Gastroenterology Report最新文献

{"title":"Prediction of major liver-related events in the population using prognostic models.","authors":"Fredrik Åberg, Ville Männistö","doi":"10.1093/gastro/goaf028","DOIUrl":"10.1093/gastro/goaf028","url":null,"abstract":"<p><p>Liver disease poses a significant global health burden, with steatotic liver disease related to metabolic dysfunction and/or alcohol use being the most prevalent type. Current risk stratification strategies emphasize detecting advanced fibrosis as a surrogate marker for liver-related events (LREs), such as hospitalization, liver cancer, or death. However, fibrosis alone does not adequately predict imminent outcomes, particularly in fast-progressing individuals without advanced fibrosis at evaluation. This underscores the need for models designed specifically to predict LREs, enabling timely interventions. The Chronic Liver Disease (CLivD) risk score, the dynamic aspartate aminotransferase-to-alanine aminotransferase ratio (dAAR), and the Cirrhosis Outcome Risk Estimator (CORE) were explicitly developed to predict LRE risk rather than detect fibrosis. Derived from general population cohorts, these models incorporate either standard liver enzymes (dAAR and CORE) or risk factors (CLivD), enabling broad application in primary care and population-based settings. They directly estimate the risk of future LREs, improving on traditional fibrosis-focused approaches. Conversely, widely used models like the Fibrosis-4 index and newer ones, such as the LiverRisk and LiverPRO scores, were initially developed to detect significant/advanced fibrosis or liver stiffness. While not designed for LRE prediction, they have later been analyzed for this purpose. Integrating fibrosis screening with LRE-focused models like CLivD, dAAR, and CORE can help healthcare systems adopt proactive, preventive care. This approach emphasizes identifying individuals at imminent risk of severe outcomes, potentially ensuring better resource allocation and personalized interventions.</p>","PeriodicalId":54275,"journal":{"name":"Gastroenterology Report","volume":"13 ","pages":"goaf028"},"PeriodicalIF":3.8,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143651886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Los Angeles-B esophagitis is a conclusive diagnostic evidence for gastroesophageal reflux disease: the validation of Lyon Consensus 2.0.","authors":"Jing Chen, Peiwen Dong, Songfeng Chen, Qianjun Zhuang, Mengyu Zhang, Kaidi Sun, Feng Tang, Qiong Wang, Yinglian Xiao","doi":"10.1093/gastro/goaf004","DOIUrl":"10.1093/gastro/goaf004","url":null,"abstract":"<p><strong>Background and aims: </strong>Recently, Lyon Consensus 2.0 recommended Los Angeles (LA)-B esophagitis as conclusive evidence and LA-A esophagitis as borderline evidence for gastroesophageal reflux disease (GERD). This study aimed to investigate the diagnostic value of LA-B and LA-A esophagitis.</p><p><strong>Methods: </strong>Patients with typical reflux symptoms who underwent endoscopy examination and received acid-suppressive therapy from two tertiary hospitals [the First Affiliated Hospital of Sun Yat-sen University (Guangzhou, P. R. China) and the Third People's Hospital of Chengdu (Chengdu, P. R. China)] were retrospectively included. Acid-suppression response rates, endoscopy results, motility, and reflux parameters were compared between patients with different grades of esophagitis.</p><p><strong>Results: </strong>In total, 401 patients were enrolled, among whom 254 were without reflux esophagitis (RE), 51 had LA-A esophagitis, 44 had LA-B esophagitis, and 52 had LA-C/D esophagitis. Patients with LA-B esophagitis and LA-C/D esophagitis had significantly higher acid-suppressive response rates than non-RE patients (<i>P </i><<i> </i>0.05), whereas no significant difference was found between patients with LA-A esophagitis and non-RE patients (non-RE vs LA-A vs LA-B vs LA-C/D: 52.4% vs 70.6% vs 75.0% vs 82.7%). Among patients with LA-A esophagitis, those with a number of reflux episodes that exceeded 80 per day (90.0% vs 52.4%, <i>P </i>=<i> </i>0.044) or hypotensive esophagogastric junction (72.4% vs 52.4%, <i>P </i>=<i> </i>0.040) had significantly higher acid-suppressive response rates than non-RE patients.</p><p><strong>Conclusions: </strong>LA-B esophagitis can be regarded as conclusive evidence for GERD and initiate acid-suppressive therapy. LA-A esophagitis did not establish a definite GERD diagnosis alone. When combined with adjunctive or supportive evidence, the acid-suppressive therapy response rate of LA-A esophagitis improved.</p>","PeriodicalId":54275,"journal":{"name":"Gastroenterology Report","volume":"13 ","pages":"goaf004"},"PeriodicalIF":3.8,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143626988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nedd4L signaling contributes to carbon tetrachloride-induced liver fibrosis in female mice and is associated with enteric dysbacteriosis.","authors":"Cheng Chen, Yanghui Bi, Bangtao Chen, Song He","doi":"10.1093/gastro/goaf022","DOIUrl":"10.1093/gastro/goaf022","url":null,"abstract":"<p><strong>Background: </strong>Liver fibrosis is characterized by hepatic stellate cell (HSC) activation and collagen overproduction, but its pathogenesis remains largely unknown. This study aimed to uncover the role of neural precursor cell expressed developmentally downregulated 4-like (Nedd4L) signaling in liver fibrosis and its relationship with gut microbiota.</p><p><strong>Methods: </strong>Intraperitoneal injection of carbon tetrachloride (CCl₄) was used to induce liver fibrosis in 8-week-old female C57BL/6J mice with <i>Nedd4L</i> knockout or administration of the Nedd4L protein phosphorylation inhibitor EMD638683. HSCs isolated from mice were activated with transforming growth factor-beta 1 (TGFβ1) with or without EMD638683.</p><p><strong>Results: </strong>An approximately 3-fold elevation in <i>Nedd4L</i> mRNA was observed in hepatocytes and liver tissues, and significantly higher hepatic Nedd4L phosphorylation was observed in fibrotic mice than in non-fibrotic mice. <i>Nedd4L</i> mRNA level in HSCs isolated from fibrotic livers and Nedd4L protein level in TGFβ1-stimulated HSCs from wild-type livers remained unchanged. In isolated HSCs, TGFβ1-induced Nedd4L phosphorylation and cell activation were suppressed with EMD638683. In CCl₄-treated mice, EMD638683 alleviated liver fibrosis and induced a relative increase in fecal <i>Bacteroides</i>, <i>Parabacteroides</i>, <i>Erysipelatoclostridium</i>, <i>Blautia</i>, and <i>Klebsiella</i>, whereas Nedd4L deficiency predisposed mice to liver injury and liver fibrosis with a remarkable reduction in fecal <i>Lactobacillus</i>, <i>Enterorhabdus</i>, and <i>Bacteroides</i>.</p><p><strong>Conclusion: </strong>Hepatic Nedd4L signaling contributes to CCl₄-induced liver fibrosis in female mice, which is associated with alterations in the gut microbiota, and Nedd4L phosphorylation is involved in TGFβ1-mediated HSC activation.</p>","PeriodicalId":54275,"journal":{"name":"Gastroenterology Report","volume":"13 ","pages":"goaf022"},"PeriodicalIF":3.8,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Etiologies of exocrine pancreatic insufficiency.","authors":"Chengji Tang, Jia Zhou, Yinghui Song, Sulai Liu","doi":"10.1093/gastro/goaf019","DOIUrl":"10.1093/gastro/goaf019","url":null,"abstract":"<p><p>Exocrine pancreatic insufficiency (EPI) is a major cause of maldigestion and malnutrition, resulting from primary pancreatic diseases or other conditions. As the prevalence of EPI continues to rise, accurate identification of its etiology has become critical for the diagnosis and treatment of pancreatic secretory insufficiency. EPI can result from both pancreatic and non-pancreatic disorders. Pancreatic disorders include acute and chronic pancreatitis, pancreatic tumors, cystic fibrosis, procedures that involve pancreatic resection, and other rare causes. Non-pancreatic disorders of EPI include diabetes mellitus, celiac disease, inflammatory bowel disease, gastrointestinal and esophagectomy surgery, as well as advanced patient age. This review aims to provide a comprehensive analysis of the literature on EPI etiology, with a thorough overview to support its consideration as a potential diagnosis.</p>","PeriodicalId":54275,"journal":{"name":"Gastroenterology Report","volume":"13 ","pages":"goaf019"},"PeriodicalIF":3.8,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential function of hepatic Niemann-Pick C1-like 1: cholesterol homeostasis regulation of the canalicular lipid bilayer membrane.","authors":"Hongtan Chen, Pingfan Mo, Guoqiang Xu","doi":"10.1093/gastro/goaf010","DOIUrl":"10.1093/gastro/goaf010","url":null,"abstract":"<p><p>Niemann-Pick C1-like 1 (NPC1L1) is distributed in the human liver and intestine but only slightly expressed in the mouse liver. While it is well established that intestinal NPC1L1 is crucial for the absorption of exogenous cholesterol, the physiological and pathological roles of canalicular membrane-localized NPC1L1 in human hepatic cholesterol transport remain unclear. In this review, we discussed the potential function of human hepatic NPC1L1 and proposed that the disparity in NPC1L1 abundance between humans and mice in the liver may be attributable to their distinct bile hydrophobicity. Human hepatic NPC1L1 might interact with other proteins in the canalicular membrane, regulate membrane cholesterol homeostasis, and contribute to the stability of the canalicular lipid bilayer membrane in response to the greater detergent properties of human bile salts. We hoped to provide novel perspectives on hepatic NPC1L1 for future investigations.</p>","PeriodicalId":54275,"journal":{"name":"Gastroenterology Report","volume":"13 ","pages":"goaf010"},"PeriodicalIF":3.8,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reassessing the role of nitric oxide in the pathogenesis of sphincter of Oddi dysfunction.","authors":"Haonan Lin, Yixuan Liang, Wangqiang Zhao, Junwei Cao, Tianqi Wang, Changmiao Wang","doi":"10.1093/gastro/goaf001","DOIUrl":"10.1093/gastro/goaf001","url":null,"abstract":"<p><p>The pathogenic mechanisms underlying sphincter of Oddi dysfunction (SOD) remain incompletely understood, and it often leads to severe symptoms encompassing nausea, vomiting, and abdominal pain. New evidence now suggests correlations between nitric oxide (NO) and SOD. In this review, we summarized the factors influencing SOD pathogenesis via NO and its derivative, the peroxynitrite anion. NO appears to enhance SOD progression by modulating sphincter of Oddi (SO) contractions via NO-sGC-cGMP signaling or inducing the apoptosis of enteric neurons, interstitial cells of Cajal, smooth muscle cells, and other cellular components via peroxynitrite anion-mediated organelle damage. Thus, a comprehensive understanding of SOD will provide a foundation for the identification of potential drugs and treatment approaches.</p>","PeriodicalId":54275,"journal":{"name":"Gastroenterology Report","volume":"13 ","pages":"goaf001"},"PeriodicalIF":3.8,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11882319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143568837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An unusual gastric submucosal prominence diagnosed as hereditary hemorrhagic telangiectasia.","authors":"Likun Zhong, Hua Lin, Jianwen Nong, Nan Yi, Yunxiao Liang","doi":"10.1093/gastro/goaf007","DOIUrl":"10.1093/gastro/goaf007","url":null,"abstract":"","PeriodicalId":54275,"journal":{"name":"Gastroenterology Report","volume":"13 ","pages":"goaf007"},"PeriodicalIF":3.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11855286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary solitary fibrous tumor of the liver: an uncommon neoplasm.","authors":"Shu Sasaki, Luis Veloza, Christine Sempoux, Didier Sarazin, Emilie Uldry, Nermin Halkic, Ismail Labgaa","doi":"10.1093/gastro/goaf012","DOIUrl":"10.1093/gastro/goaf012","url":null,"abstract":"","PeriodicalId":54275,"journal":{"name":"Gastroenterology Report","volume":"13 ","pages":"goaf012"},"PeriodicalIF":3.8,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143469986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Micro-environmental changes indicate potential for subclinical intestinal tissue damage in early-age-onset colorectal cancer patients.","authors":"Sean G Kraus, Katherine A Johnson, Philip B Emmerich, Linda Clipson, Cheri A Pasch, Wei Zhang, Kristina A Matkowskyj, Dustin A Deming","doi":"10.1093/gastro/goaf015","DOIUrl":"10.1093/gastro/goaf015","url":null,"abstract":"<p><strong>Background: </strong>While improved screening rates have contributed to an overall decrease in the incidence of colorectal cancer (CRC), the incidence of early-age-onset CRC (EAO CRC; age <50 years) has increased. Here, we characterize the genetic alterations and tumor microenvironment (TME) for EAO and later-age-onset (LAO) CRCs to identify relevant biological differences that might point to etiologic factors.</p><p><strong>Methods: </strong>A cohort of EAO (<i>n </i>=<i> </i>60) and LAO (<i>n </i>=<i> </i>93) CRC patients were evaluated for mutations by using targeted DNA sequencing and for TME differences by using immunohistochemistry and immunofluorescence. The Cancer Genome Atlas (TCGA) PanCancer Atlas colorectal adenocarcinoma cohort was evaluated for transcriptional changes between EAO (<i>n </i>=<i> </i>82) and LAO (<i>n </i>=<i> </i>510) patients.</p><p><strong>Results: </strong><i>KRAS</i> and <i>BRAF</i> mutations were less frequent in EAO CRCs. Gene-set enrichment analysis of TCGA data revealed the downregulation of immune-related pathways in EAO CRCs. Both age cohorts had similar numbers of CD8⁺ tumor-infiltrating lymphocytes (TILs), although LAO patients had more CD4⁺ TILs and Th1-polarized CD4s. While significant associations between immune subsets and versican (VCAN), versikine, and alpha-smooth muscle actin (αSMA) were found, none of these trends differed between age cohorts. EAO patients trended towards greater VCAN accumulation in adjacent normal tissue, lower rates of VCAN proteolysis, and decreased αSMA accumulation vs LAO patients.</p><p><strong>Conclusions: </strong>Overall, established EAO cancers are similar to LAO cancers in mutational profile and key TME features. High VCAN and αSMA expression in adjacent normal colon indicates a presence of factors that are associated with increased intestinal subclinical inflammation. Future mechanistic studies will be conducted to better understand the importance of these findings and related processes should be prioritized as potential etiologic factors for EAO tumorigenesis.</p>","PeriodicalId":54275,"journal":{"name":"Gastroenterology Report","volume":"13 ","pages":"goaf015"},"PeriodicalIF":3.8,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842056/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143469984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk-stratified hepatocellular carcinoma surveillance in non-cirrhotic patients with MASLD.","authors":"Ke Mi, Tingdan Ye, Lin Zhu, Calvin Q Pan","doi":"10.1093/gastro/goaf018","DOIUrl":"10.1093/gastro/goaf018","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is rapidly emerging as the leading global liver disorder and is poised to become the primary cause of hepatocellular carcinoma (HCC). Research indicates that nearly 50% of HCC cases in MASLD patients occur without cirrhosis, often presenting with more advanced and larger tumors. Despite this, current guidelines primarily focus on HCC screening in cirrhotic patients, with limited guidance for non-cirrhotic MASLD individuals. This narrative review seeks to identify key risk factors for HCC development, consolidate available screening methods, and propose a practical, risk-stratified algorithm for HCC surveillance in non-cirrhotic MASLD patients. We conducted a comprehensive review of studies published between 2017 and 2023 using PubMed, Embase, and CNKI, focusing on HCC risk factors and emerging screening strategies for non-cirrhotic MASLD cohorts. Key risk factors for HCC development in these patients include male sex, age over 65, hypertension, diabetes, mild alcohol consumption, smoking, dyslipidemia, elevated alanine aminotransferase levels, and a platelet count ≤ 150 × 10⁹/L. Among the screening methods evaluated, circulating free DNA, alpha-fetoprotein (AFP) combined with protein induced by vitamin K absence or antagonist-II (PIVKA-II), and the GALAD score (incorporating Glypican-3, AFP, alpha-1-Antitrypsin, and des-gamma-carboxy prothrombin) demonstrated the highest performance. Based on these findings, we proposed a risk-stratified HCC surveillance algorithm that integrates GALAD and PIVKA-II into the existing sonography and AFP screening protocols. This review aims to provide clinicians with actionable recommendations for HCC screening in non-cirrhotic MASLD patients.</p>","PeriodicalId":54275,"journal":{"name":"Gastroenterology Report","volume":"13 ","pages":"goaf018"},"PeriodicalIF":3.8,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143469988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}