Elsa L. S. A. van Liere, Dewkoemar Ramsoekh, Emma Daulton, Maya Dakkak, Joris M. van Lingen, Trenton K. Stewart, Sofie Bosch, Beatriz Carvalho, Evelien Dekker, Maarten A. J. M. Jacobs, Jan Jacob Koornstra, Johan P. Kuijvenhoven, Monique E. van Leerdam, Tim G. J. de Meij, Gerrit A. Meijer, Manon C. W. Spaander, James A. Covington, Nanne K. H. de Boer
Non-invasive biomarkers may reduce post-colonoscopy colorectal cancer (CRC) rates and colonoscopy overuse in Lynch syndrome. Unlike faecal immunochemical test (FIT), faecal volatile organic compounds (VOCs) may accurately detect both advanced and non-advanced colorectal neoplasia.
{"title":"Faecal Volatile Organic Compounds to Detect Colorectal Neoplasia in Lynch Syndrome—A Prospective Longitudinal Multicentre Study","authors":"Elsa L. S. A. van Liere, Dewkoemar Ramsoekh, Emma Daulton, Maya Dakkak, Joris M. van Lingen, Trenton K. Stewart, Sofie Bosch, Beatriz Carvalho, Evelien Dekker, Maarten A. J. M. Jacobs, Jan Jacob Koornstra, Johan P. Kuijvenhoven, Monique E. van Leerdam, Tim G. J. de Meij, Gerrit A. Meijer, Manon C. W. Spaander, James A. Covington, Nanne K. H. de Boer","doi":"10.1111/apt.18328","DOIUrl":"https://doi.org/10.1111/apt.18328","url":null,"abstract":"Non-invasive biomarkers may reduce post-colonoscopy colorectal cancer (CRC) rates and colonoscopy overuse in Lynch syndrome. Unlike faecal immunochemical test (FIT), faecal volatile organic compounds (VOCs) may accurately detect both advanced and non-advanced colorectal neoplasia.","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"23 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142448931","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":"Editorial: To Stop or Not to Stop, Is It Still a Question? Authors' Reply.","authors":"Jeongkuk Seo,Byong Duk Ye","doi":"10.1111/apt.18341","DOIUrl":"https://doi.org/10.1111/apt.18341","url":null,"abstract":"","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"3 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142447980","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}
<p>Antiretroviral therapy (ART) has revolutionised the clinical management of HIV infection. With access and adherence to ART, people living with HIV (PLHIV) are having much improved life expectancy, albeit challenged by earlier onset and higher prevalence of comorbidities, including liver diseases. In the current issue of the Journal, Allende et al compares liver biopsies of 107 PLHIV with metabolic dysfunction-associated steatotic liver disease (MASLD) to matched controls,<span><sup>1</sup></span> concluding that PLHIV had less pronounced steatohepatitis but higher grade fibrosis. Notably, 21% of PLHIV had advanced fibrosis, and PLHIV had a 42% higher risk of fibrosis compared with matched controls.</p><p>The association of HIV infection with liver fibrosis has long been known. The actual incidence and its variation with populations is still far from clear. In an European multi-centre prospective cohort study, steatosis was present in two thirds of PLHIV (who had risk factors for MASLD), of whom 11.3% had advanced fibrosis.<span><sup>2</sup></span> In a systematic review involving 10 studies from six countries, the prevalence of NAFLD and fibrosis among PLHIV were 35% and 22%, respectively.<span><sup>3</sup></span> Targeting low-and-middle-income countries, a prospective cohort enrolling over 2000 PLHIV reported an overall prevalence of 28.4% and 7.6% for steatosis and fibrosis, respectively.<span><sup>4</sup></span> Comparability of these studies is low because of the differences in recruitment criteria, measures of steatosis/fibrosis, timing in relation to the HIV diagnosis and probable differences in population characteristics. Prospective cohort studies and the standardised adoption of the new term MASLD could hopefully clarify the situation from ongoing and future studies.</p><p>A more important implication from the study by Allende et al is that HIV-specific factors are at play that contribute to fibrosis in HIV-associated MASLD,<span><sup>1</sup></span> making it an important metabolic comorbidity in the ART era. For PLHIV, liver fibrosis could arise from viral hepatitis co-infections, be related to concurrent metabolic disease conditions (diabetes, metabolic syndrome, obesity, drug and alcohol exposure), and HIV-related factors, including chronic inflammation, immune activation, exposure of older generations of nucleotide reverse transcriptase inhibitors and changes in intestinal microbiota. In particular, 9.7% of PLHIV in this cohort had normal body mass index (compared with 3.9% in controls).<span><sup>1</sup></span> HIV-related factors may play a more important role in MASLD among lean than obese PLHIV.</p><p> <span><sup>4</sup></span> </p><p>The screening of PLHIV for liver fibrosis could be an effective strategy to reduce morbidity, though specific pharmacological treatment for fibrosis is yet to be available.<span><sup>5</sup></span> The European AIDS Clinical Society guidelines recommend case-based screeni
{"title":"Editorial: Enhancing targeted screening of people living with HIV for liver fibrosis","authors":"Shui-Shan Lee, Grace Chung-Yan Lui","doi":"10.1111/apt.18273","DOIUrl":"10.1111/apt.18273","url":null,"abstract":"<p>Antiretroviral therapy (ART) has revolutionised the clinical management of HIV infection. With access and adherence to ART, people living with HIV (PLHIV) are having much improved life expectancy, albeit challenged by earlier onset and higher prevalence of comorbidities, including liver diseases. In the current issue of the Journal, Allende et al compares liver biopsies of 107 PLHIV with metabolic dysfunction-associated steatotic liver disease (MASLD) to matched controls,<span><sup>1</sup></span> concluding that PLHIV had less pronounced steatohepatitis but higher grade fibrosis. Notably, 21% of PLHIV had advanced fibrosis, and PLHIV had a 42% higher risk of fibrosis compared with matched controls.</p><p>The association of HIV infection with liver fibrosis has long been known. The actual incidence and its variation with populations is still far from clear. In an European multi-centre prospective cohort study, steatosis was present in two thirds of PLHIV (who had risk factors for MASLD), of whom 11.3% had advanced fibrosis.<span><sup>2</sup></span> In a systematic review involving 10 studies from six countries, the prevalence of NAFLD and fibrosis among PLHIV were 35% and 22%, respectively.<span><sup>3</sup></span> Targeting low-and-middle-income countries, a prospective cohort enrolling over 2000 PLHIV reported an overall prevalence of 28.4% and 7.6% for steatosis and fibrosis, respectively.<span><sup>4</sup></span> Comparability of these studies is low because of the differences in recruitment criteria, measures of steatosis/fibrosis, timing in relation to the HIV diagnosis and probable differences in population characteristics. Prospective cohort studies and the standardised adoption of the new term MASLD could hopefully clarify the situation from ongoing and future studies.</p><p>A more important implication from the study by Allende et al is that HIV-specific factors are at play that contribute to fibrosis in HIV-associated MASLD,<span><sup>1</sup></span> making it an important metabolic comorbidity in the ART era. For PLHIV, liver fibrosis could arise from viral hepatitis co-infections, be related to concurrent metabolic disease conditions (diabetes, metabolic syndrome, obesity, drug and alcohol exposure), and HIV-related factors, including chronic inflammation, immune activation, exposure of older generations of nucleotide reverse transcriptase inhibitors and changes in intestinal microbiota. In particular, 9.7% of PLHIV in this cohort had normal body mass index (compared with 3.9% in controls).<span><sup>1</sup></span> HIV-related factors may play a more important role in MASLD among lean than obese PLHIV.</p><p>\u0000 <span><sup>4</sup></span>\u0000 </p><p>The screening of PLHIV for liver fibrosis could be an effective strategy to reduce morbidity, though specific pharmacological treatment for fibrosis is yet to be available.<span><sup>5</sup></span> The European AIDS Clinical Society guidelines recommend case-based screeni","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"60 10","pages":"1453-1454"},"PeriodicalIF":6.6,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.18273","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142444050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>The global fight against viral hepatitis started in 2016 and, based on the WHO's strategy to reduce infection rate by 90% and deaths by 65% until 2030, has made significant strides recently. Despite this fact, the Global Hepatitis Report in 2024 reveals that viral hepatitis killed over a million people last year, so there is still a lot of job to do to overcome barriers worldwide.<span><sup>1, 2</sup></span> In this context, independent of every country's politics, microelimination efforts have proved quite effective and useful.</p><p>Under this aim, the authors of a recent paper in AP&T used an intelligent method to identify hepatitis patients (not only C but also B and D) who were not linked to care.<span><sup>3</sup></span> They retrieved the records of 3731 patients from the Central Laboratory database of the Northern Barcelona Health Area and identified an alarming gap between diagnosis and management of hepatitis cases. Respectively, 38% HBsAg, 29% anti-δ positive and 59% HCV RNA positive individuals did not receive the appropriate care. The disconnection between diagnosis and healthcare delivery demonstrates how intricate it is to deal with chronic viral hepatitis, whereby the impediments differ according to patient populations affected.<span><sup>1</sup></span></p><p>Next, the authors proceeded a step further and tried to reintegrate the lost patients by systematically identifying and contacting them (up to 5 telephone calls and by post!). Finally, 47.2% of eligible patients (64% hepatitis B, 27% C and 100% D) were successfully linked to care. This is one of the most impressive aspects of the study that looks into whether a targeted intervention strategy is effective or not. The results can be considered a great success, especially regarding the ‘new (old) kid in town’—hepatitis D, which is mostly underdiagnosed but happens to be in the most severe among viral hepatitis infections.</p><p>So, can even the most challenging cases be brought back into care with the right approach? This is less true regarding hepatitis C patients, who present considerable difficulties in re-engaging. In fact, social factors such as instability, unwillingness to use healthcare services and outmoded beliefs about treatment challenges contributed to a lower success rate. All interventions targeting this population should therefore encompass more than clinical strategies to address the social determinants of health that impede patient engagement.<span><sup>4</sup></span> Better coordination of patient data across regions is one key recommendation to help keep track of patients who move and maintain continuity of care. Additionally, closer integration of social services with health care can provide the necessary assistance to bring back socially marginalized patients as well as those who have lost trust in the healthcare system.</p><p>As the global health community continues its efforts to eliminate viral hepatitis, there is a clear reminder of how far we ha
{"title":"Editorial: Viral hepatitis elimination: Still a big challenge: Care is not only for C","authors":"Nikolaos Papadopoulos, Melanie Deutsch","doi":"10.1111/apt.18251","DOIUrl":"10.1111/apt.18251","url":null,"abstract":"<p>The global fight against viral hepatitis started in 2016 and, based on the WHO's strategy to reduce infection rate by 90% and deaths by 65% until 2030, has made significant strides recently. Despite this fact, the Global Hepatitis Report in 2024 reveals that viral hepatitis killed over a million people last year, so there is still a lot of job to do to overcome barriers worldwide.<span><sup>1, 2</sup></span> In this context, independent of every country's politics, microelimination efforts have proved quite effective and useful.</p><p>Under this aim, the authors of a recent paper in AP&T used an intelligent method to identify hepatitis patients (not only C but also B and D) who were not linked to care.<span><sup>3</sup></span> They retrieved the records of 3731 patients from the Central Laboratory database of the Northern Barcelona Health Area and identified an alarming gap between diagnosis and management of hepatitis cases. Respectively, 38% HBsAg, 29% anti-δ positive and 59% HCV RNA positive individuals did not receive the appropriate care. The disconnection between diagnosis and healthcare delivery demonstrates how intricate it is to deal with chronic viral hepatitis, whereby the impediments differ according to patient populations affected.<span><sup>1</sup></span></p><p>Next, the authors proceeded a step further and tried to reintegrate the lost patients by systematically identifying and contacting them (up to 5 telephone calls and by post!). Finally, 47.2% of eligible patients (64% hepatitis B, 27% C and 100% D) were successfully linked to care. This is one of the most impressive aspects of the study that looks into whether a targeted intervention strategy is effective or not. The results can be considered a great success, especially regarding the ‘new (old) kid in town’—hepatitis D, which is mostly underdiagnosed but happens to be in the most severe among viral hepatitis infections.</p><p>So, can even the most challenging cases be brought back into care with the right approach? This is less true regarding hepatitis C patients, who present considerable difficulties in re-engaging. In fact, social factors such as instability, unwillingness to use healthcare services and outmoded beliefs about treatment challenges contributed to a lower success rate. All interventions targeting this population should therefore encompass more than clinical strategies to address the social determinants of health that impede patient engagement.<span><sup>4</sup></span> Better coordination of patient data across regions is one key recommendation to help keep track of patients who move and maintain continuity of care. Additionally, closer integration of social services with health care can provide the necessary assistance to bring back socially marginalized patients as well as those who have lost trust in the healthcare system.</p><p>As the global health community continues its efforts to eliminate viral hepatitis, there is a clear reminder of how far we ha","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"60 10","pages":"1451-1452"},"PeriodicalIF":6.6,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.18251","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142444113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Letter: Muddle of serum sPD-1 and sPD-L1 levels and association with HBsAg clearance in HBeAg-negative CHB patients on IFN therapy","authors":"Ankur Jindal","doi":"10.1111/apt.18268","DOIUrl":"10.1111/apt.18268","url":null,"abstract":"","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"60 10","pages":"1503-1504"},"PeriodicalIF":6.6,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142444051","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}
<p>Inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), affects several million people worldwide, mainly in the Western world. However, the incidence is sharply rising in newly industrialized countries.<span><sup>1, 2</sup></span> The adoption of a Western lifestyle, particularly a diet high in sugar, fat and ultra-processed foods, may contribute to this trend.<span><sup>2</sup></span></p><p>As a result, dietary compounds have been investigated for their role in the pathogenesis of IBD.<span><sup>3, 4</sup></span> Among these, advanced glycation end products (AGEs), which are formed during thermal processing of foods, have come to the fore as they increase oxidative stress and inflammation.<span><sup>5</sup></span> Studies have linked AGEs to alterations in the gut microbiome and to pro-inflammatory immune responses.<span><sup>6</sup></span> However, evidence on their role in the risk of developing IBD remains sparse and inconclusive.<span><sup>7, 8</sup></span></p><p>Jiang et al. have reported novel findings from a cohort based on the UK Biobank, including 121,978 individuals without IBD.<span><sup>9</sup></span> Of these, 671 (0.55%) developed IBD during a median follow-up of almost 14 years. Their intake of three AGEs was estimated by dietary questionnaires. Interestingly, the authors found that one of the AGEs was associated with an increased risk of developing IBD, but only CD (adjusted hazard ratio: 1.09; 95% CI: 1.01–1.18). In stratified analyses, the association was strongest in the overweight, the physically inactive and non-smokers. The authors used polygenic risk scores to explore the interaction of diet with the background genetic risk. They found that all three AGEs were associated with a higher risk of CD in individuals at high genetic risk but, again, saw no association for UC.</p><p>Strengths of their study are its large population and the comprehensive genetic profiling. Major limitations include the lack of information on dietary changes over time and measurement bias due to the use of dietary questionnaires to estimate AGEs. Because exact concentrations of AGEs are unknown, these data do not provide sufficient evidence to link these associations to a specific AGE or signalling pathway.</p><p>Nevertheless, this study has elegantly demonstrated the importance of diet in the development of IBD, especially in those with a high background genetic risk. However, several questions remain unanswered. Are AGEs the primary culprit or other compounds present in ultra-processed food and if yes, which specific AGE molecules or pathways are involved? Is there a dose–response relationship between AGEs and the risk of IBD? Can individuals with a high genetic risk of IBD prevent or delay disease onset by maintaining a healthy lifestyle and avoiding high intake of AGEs? In addition, the finding of a stronger association in overweight and physically inactive individuals raises the question of whether the
炎症性肠病 (IBD) 包括克罗恩病 (CD) 和溃疡性结肠炎 (UC)，全世界有几百万人受其影响，主要是在西方国家。2 因此，人们对膳食化合物在 IBD 发病机制中的作用进行了研究。3, 4 其中，在食品热加工过程中形成的高级糖化终产物（AGEs）因会增加氧化应激和炎症而受到关注。研究表明，AGEs 与肠道微生物组的改变以及促炎症免疫反应有关。6 然而，有关 AGEs 在 IBD 发病风险中的作用的证据仍然稀少，且尚无定论。7, 8Jiang 等人报告了基于英国生物库（UK Biobank）的一个队列的新发现，该队列包括 121,978 名未患 IBD 的个体。他们对三种 AGE 的摄入量是通过饮食调查问卷估算出来的。有趣的是，作者发现其中一种 AGE 与 IBD 患病风险的增加有关，但只与 CD 有关（调整后危险比：1.09；95% CI：1.01-1.18）。在分层分析中，超重者、不运动者和非吸烟者的相关性最强。作者使用多基因风险评分来探讨饮食与背景遗传风险之间的相互作用。他们发现，在遗传风险较高的人群中，所有三种 AGEs 都与较高的 CD 风险有关，但同样与 UC 无关。其主要局限性包括缺乏有关饮食随时间变化的信息，以及由于使用饮食问卷估算 AGEs 而产生的测量偏差。由于 AGEs 的确切浓度尚不清楚，这些数据并不能提供足够的证据将这些关联与特定的 AGE 或信号通路联系起来。尽管如此，这项研究还是很好地证明了饮食在 IBD 发病中的重要性，尤其是在那些具有高背景遗传风险的人群中。然而，仍有几个问题没有得到解答。AGEs是罪魁祸首还是超加工食品中的其他化合物？AGE 与 IBD 风险之间是否存在剂量反应关系？具有 IBD 高遗传风险的人能否通过保持健康的生活方式和避免摄入大量 AGE 预防或推迟疾病的发生？此外，在超重和缺乏运动的人群中发现了更强的关联性，这就提出了一个问题：代谢综合征与慢性低度炎症是否可能是慢性肠道炎症的真正导火索？要实现这一目标，需要进一步开展以人群为基础的研究，对膳食摄入量进行纵向测量，并对膳食分子进行细化研究。我们相信这些努力是值得的。毕竟，饮食是可以改变的，而遗传--至少现在是静态的。法希姆-易卜拉希米：构思；写作--原稿；写作--审阅和编辑；方法论。安德斯-福斯项目管理；监督；方法论；写作-原稿；写作-审阅和编辑；构思：本研究部分由瑞士国家科学基金会资助（资助编号 P500PM_210866）。Bengt Ihre 基金会（资助编号 SLS-974469）、Bengt Ihre 奖学金（2023-1）和瑞典医学会（资助编号 SLS-973638）也为本研究提供了资助。如需查看本文，请访问 https://doi.org/10.1111/apt.18218
{"title":"Editorial: Advanced glycation end products - a dietary culprit for IBD in the genetically susceptible?","authors":"Fahim Ebrahimi, Anders Forss","doi":"10.1111/apt.18240","DOIUrl":"10.1111/apt.18240","url":null,"abstract":"<p>Inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), affects several million people worldwide, mainly in the Western world. However, the incidence is sharply rising in newly industrialized countries.<span><sup>1, 2</sup></span> The adoption of a Western lifestyle, particularly a diet high in sugar, fat and ultra-processed foods, may contribute to this trend.<span><sup>2</sup></span></p><p>As a result, dietary compounds have been investigated for their role in the pathogenesis of IBD.<span><sup>3, 4</sup></span> Among these, advanced glycation end products (AGEs), which are formed during thermal processing of foods, have come to the fore as they increase oxidative stress and inflammation.<span><sup>5</sup></span> Studies have linked AGEs to alterations in the gut microbiome and to pro-inflammatory immune responses.<span><sup>6</sup></span> However, evidence on their role in the risk of developing IBD remains sparse and inconclusive.<span><sup>7, 8</sup></span></p><p>Jiang et al. have reported novel findings from a cohort based on the UK Biobank, including 121,978 individuals without IBD.<span><sup>9</sup></span> Of these, 671 (0.55%) developed IBD during a median follow-up of almost 14 years. Their intake of three AGEs was estimated by dietary questionnaires. Interestingly, the authors found that one of the AGEs was associated with an increased risk of developing IBD, but only CD (adjusted hazard ratio: 1.09; 95% CI: 1.01–1.18). In stratified analyses, the association was strongest in the overweight, the physically inactive and non-smokers. The authors used polygenic risk scores to explore the interaction of diet with the background genetic risk. They found that all three AGEs were associated with a higher risk of CD in individuals at high genetic risk but, again, saw no association for UC.</p><p>Strengths of their study are its large population and the comprehensive genetic profiling. Major limitations include the lack of information on dietary changes over time and measurement bias due to the use of dietary questionnaires to estimate AGEs. Because exact concentrations of AGEs are unknown, these data do not provide sufficient evidence to link these associations to a specific AGE or signalling pathway.</p><p>Nevertheless, this study has elegantly demonstrated the importance of diet in the development of IBD, especially in those with a high background genetic risk. However, several questions remain unanswered. Are AGEs the primary culprit or other compounds present in ultra-processed food and if yes, which specific AGE molecules or pathways are involved? Is there a dose–response relationship between AGEs and the risk of IBD? Can individuals with a high genetic risk of IBD prevent or delay disease onset by maintaining a healthy lifestyle and avoiding high intake of AGEs? In addition, the finding of a stronger association in overweight and physically inactive individuals raises the question of whether the ","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"60 10","pages":"1449-1450"},"PeriodicalIF":6.6,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.18240","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142447977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Letter: Gut microbiota—An overlooked therapeutic target in the prevention of post-operative recurrence of Crohn's disease","authors":"D. Bogatic, R. V. Bryant","doi":"10.1111/apt.18258","DOIUrl":"10.1111/apt.18258","url":null,"abstract":"","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"60 10","pages":"1501-1502"},"PeriodicalIF":6.6,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142447979","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":"Editorial: To Stop Or Not To Stop: Is It Still A Question?","authors":"Stephan R Vavricka,Thomas Greuter","doi":"10.1111/apt.18298","DOIUrl":"https://doi.org/10.1111/apt.18298","url":null,"abstract":"","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"71 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142447978","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}
Philip N. Newsome, Arun J. Sanyal, Kristiane A. Engebretsen, Iris Kliers, Laura Østergaard, Denise Vanni, Elisabetta Bugianesi, Mary E. Rinella, Michael Roden, Vlad Ratziu
Semaglutide, a glucagon-like peptide-1 receptor agonist, has demonstrated potential beneficial effects in metabolic dysfunction-associated steatohepatitis (MASH).
{"title":"Semaglutide 2.4 mg in Participants With Metabolic Dysfunction-Associated Steatohepatitis: Baseline Characteristics and Design of the Phase 3 ESSENCE Trial","authors":"Philip N. Newsome, Arun J. Sanyal, Kristiane A. Engebretsen, Iris Kliers, Laura Østergaard, Denise Vanni, Elisabetta Bugianesi, Mary E. Rinella, Michael Roden, Vlad Ratziu","doi":"10.1111/apt.18331","DOIUrl":"https://doi.org/10.1111/apt.18331","url":null,"abstract":"Semaglutide, a glucagon-like peptide-1 receptor agonist, has demonstrated potential beneficial effects in metabolic dysfunction-associated steatohepatitis (MASH).","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"66 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142440377","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}
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