Digestion最新文献

{"title":"Inhibitory Effects of Probiotic and Gastro-Intestinal Bacteria on Helicobacter pylori in vitro.","authors":"Johannes Raphael Westphal, Nadine Koch, Lukas Macke, Riccardo Vasapolli, Didem Saka, Ramiro Vilchez-Vargas, Tianjun Song, Peter Malfertheiner, Christian Schulz","doi":"10.1159/000543447","DOIUrl":"10.1159/000543447","url":null,"abstract":"<p><strong>Introduction: </strong>Helicobacter pylori is a highly prevalent pathogen affecting approximately 50% of the world population, causing chronic gastritis and subsequently adenocarcinoma. Antibiotic resistance rates in H. pylori are increasing, thus demanding alternative treatment options. Some beneficial bacteria, including probiotics and gastrointestinal commensals, were shown to inhibit H. pylori growth, viability, and initial attachment to the gastric epithelium.</p><p><strong>Methods: </strong>In this review, we systematically summarized the currently available literature for in vitro inhibition of H. pylori through beneficial bacteria from the Lactobacillales order. We performed research on PubMed and Google Scholar in accordance with the PRISMA guidelines.</p><p><strong>Results: </strong>A multitude of species were shown to possess anti-H. pylori activity, although the majority of investigated bacteria belonged to only one bacterial genus: Lactobacillus. Anti-H. pylori activity was mediated through transcriptional modulation of virulence factors, competition for binding sites, the induction of a dormancy state of H. pylori, and the secretion of anti-H. pylori compounds.</p><p><strong>Conclusion: </strong>Many bacterial compounds that show probiotic properties are capable of inhibiting H. pylori in in vitro experiments. However, a huge variety of test methods to detect anti-H. pylori effects demands standardization.</p>","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"349-364"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"C-Kit Immunohistochemical Expression as a Complementary Method to Assess Mast Cell Density in Helicobacter pylori-Mediated Gastritis.","authors":"Ava T Ismael, Rafal A Abdulhameed, Bushra A Hamdi, Rawaz D Tawfeeq, Aram Ommar","doi":"10.1159/000541387","DOIUrl":"10.1159/000541387","url":null,"abstract":"<p><strong>Introduction: </strong>Chronic gastritis is a group of conditions commonly characterized by stomach lining inflammation. The study aimed to investigate the clinical and pathological aspects that play a role in its development. Additionally, the study examines the use of CD117 as an immunohistochemistry marker in evaluating mast cell density (MCD).</p><p><strong>Methods: </strong>This retrospective, cross-sectional study was conducted in Iraqi Kurdistan with a sample size of 380 patients. Patient data included gastritis type, neutrophil infiltration severity, mononuclear cell infiltration within the lamina propria, intestinal metaplasia, and glandular atrophy, which were categorized and given a score. The CD117 level was identified using an anti-human rabbit polyclonal antibody.</p><p><strong>Results: </strong>A statistically significant association was revealed between Helicobacter pylori-mediated gastritis and non-specific gastritis with age, activity, H. pylori and MCD, dysplasia, and malignancy. Meanwhile, no association was found with gender, inflammatory infiltrate, intestinal metaplasia, and glandular atrophy. C-Kit exhibited a marked increase in MCD in patients with H. pylori-mediated gastritis, intestinal metaplasia, atrophy, and gastric carcinoma. However, a significant decrease in MCD was observed on repeating endoscopy evaluations for patients after treatment.</p><p><strong>Conclusion: </strong>Regions that exhibit severe inflammation, metaplasia, atrophy, and carcinoma demonstrated an increase in MCD with H. pylori-mediated gastritis. A detailed investigation in clinical practice to screen early diagnosis and treatment needs to be performed in high H. pylori prevalence.</p>","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"23-29"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142282035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NEIL3 Upregulated by TFAP2A Promotes M2 Polarization of Macrophages in Liver Cancer via the Mediation of Glutamine Metabolism.","authors":"Fabiao Zhang, Binfeng Wang, Wenlong Zhang, Yongfu Xu, Caiming Zhang, Xiangyang Xue","doi":"10.1159/000540804","DOIUrl":"10.1159/000540804","url":null,"abstract":"<p><strong>Introduction: </strong>Tumor-associated macrophages, which are part of the tumor microenvironment, are a major factor in cancer progression. However, a complete understanding of the regulatory mechanism of M2 polarization of macrophages (Mø) in liver cancer is yet to be established. This study aimed to investigate the potential mechanism by which NEIL3 influenced M2 Mø polarization in liver cancer.</p><p><strong>Methods: </strong>Bioinformatics analysis analyzed NEIL3 expression and its enriched pathways in liver cancer tissue, as well as its correlation with pathway genes. The upstream transcription factor of NEIL3, TFAP2A, was predicted and its expression in liver cancer tissue was analyzed. The binding relationship between the two was analyzed by dual-luciferase reporter and chromatin immunoprecipitation experiments. qRT-PCR assessed NEIL3 and TFAP2A levels in liver cancer cells. Cell viability was detected by CCK-8, while CD206 and CD86 expression was detected by immunofluorescence. IL-10 and CCR2 expressions were assessed using qRT-PCR, and M2 Mø quantity was detected using flow cytometry. Reagent kits tested glutamine (Gln) consumption, α-ketoglutarate, and glutamate content, as well as NADPH/NADP+ and GSH/GSSG ratios. Expression of Gln transport proteins was detected using Western blot. An animal model was established to investigate the influence of NEIL3 expression on liver cancer growth.</p><p><strong>Results: </strong>NEIL3 was highly expressed in liver cancer and promoted Mø M2 polarization through Gln metabolism. TFAP2A was identified as the upstream transcription factor of NEIL3 and was highly expressed in liver cancer. Rescue experiments presented that overexpression of NEIL3 reversed the suppressive effect of TFAP2A knockdown on Mø M2 polarization in liver cancer. In vivo experiments demonstrated that the knockdown of NEIL3 could significantly repress the growth of xenograft tumors.</p><p><strong>Conclusion: </strong>This study suggested that the TFAP2A/NEIL3 axis promoted Mø M2 polarization through Gln metabolism, providing a theoretical basis for immune therapy targeting the liver cancer TME.</p>","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"30-44"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence-Based Clinical Guidelines for Chronic Constipation 2023.","authors":"Eikichi Ihara, Noriaki Manabe, Hidenori Ohkubo, Naotaka Ogasawara, Haruei Ogino, Kazuki Kakimoto, Motoyori Kanazawa, Hidejiro Kawahara, Chika Kusano, Shiko Kuribayashi, Akinari Sawada, Tomohisa Takagi, Shota Takano, Toshihiko Tomita, Toshihiro Noake, Mariko Hojo, Ryota Hokari, Tatsuhiro Masaoka, Tomohiko Machida, Noboru Misawa, Yoshiyuki Mishima, Hiroshi Yajima, Sayuri Yamamoto, Hiroshi Yamawaki, Tatsuya Abe, Yasumi Araki, Kunio Kasugai, Takeshi Kamiya, Akira Torii, Atsushi Nakajima, Koji Nakada, Shin Fukudo, Yasuhiro Fujiwara, Hiroto Miwa, Hiromi Kataoka, Akihito Nagahara, Kazuhide Higuchi","doi":"10.1159/000540912","DOIUrl":"10.1159/000540912","url":null,"abstract":"&lt;p&gt;&lt;p&gt;The Japan Gastroenterological Association published the first version of its clinical guidelines for chronic constipation 2023. Based on the latest evidence, these guidelines describe the definition, classification, diagnostic criteria, diagnostic testing methods, epidemiology, pathophysiology, and treatment of chronic constipation. They include flowcharts for both diagnosis and treatment of chronic constipation. In the treatment of chronic constipation, the first step involves differentiating between secondary forms, such as organic disease-associated constipation, systemic disease-associated constipation, and drug-induced constipation. The next step is to determine whether the chronic constipation stems from a motility disorder, a form of primary chronic constipation. For functional constipation and constipation-predominant irritable bowel syndrome, treatment should be initiated after evaluating symptoms like reduced bowel movement frequency type or defecation difficulty type. The first line of treatment includes the improvement of lifestyle habits and diet therapy. The first drugs to consider for oral treatment are osmotic laxatives. If these are ineffective, secretagogues and ileal bile acid transporter inhibitors are candidates. However, stimulant laxatives are exclusively designated for as-needed use. Probiotics, bulk-forming laxatives, prokinetics, and Kampo medicines, for which there is insufficient evidence, are considered alternative or complementary therapy. Providing the best clinical strategies for chronic constipation therapy in Japan, these clinical guidelines for chronic constipation 2023 should prove useful for its treatment worldwide. The Japan Gastroenterological Association published the first version of its clinical guidelines for chronic constipation 2023. Based on the latest evidence, these guidelines describe the definition, classification, diagnostic criteria, diagnostic testing methods, epidemiology, pathophysiology, and treatment of chronic constipation. They include flowcharts for both diagnosis and treatment of chronic constipation. In the treatment of chronic constipation, the first step involves differentiating between secondary forms, such as organic disease-associated constipation, systemic disease-associated constipation, and drug-induced constipation. The next step is to determine whether the chronic constipation stems from a motility disorder, a form of primary chronic constipation. For functional constipation and constipation-predominant irritable bowel syndrome, treatment should be initiated after evaluating symptoms like reduced bowel movement frequency type or defecation difficulty type. The first line of treatment includes the improvement of lifestyle habits and diet therapy. The first drugs to consider for oral treatment are osmotic laxatives. If these are ineffective, secretagogues and ileal bile acid transporter inhibitors are candidates. However, stimulant laxatives are exclusively designated for","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"62-89"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11825134/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142003881","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":"Akkermansia muciniphila and Its Extracellular Vesicles Affect Endocannabinoid System in in vitro Model.","authors":"Pegah Noori, Fattah Sotoodehnejadnematalahi, Pooneh Rahimi, Seyed Davar Siadat","doi":"10.1159/000543446","DOIUrl":"10.1159/000543446","url":null,"abstract":"<p><strong>Introduction: </strong>Recent studies indicate that the gut microbiota controls the host's immune system. Probiotics use different signaling pathways to regulate intestinal permeability, barrier integrity, and energy balance.</p><p><strong>Methods: </strong>This research examined how Akkermansia muciniphila and its extracellular vesicles (EVs) impact inflammation and genes related to the endocannabinoid system in the STC-1 cell line through RT-PCR and ELISA assays.</p><p><strong>Results: </strong>The study's results indicated that EVs had a significant impact on GLP-1 expression compared to the multiplicity of infections (MOI) ratio. Notably, there was a substantial increase in the expression of PYY and GLP-1 genes across all treatments (p < 0.05). Conversely, the expression of CB-1, CB-2, and FAAH genes notably decreased in the STC-1 cell line when treated with MOI 50 of A. muciniphila and an EV concentration of 100 μg/mL (p < 0.05). Both MOI 50 of A. muciniphila and an EV concentration of 100 μg/mL significantly enhanced the expression of the TLR-2 gene. In contrast, EVs at a concentration of 100 μg/mL substantially reduced TLR-4 gene expression. A. muciniphila-derived EVs notably decreased the levels of inflammatory cytokines (TNF-α and IL-6), while increasing IL-10 expression at MOI 100 and an EV concentration of 100 μg/mL. These findings suggest that A. muciniphila and its EVs could regulate the expression of specific genes, serving as targets for maintaining host energy balance.</p><p><strong>Conclusions: </strong>In summary, this study illustrates that A. muciniphila-derived EVs exhibit anti-inflammatory properties and have the potential to modulate gene expression in cases of obesity and gastrointestinal tract inflammation.</p>","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"338-348"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endoscopic and Clinicopathological Features of a Colorectal Mucin-Rich Variant of Traditional Serrated Adenoma.","authors":"Eiji Kamba, Takashi Murakami, Naoki Tsugawa, Yudai Otsuki, Kei Nomura, Yuichiro Kadomatsu, Hirofumi Fukushima, Tsuyoshi Saito, Tomoyoshi Shibuya, Takashi Yao, Akihito Nagahara","doi":"10.1159/000543700","DOIUrl":"10.1159/000543700","url":null,"abstract":"<p><strong>Introduction: </strong>The mucin-rich variant of traditional serrated adenoma (MR-TSA), pathologically defined by the presence of goblet cells comprising over 50% of the lesion compared to the absorptive epithelial eosinophilic cytoplasm, was recently introduced as one morphological variants of traditional serrated adenoma (TSA). This study aimed to characterize the endoscopic and clinicopathological characteristics of MR-TSAs.</p><p><strong>Methods: </strong>Lesions pathologically diagnosed as TSAs at our hospital between 2011 and 2023 were reviewed. We analyzed the endoscopic and clinicopathological features of 49 MR-TSAs and 236 conventional TSAs (C-TSAs). Furthermore, immunohistochemical and genetic analyses were performed to ensure that there were no discrepancies with our previous study.</p><p><strong>Results: </strong>MR-TSAs, like C-TSAs, were often located in the sigmoid colon and rectum, with no significant difference in lesion size. Macroscopically, MR-TSAs frequently appeared as type 0-Is with a weak reddish color and had a mucous cap, less often exhibiting a pinecone-like or coral-shaped appearance compared to C-TSAs (p < 0.001). Magnifying endoscopy showed expanded crypt openings in 80% of MR-TSAs (p < 0.001). Both groups had similar IIIH and IVH pit patterns. Immunohistochemical analysis revealed that MUC5AC was expressed more frequently in MR-TSAs than in C-TSAs. Additionally, genetic analysis showed that MR-TSAs more frequently harbored the BRAF mutation than C-TSAs (p < 0.001), whereas MR-TSAs less frequently harbored the KRAS mutation than C-TSAs (p = 0.047).</p><p><strong>Conclusion: </strong>MR-TSAs, frequently harboring the BRAF but not KRAS mutation, exhibited several distinct endoscopic findings, including a sessile morphology, lack of pinecone-like or coral-like appearance, weak reddish color, and mucous cap.</p>","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"314-326"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12324798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482538","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":"Impact of Helicobacter pylori on Immune Checkpoint Inhibition in Hepatocellular Carcinoma: A Multicenter Study.","authors":"Najib Ben Khaled, Christian Schulz, Marianna Alunni-Fabbroni, Kathrin Bronny, Leonie S Jochheim, Behnam Kalali, Osman Öcal, Max Seidensticker, Ignazio Piseddu, Stefan Enssle, Monika Karin, Julia S Schneider, Theresa Strasoldo-Graffemberg, Nadine Koch, Lukas Macke, Florian P Reiter, Christian M Lange, Yinghong Wang, Enrico N De Toni, Markus Gerhard, Julia Mayerle, Jens Ricke, Peter Malfertheiner","doi":"10.1159/000542847","DOIUrl":"10.1159/000542847","url":null,"abstract":"<p><strong>Introduction: </strong>Immunomodulating effects of Helicobacter pylori (H. pylori) have been shown to inhibit antitumor immunity. Resistance to immune checkpoint inhibitor (ICI)-based therapies is common among patients with hepatocellular carcinoma (HCC). This study aimed to assess the effect of H. pylori on the outcomes of ICI in patients with HCC.</p><p><strong>Methods: </strong>We conducted a multicenter study in patients with HCC across a broad range of treatments. Patients received either ICI-based combination regimens or sorafenib-based therapy. H. pylori serostatus and virulence factors were determined and correlated with overall survival (OS), progression-free survival (PFS), and safety across the treatment modalities.</p><p><strong>Results: </strong>180 patients with HCC were included; among these, 64 were treated with ICI-based regimen and 116 with sorafenib-based regimen. In patients treated with ICI, median OS was shorter in H. pylori-positive patients (10.9 months in H. pylori-positive vs. 18.3 months; p = 0.0384). H. pylori positivity was associated with a shorter PFS in ICI recipients (3.9 months vs. 6.8 months, p = 0.0499). In patients treated with sorafenib, median OS was not shorter among H. pylori-positive patients (13.4 months in H. pylori-positive vs. 10.6 months; p = 0.3353). Immune-related adverse events and rates of gastrointestinal bleeding were comparable between H. pylori-positive and -negative patients.</p><p><strong>Conclusion: </strong>H. pylori seropositivity was linked to poorer outcomes in patients with HCC treated with ICI. This association was not observed among patients receiving sorafenib-based therapies.</p>","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"303-313"},"PeriodicalIF":3.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143457030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Surveillance after Endoscopic Resection for Colorectal Tumors: A Comprehensive Review.","authors":"Kinichi Hotta, Takahisa Matsuda, Yasushi Sano, Takahiro Fujii, Yutaka Saito","doi":"10.1159/000542665","DOIUrl":"10.1159/000542665","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;The goal of surveillance after the endoscopic resection of colorectal tumors is to reduce colorectal cancer (CRC) incidence and mortality. Considering the effective use of the limited endoscopic capacity and the cost of surveillance, it is desirable to develop a surveillance program that is as minimal as possible. In Europe (European Society of Gastrointestinal Endoscopy [ESGE]) and the USA (Multi-Society Task Force [MSTF]), after the results of the National Polyp Study (NPS) were established, guidelines were developed that stratified risk based on initial endoscopy, and surveillance programs for each risk group were proposed. More than 10 years later, the \"colonoscopy screening and surveillance guidelines\" were developed with the basic principle of \"aiming for zero CRC deaths during surveillance, bowel preservation, and emphasis on patient quality of life\" as the guideline principles in Japan.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Summary: &lt;/strong&gt;Randomized controlled trials to evaluate the appropriate surveillance intervals after endoscopic resection of colorectal tumors, the NPS, the Nottingham Study, and the Japan Polyp Study (JPS), are summarized. The ESGE, USMSTF, and Japanese guidelines compared low-risk adenoma, high-risk adenoma, advanced neoplasia, piecemeal resection, and serrated lesions by category.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Key messages: &lt;/strong&gt;Surveillance guidelines based on risk stratification were developed in Japan. Guidelines are meaningful only when they are effectively utilized in clinical practice. They must also be revised based on new evidence. It is hoped that new knowledge will be accumulated, especially in Japan, on topics that are currently lacking.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;The goal of surveillance after the endoscopic resection of colorectal tumors is to reduce colorectal cancer (CRC) incidence and mortality. Considering the effective use of the limited endoscopic capacity and the cost of surveillance, it is desirable to develop a surveillance program that is as minimal as possible. In Europe (European Society of Gastrointestinal Endoscopy [ESGE]) and the USA (Multi-Society Task Force [MSTF]), after the results of the National Polyp Study (NPS) were established, guidelines were developed that stratified risk based on initial endoscopy, and surveillance programs for each risk group were proposed. More than 10 years later, the \"colonoscopy screening and surveillance guidelines\" were developed with the basic principle of \"aiming for zero CRC deaths during surveillance, bowel preservation, and emphasis on patient quality of life\" as the guideline principles in Japan.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Summary: &lt;/strong&gt;Randomized controlled trials to evaluate the appropriate surveillance intervals after endoscopic resection of colorectal tumors, the NPS, the Nottingham Study, and the Japan Polyp Study (JPS), are summarized. The ESGE, USMSTF, and Japanese guidelines compared low-risk adenoma, high-risk adenoma, advanced neoplasia, p","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"131-137"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686425","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":"New Progress in the Study of Pathogenesis of Alcoholic Pancreatitis.","authors":"Hanhui Li, Xiaoping Tan, Jie Li, Qing Zhang","doi":"10.1159/000542548","DOIUrl":"10.1159/000542548","url":null,"abstract":"<p><strong>Background: </strong>Alcoholic pancreatitis is a progressive condition characterized by susceptibility to recurrence, progression to chronic pancreatitis, complications, and high morbidity.</p><p><strong>Summary: </strong>The main causes include long-term alcoholism, excessive drinking, the toxic effects of alcohol metabolites, interactions with biliary diseases, and genetic factors. Alcohol is the second leading cause of acute pancreatitis (AP) in the USA, accounting for one-third of all AP cases. A follow-up study on readmission revealed that the readmission rate of alcoholic acute pancreatitis (AAP) patients within 11 months was 43.1%, of which men dominated the admissions and readmissions of AAP. Among this population, 82.3% have alcohol use disorder, over half have tobacco use disorders, 6.7% have tobacco use disorder, 4.5% have opioid use disorder, and 18.5% of patients exhibit signs of potential alcoholic chronic pancreatitis. Numerous animal and clinical studies suggest that alcohol alone does not cause pancreatitis; rather, additional factors such as smoking, endotoxin lipopolysaccharide (LPS), genetic mutations, or other genetic predispositions - are necessary for the disease's progression.</p><p><strong>Key messages: </strong>Given the high rates of admission and readmission for alcoholic pancreatitis, it is essential to further investigate its pathogenesis and pathological processes to develop more effective treatment strategies. Therefore, this paper summarizes the current understanding of the pathogenesis and treatment status of alcoholic pancreatitis, drawing on recently published literature and data to provide insights and references for future research and treatment efforts.</p>","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"212-226"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143002057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Link between Metabolic Syndrome and the Brain.","authors":"Spyridon Zouridis, Ahmad Basil Nasir, Patricia Aspichueta, Wing-Kin Syn","doi":"10.1159/000541696","DOIUrl":"10.1159/000541696","url":null,"abstract":"<p><strong>Background: </strong>Metabolic syndrome (MetS) is a cluster of cardiometabolic conditions that has been linked to high risk for cardiovascular disease, liver complications, and several malignancies. More recently, MetS has been associated with cognitive dysfunction.</p><p><strong>Summary: </strong>Studies have shown an association with minimal cognitive impairment, progression to vascular dementia, and even Alzheimer's disease. MetS components have been individually explored, and glucose intolerance has the strongest association with impairment in several cognitive domains. Several hypotheses have been proposed regarding the pathophysiology underlying the MetS-cognitive dysfunction association, and even though insulin resistance plays a major role, more studies are needed to elucidate this topic. Moreover, several other factors contributing to this association have been identified. Liver disease and more specifically metabolic dysfunction-associated steatotic liver disease can on its own contribute to cognitive decline through systemic inflammation and higher ammonia levels. Gut dysbiosis that has also been identified in MetS can also lead to cognitive impairment through several mechanisms that result in neurotoxicity. Finally, there are several other factors that may modify the MetS-cognitive dysfunction relationship, such as lifestyle, diet, education status, and age. More recently, circadian syndrome was explored and was found to be even more strongly associated with cognitive impairment.</p><p><strong>Key message: </strong>MetS is associated with cognitive decline. Certain cardiometabolic risk factors have a stronger association with cognitive impairment, and there are several factors that may modify this relationship. The aim of this review was to assess and summarize the existing body of evidence on the association between MetS and cognitive impairment and identify areas that necessitate further investigation.</p>","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"203-211"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12129422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380202","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}