚系多基因panel检测：一项系统评价与荟萃分析PMID:日期:2026-09-03Colorectal cancer can arise from an inherited genetic background, but the diagnostic yield of multigene germline panel testing in patients diagnosed with colorectal cancer remains uncertain. The aim of this study was to quantify such yield. In this systematic review and meta-analysis, we searched PubMed (MEDLINE), Embase, Scopus, and the Cochrane Central Register of Controlled Trials from database inception to Aug 2, 2025, for studies published in English reporting the results of germline multigene panel testing of at least five genes using next-generation sequencing in unselected patients with colorectal cancer. Eligible study designs included cross-sectional and cohort studies, and clinic-based series in which all consecutive patients with colorectal cancer were offered multigene panel testing. Two independent reviewers, masked from each other's decisions, screened records and extracted summary data and individual participant data, with conflicts resolved by a third reviewer. Risk of bias was assessed using the Newcastle-Ottawa Scale. The primary outcome was the person-level prevalence (diagnostic rate) of at least one pathogenic or likely pathogenic variant in cancer predisposition genes. Analyses were stratified by age at colorectal cancer diagnosis and gene penetrance. Random-effects meta-analyses estimated pooled prevalence. Heterogeneity was quantified using the I statistic. Meta-regression evaluated the effect of age at colorectal cancer diagnosis, panel size, family history, and publication year on diagnostic rates. This study was registered in PROSPERO, CRD42025649177. Of 2707 records identified, 1682 duplicates were removed and screening excluded a further 985 records. 40 articles underwent full-text review, of which 21 met eligibility criteria and were included (ten [48%] at low, nine [43%] at moderate, and two [10%] at high risk of bias). Across 6925 individuals with colorectal cancer, the pooled rate of any pathogenic or likely pathogenic variant was 15·2% (95% CI 12·8-18·1; 1061/6925; I=84·1%; k=12), with high-penetrance variants identified in 7·9% (5·9-10·5; 551/6909; I=88·4%; k=11) and high-penetrance colorectal cancer predisposition variants in 5·4% (3·5-8·6; 408/6909; I=93·4%; k=11). In early-onset colorectal cancer (age at diagnosis <50 years), yields were 17·7% (15·0-20·7; 1113/7444; I=85·7%; k=16) for any pathogenic or likely pathogenic variant, 14·2% (11·7-17·3; 917/7409; I=85·7%; k=15) for high-penetrance variants, and 12·2% (9·5-15·5; 788/7409; I=89·5%; k=15) for high-penetrance colorectal cancer predisposition variants. In late-onset colorectal cancer (age at diagnosis ≥50 years), yields were 13·0% (10·8-15·7; 711/5243; I=73·3%; k=11) for all variants, 6·5% (4·4-9·5; 349/5227; I=86·4%; k=10) for high-penetrance variants, and 3·8% (2·0-7·5; 234/5227; I=90·3%; k=10) for high-penetrance colorectal cancer predisposition variants. In meta-regression analyses, panel size and publication year did not affect yields. A higher prevalence of first-degree family history of colorectal cancer correlated with increased overall and colorectal cancer-specific variant yields, but not with non-colorectal variant yields. There was a progressive decline in yield with increasing age at colorectal cancer diagnosis, although the yield for high-penetrance variants remained greater than 5% up to age 67 years (95% CI 59-75). The yield of multigene panel testing is considerable in unselected patients with colorectal cancer, even beyond early-onset disease. The yield of high-penetrance germline variants remains above recognised testing thresholds up to age 67 years, providing a benchmark of universal testing for further study. Italian Ministry of University, EU-Next Generation EU, and National Cancer Institute.
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10. Incidence of inflammatory bowel disease in Jakarta, Indonesia, 2021-24.
PMID:日期:2026-09-01该文献暂无摘要。