Pub Date : 2024-11-01Epub Date: 2024-09-20DOI: 10.1016/S2468-1253(24)00264-4
Shahida Din, Jonathan Segal, Jonathan Blackwell, Beatriz Gros, Christopher J Black, Alexander C Ford
<p><strong>Background: </strong>Randomised placebo-controlled trials are the gold standard to assess novel drugs in ulcerative colitis and Crohn's disease. However, there might be risks associated with receiving placebo. We aimed to examine the harms associated with receiving placebo in trials of licensed biologics and small molecules for the induction of remission in ulcerative colitis and luminal Crohn's disease in a meta-analysis.</p><p><strong>Methods: </strong>We performed a systematic review and meta-analysis. We searched MEDLINE, Embase, Embase Classic, and the Cochrane Central Register of Controlled Trials from database inception to May 30, 2024, for randomised placebo-controlled trials of licensed biologics and small molecules for induction of remission in adults (≥18 years) with moderately to severely active ulcerative colitis or luminal Crohn's disease reporting data on adverse events over a minimum treatment period of 4 weeks. There were no prespecified study exclusion criteria. We extracted summary data and pooled data using a random-effects model for any treatment-emergent adverse event, any drug-related adverse event, infection, worsening of inflammatory bowel disease (IBD) activity, withdrawal due to adverse events, serious adverse events, serious infection, serious worsening of IBD activity, or venous thromboembolic events (VTEs), reporting relative risks (RRs) with 95% CIs. The protocol for this meta-analysis was registered with PROSPERO (CRD42024527341).</p><p><strong>Findings: </strong>The search identified 10 826 citations, of which 47 trials including 20 987 patients (14 267 [68·0%] receiving active drug and 6720 [32·0%] receiving placebo) were eligible. The risk of any treatment-emergent adverse event was no different with active drug than with placebo (7660/14 267 [53·7%] patients on active drug vs 3758/6720 [55·9%] on placebo; RR 0·97, 95% CI 0·94-1·00; I<sup>2</sup> =36%). However, the risks of worsening of IBD activity (563/13 473 [4·2%] vs 530/6252 [8·5%]; 0·48, 0·40-0·59; I<sup>2</sup> =54%), withdrawal due to adverse event (401/13 363 [3·0%] vs 299/6267 [4·8%]; 0·62, 0·48-0·79; I<sup>2</sup> =46%), serious adverse event (682/14 267 [4·8%] vs 483/6720 [7·2%]; 0·69, 0·59-0·80; I<sup>2</sup> =30%), serious infection (140/14 194 [1·0%] vs 91/6647 [1·4%]; 0·67, 0·50-0·89; I<sup>2</sup> =0%), serious worsening of IBD activity (187/11 271 [1·7%] vs 189/5056 [3·7%]; 0·45, 0·34-0·60; I<sup>2</sup> =27%), or VTEs (13/7542 [0·2%] vs 12/2981 [0·4%]; 0·45, 0·21-0·94; I<sup>2</sup> =0%) were all significantly lower with active drug than placebo. Numbers needed to treat with active drug to avoid these potentially serious adverse events ranged from 23 for worsening of IBD activity to 452 for VTEs. 27 randomised controlled trials were judged as low risk of bias across all domains.</p><p><strong>Interpretation: </strong>Patients with moderately to severely active IBD receiving placebo are more likely to experience significant worsenin
{"title":"Harms with placebo in trials of biological therapies and small molecules as induction therapy in inflammatory bowel disease: a systematic review and meta-analysis.","authors":"Shahida Din, Jonathan Segal, Jonathan Blackwell, Beatriz Gros, Christopher J Black, Alexander C Ford","doi":"10.1016/S2468-1253(24)00264-4","DOIUrl":"10.1016/S2468-1253(24)00264-4","url":null,"abstract":"<p><strong>Background: </strong>Randomised placebo-controlled trials are the gold standard to assess novel drugs in ulcerative colitis and Crohn's disease. However, there might be risks associated with receiving placebo. We aimed to examine the harms associated with receiving placebo in trials of licensed biologics and small molecules for the induction of remission in ulcerative colitis and luminal Crohn's disease in a meta-analysis.</p><p><strong>Methods: </strong>We performed a systematic review and meta-analysis. We searched MEDLINE, Embase, Embase Classic, and the Cochrane Central Register of Controlled Trials from database inception to May 30, 2024, for randomised placebo-controlled trials of licensed biologics and small molecules for induction of remission in adults (≥18 years) with moderately to severely active ulcerative colitis or luminal Crohn's disease reporting data on adverse events over a minimum treatment period of 4 weeks. There were no prespecified study exclusion criteria. We extracted summary data and pooled data using a random-effects model for any treatment-emergent adverse event, any drug-related adverse event, infection, worsening of inflammatory bowel disease (IBD) activity, withdrawal due to adverse events, serious adverse events, serious infection, serious worsening of IBD activity, or venous thromboembolic events (VTEs), reporting relative risks (RRs) with 95% CIs. The protocol for this meta-analysis was registered with PROSPERO (CRD42024527341).</p><p><strong>Findings: </strong>The search identified 10 826 citations, of which 47 trials including 20 987 patients (14 267 [68·0%] receiving active drug and 6720 [32·0%] receiving placebo) were eligible. The risk of any treatment-emergent adverse event was no different with active drug than with placebo (7660/14 267 [53·7%] patients on active drug vs 3758/6720 [55·9%] on placebo; RR 0·97, 95% CI 0·94-1·00; I<sup>2</sup> =36%). However, the risks of worsening of IBD activity (563/13 473 [4·2%] vs 530/6252 [8·5%]; 0·48, 0·40-0·59; I<sup>2</sup> =54%), withdrawal due to adverse event (401/13 363 [3·0%] vs 299/6267 [4·8%]; 0·62, 0·48-0·79; I<sup>2</sup> =46%), serious adverse event (682/14 267 [4·8%] vs 483/6720 [7·2%]; 0·69, 0·59-0·80; I<sup>2</sup> =30%), serious infection (140/14 194 [1·0%] vs 91/6647 [1·4%]; 0·67, 0·50-0·89; I<sup>2</sup> =0%), serious worsening of IBD activity (187/11 271 [1·7%] vs 189/5056 [3·7%]; 0·45, 0·34-0·60; I<sup>2</sup> =27%), or VTEs (13/7542 [0·2%] vs 12/2981 [0·4%]; 0·45, 0·21-0·94; I<sup>2</sup> =0%) were all significantly lower with active drug than placebo. Numbers needed to treat with active drug to avoid these potentially serious adverse events ranged from 23 for worsening of IBD activity to 452 for VTEs. 27 randomised controlled trials were judged as low risk of bias across all domains.</p><p><strong>Interpretation: </strong>Patients with moderately to severely active IBD receiving placebo are more likely to experience significant worsenin","PeriodicalId":56028,"journal":{"name":"Lancet Gastroenterology & Hepatology","volume":" ","pages":"1020-1029"},"PeriodicalIF":30.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142301849","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}
Pub Date : 2024-11-01Epub Date: 2024-09-20DOI: 10.1016/S2468-1253(24)00231-0
Andrea Shin
Gastroparesis is a disorder of delayed gastric emptying with associated symptoms of postprandial fullness, early satiety, nausea, vomiting, bloating, and abdominal pain. Functional dyspepsia is an upper gastrointestinal disorder of gut-brain interaction that presents with similar symptoms but is defined according to symptom patterns rather than gastric motor dysfunction. Although delayed gastric emptying is a defining feature of gastroparesis, other aspects of gastric neuromuscular dysfunction, such as gastric accommodation and visceral hypersensitivity might contribute to symptoms. Similarly, although functional dyspepsia is not defined by impaired gastric emptying, disordered gastric motility might underlie pathogenesis in some patients with functional dyspepsia. In the last decade, it has been increasingly recognised that these two disorders might represent varying presentations along a common continuum of neuromuscular dysfunction, although with differentiating features with respect to outcomes, diagnosis, and treatments. In this Review, an overview of gastroparesis and functional dyspepsia from the perspective of gastric motility is provided, discussing what is distinct and what is shared between these disorders.
{"title":"Disorders of gastric motility.","authors":"Andrea Shin","doi":"10.1016/S2468-1253(24)00231-0","DOIUrl":"10.1016/S2468-1253(24)00231-0","url":null,"abstract":"<p><p>Gastroparesis is a disorder of delayed gastric emptying with associated symptoms of postprandial fullness, early satiety, nausea, vomiting, bloating, and abdominal pain. Functional dyspepsia is an upper gastrointestinal disorder of gut-brain interaction that presents with similar symptoms but is defined according to symptom patterns rather than gastric motor dysfunction. Although delayed gastric emptying is a defining feature of gastroparesis, other aspects of gastric neuromuscular dysfunction, such as gastric accommodation and visceral hypersensitivity might contribute to symptoms. Similarly, although functional dyspepsia is not defined by impaired gastric emptying, disordered gastric motility might underlie pathogenesis in some patients with functional dyspepsia. In the last decade, it has been increasingly recognised that these two disorders might represent varying presentations along a common continuum of neuromuscular dysfunction, although with differentiating features with respect to outcomes, diagnosis, and treatments. In this Review, an overview of gastroparesis and functional dyspepsia from the perspective of gastric motility is provided, discussing what is distinct and what is shared between these disorders.</p>","PeriodicalId":56028,"journal":{"name":"Lancet Gastroenterology & Hepatology","volume":" ","pages":"1052-1064"},"PeriodicalIF":30.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142309196","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}
Pub Date : 2024-11-01Epub Date: 2024-09-20DOI: 10.1016/S2468-1253(24)00233-4
Beatriz Gros, Jonathan Blackwell, Jonathan Segal, Christopher J Black, Alexander C Ford, Shahida Din
<p><strong>Background: </strong>Randomised placebo-controlled trials for the induction of inflammatory bowel disease (IBD) remission involve potential harms to those receiving placebo. Whether these harms are also apparent with placebo during maintenance of remission trials in IBD is unclear. We aimed to examine the potential harms associated with receiving placebo in trials of licensed biologics and small molecules for maintenance of remission of ulcerative colitis and luminal Crohn's disease in a meta-analysis.</p><p><strong>Methods: </strong>We performed a systematic review and meta-analysis. We searched several medical literature databases including MEDLINE (from Jan 1, 1946, to May 31, 2024), Embase and Embase Classic (Jan 1, 1947, to May 31, 2024), and the Cochrane Central Register of Controlled Trials from database inception to May 31, 2024, for randomised placebo-controlled trials of licensed biologics and small molecules for maintenance of remission in adults with IBD reporting data on adverse events over a period of 20 weeks or more. There were no language restrictions or prespecified exclusion criteria. We extracted summary data and pooled data using a random-effects model for any treatment-emergent adverse event, drug-related adverse event, infection, worsening of IBD activity, withdrawal due to adverse events, serious adverse events, serious infection, serious worsening of IBD activity, or venous thromboembolic events, reporting relative risks (RRs) for placebo versus active drug with 95% CIs for each outcomes. The protocol for this meta-analysis was registered with PROSPERO (CRD42024542624).</p><p><strong>Findings: </strong>Our search identified 10 826 citations, of which 45 trials including 16 562 patients (10 319 [62·3%] receiving active drug and 6243 [37·7%] placebo) were eligible. The risks of any treatment-emergent adverse event (7297/9546 [76·4%] patients on active drug vs 4415/5850 [75·5%] on placebo; RR 1·01, 95% CI 0·99-1·04; I<sup>2</sup> =47%), serious infection (260/10 242 [2·5%] vs 155/6149 [2·5%]; 0·97, 0·79-1·19; I<sup>2</sup> =0%), or venous thromboembolic event (12/4729 [0·3%] vs 9/2691 [0·3%]; 0·72, 0·31-1·66; I<sup>2</sup> =0%) were not significantly lower with active drug than placebo. The risks of any infection (3208/8038 [39·9%] vs 1713/4809 [35·6%]; 1·14, 1·05-1·23; I<sup>2</sup> =60%) or any drug-related adverse event (1094/2997 [36·5%] vs 609/1950 [31·2%]; 1·24, 1·02-1·50; I<sup>2</sup> =75%) were higher with active drug than placebo. However, the risks of any worsening of IBD activity (1038/8090 [12·8%] vs 1181/5191 [22·8%]; 0·58, 0·52-0·64; I<sup>2</sup> =40%), any withdrawal due to adverse events (610/10 282 [5·9%] vs 561/6207 [9·0%]; 0·71, 0·60-0·84; I<sup>2</sup> =43%), any serious adverse events (1066/10 292 [10·4%] vs 742/6198 [12·0%]; 0·85, 0·77-0·94; I<sup>2</sup> =17%), or any serious worsening of IBD activity (101/5707 [1·8%] vs 143/3640 [3·9%]; 0·55, 0·42-0·71; I<sup>2</sup> =0%) were lower with
背景：用于诱导炎症性肠病（IBD）缓解的随机安慰剂对照试验可能会对接受安慰剂治疗的患者造成伤害。目前尚不清楚在 IBD 的缓解维持试验中安慰剂是否也会造成这些伤害。我们的目的是通过一项荟萃分析，研究在维持溃疡性结肠炎和管腔克罗恩病缓解的许可生物制剂和小分子药物试验中，接受安慰剂可能带来的危害：我们进行了系统回顾和荟萃分析。我们检索了多个医学文献数据库，包括MEDLINE（1946年1月1日至2024年5月31日）、Embase和Embase Classic（1947年1月1日至2024年5月31日），以及Cochrane对照试验中央登记册（从数据库建立之初至2024年5月31日），检索了用于维持成人IBD患者缓解的许可生物制剂和小分子药物的随机安慰剂对照试验，这些试验报告了20周或20周以上的不良事件数据。没有语言限制或预先确定的排除标准。我们提取了汇总数据，并采用随机效应模型对任何治疗引发的不良事件、药物相关不良事件、感染、IBD活动恶化、因不良事件而停药、严重不良事件、严重感染、IBD活动严重恶化或静脉血栓栓塞事件进行了汇总，报告了安慰剂与活性药物的相对风险系数（RRs）以及各结果的 95% CIs。该荟萃分析方案已在 PROSPERO（CRD42024542624）上注册：我们的搜索发现了 10 826 篇引文，其中 45 项试验包括 16 562 名患者（10 319 名患者[62-3%]接受活性药物治疗，6243 名患者[37-7%]接受安慰剂治疗）符合条件。任何治疗引发的不良事件（7297/9 546 [76-4%] 接受活性药物治疗的患者 vs 4415/5850 [75-5%] 接受安慰剂治疗的患者；RR 1-01，95% CI 0-99-1-04；I2 =47%）、严重感染（260/10 242 [2-5%] vs 155/6149 [2-5%]；严重感染（260/10 242 [2-5%] vs 155/6149 [2-5%]；0-97，0-79-1-19；I2 =0%）或静脉血栓栓塞事件（12/4729 [0-3%] vs 9/2691 [0-3%]；0-72，0-31-1-66；I2 =0%）在使用活性药物后并不显著低于安慰剂。使用活性药物发生任何感染（3208/8038 [39-9%] vs 1713/4809 [35-6%]；1-14，1-05-1-23；I2 =60%）或任何药物相关不良事件（1094/2997 [36-5%] vs 609/1950 [31-2%]；1-24，1-02-1-50；I2 =75%）的风险高于安慰剂。然而，IBD 活动恶化的风险（1038/8090 [12-8%] vs 1181/5191 [22-8%]；0-58，0-52-0-64；I2 =40%）、因不良事件而停药的风险（610/10 282 [5-9%] vs 561/6207 [9-0%]；0-71，0-60-0-84；I2 =43%）、任何严重不良事件（1066/10 292 [10-4%] vs 742/6198 [12-0%]；0-85，0-77-0-94；I2 =17%）或任何严重的 IBD 活动恶化（101/5707 [1-8%] vs 143/3640 [3-9%]；0-55，0-42-0-71；I2 =0%），活性药物均低于安慰剂。21项随机对照试验在所有领域均被判定为低偏倚风险：在IBD的维持缓解试验中，安慰剂与一些具有临床意义的潜在危害有关。在参与临床试验之前，应就这些问题向患者提供咨询，并考虑采用其他设计来测试治疗 IBD 的新药：无。
{"title":"Harms with placebo in trials of biological therapies and small molecules as maintenance therapy in inflammatory bowel disease: a systematic review and meta-analysis.","authors":"Beatriz Gros, Jonathan Blackwell, Jonathan Segal, Christopher J Black, Alexander C Ford, Shahida Din","doi":"10.1016/S2468-1253(24)00233-4","DOIUrl":"10.1016/S2468-1253(24)00233-4","url":null,"abstract":"<p><strong>Background: </strong>Randomised placebo-controlled trials for the induction of inflammatory bowel disease (IBD) remission involve potential harms to those receiving placebo. Whether these harms are also apparent with placebo during maintenance of remission trials in IBD is unclear. We aimed to examine the potential harms associated with receiving placebo in trials of licensed biologics and small molecules for maintenance of remission of ulcerative colitis and luminal Crohn's disease in a meta-analysis.</p><p><strong>Methods: </strong>We performed a systematic review and meta-analysis. We searched several medical literature databases including MEDLINE (from Jan 1, 1946, to May 31, 2024), Embase and Embase Classic (Jan 1, 1947, to May 31, 2024), and the Cochrane Central Register of Controlled Trials from database inception to May 31, 2024, for randomised placebo-controlled trials of licensed biologics and small molecules for maintenance of remission in adults with IBD reporting data on adverse events over a period of 20 weeks or more. There were no language restrictions or prespecified exclusion criteria. We extracted summary data and pooled data using a random-effects model for any treatment-emergent adverse event, drug-related adverse event, infection, worsening of IBD activity, withdrawal due to adverse events, serious adverse events, serious infection, serious worsening of IBD activity, or venous thromboembolic events, reporting relative risks (RRs) for placebo versus active drug with 95% CIs for each outcomes. The protocol for this meta-analysis was registered with PROSPERO (CRD42024542624).</p><p><strong>Findings: </strong>Our search identified 10 826 citations, of which 45 trials including 16 562 patients (10 319 [62·3%] receiving active drug and 6243 [37·7%] placebo) were eligible. The risks of any treatment-emergent adverse event (7297/9546 [76·4%] patients on active drug vs 4415/5850 [75·5%] on placebo; RR 1·01, 95% CI 0·99-1·04; I<sup>2</sup> =47%), serious infection (260/10 242 [2·5%] vs 155/6149 [2·5%]; 0·97, 0·79-1·19; I<sup>2</sup> =0%), or venous thromboembolic event (12/4729 [0·3%] vs 9/2691 [0·3%]; 0·72, 0·31-1·66; I<sup>2</sup> =0%) were not significantly lower with active drug than placebo. The risks of any infection (3208/8038 [39·9%] vs 1713/4809 [35·6%]; 1·14, 1·05-1·23; I<sup>2</sup> =60%) or any drug-related adverse event (1094/2997 [36·5%] vs 609/1950 [31·2%]; 1·24, 1·02-1·50; I<sup>2</sup> =75%) were higher with active drug than placebo. However, the risks of any worsening of IBD activity (1038/8090 [12·8%] vs 1181/5191 [22·8%]; 0·58, 0·52-0·64; I<sup>2</sup> =40%), any withdrawal due to adverse events (610/10 282 [5·9%] vs 561/6207 [9·0%]; 0·71, 0·60-0·84; I<sup>2</sup> =43%), any serious adverse events (1066/10 292 [10·4%] vs 742/6198 [12·0%]; 0·85, 0·77-0·94; I<sup>2</sup> =17%), or any serious worsening of IBD activity (101/5707 [1·8%] vs 143/3640 [3·9%]; 0·55, 0·42-0·71; I<sup>2</sup> =0%) were lower with ","PeriodicalId":56028,"journal":{"name":"Lancet Gastroenterology & Hepatology","volume":" ","pages":"1030-1040"},"PeriodicalIF":30.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142301850","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}
Pub Date : 2024-10-22DOI: 10.1016/s2468-1253(24)00265-6
Cathy Lu, Ryan Rosentreter, Claire E Parker, Julie Remillard, Stephanie R Wilson, Mark E Baker, Gauraang Bhatnagar, Jakob Begun, David H Bruining, Robert V Bryant, Britt Christensen, Brian G Feagan, Joel G Fletcher, Ilyssa Gordon, Gaylyn Henderson, Vipul Jairath, John Knudsen, Torsten Kucharzik, Kyle Lesack, Christian Maaser, Florian Rieder
Background
Diagnostic imaging using CT enterography, magnetic resonance enterography, and intestinal ultrasound are important tools in evaluating stricturing Crohn's disease. Definitions of strictures have been developed for CT enterography and magnetic resonance enterography. However, expert recommendations for definitions and treatment response of strictures on intestinal ultrasound are not available. The aim of this study was to standardise definitions, diagnosis, and treatment response criteria in small bowel stricturing Crohn's disease on intestinal ultrasound.
Methods
Using modified RAND–University of California Los Angeles Appropriateness Method, a diverse expert panel of 13 gastroenterologists, seven radiologists, and two patient representatives was assembled. A total of 466 statements on definitions and response to therapy of stricturing Crohn's disease on intestinal ultrasound were generated from a systematic review and from expert opinion, with subsequent rating for appropriateness. Two rounds of voting with an interposed survey result discussion were performed. Statements were classified as inappropriate, uncertain, or appropriate based on the median panel rating and degree of disagreement. Appropriateness was rated using a nine-point Likert scale (1 being inappropriate, 9 being highly appropriate).
Findings
A naive or anastomotic small bowel Crohn's disease stricture on intestinal ultrasound is defined by the combination of bowel wall thickening, luminal narrowing, and pre-stenotic dilation. Bowel wall thickness is defined as being more than 3 mm. Luminal narrowing is defined as either a luminal diameter reduction of more than 50% in the narrowest area and relative to a normal adjacent bowel loop, or a luminal diameter of less than 1 cm. Pre-stenotic dilation is defined as more than 2·5 cm or an increase in bowel diameter relative to a normal adjacent bowel loop. Definitions for grading hyperaemia, inflammatory fat, wall stratification, intestinal ultrasound machine technical parameters, and image acquisition were also devised. Treatment response of strictures was defined as reduction in stricture length, bowel wall thickening, luminal narrowing, pre-stenotic dilation, and motility abnormalities.
Interpretation
To our knowledge, this is the first intestinal ultrasound appropriateness rating exercise conducted for defining, diagnosing, and measuring response to therapy in small bowel stricturing Crohn's disease and informs future clinical use and intestinal ultrasound index development for clinical trials.
{"title":"International expert guidance for defining and monitoring small bowel strictures in Crohn's disease on intestinal ultrasound: a consensus statement","authors":"Cathy Lu, Ryan Rosentreter, Claire E Parker, Julie Remillard, Stephanie R Wilson, Mark E Baker, Gauraang Bhatnagar, Jakob Begun, David H Bruining, Robert V Bryant, Britt Christensen, Brian G Feagan, Joel G Fletcher, Ilyssa Gordon, Gaylyn Henderson, Vipul Jairath, John Knudsen, Torsten Kucharzik, Kyle Lesack, Christian Maaser, Florian Rieder","doi":"10.1016/s2468-1253(24)00265-6","DOIUrl":"https://doi.org/10.1016/s2468-1253(24)00265-6","url":null,"abstract":"<h3>Background</h3>Diagnostic imaging using CT enterography, magnetic resonance enterography, and intestinal ultrasound are important tools in evaluating stricturing Crohn's disease. Definitions of strictures have been developed for CT enterography and magnetic resonance enterography. However, expert recommendations for definitions and treatment response of strictures on intestinal ultrasound are not available. The aim of this study was to standardise definitions, diagnosis, and treatment response criteria in small bowel stricturing Crohn's disease on intestinal ultrasound.<h3>Methods</h3>Using modified RAND–University of California Los Angeles Appropriateness Method, a diverse expert panel of 13 gastroenterologists, seven radiologists, and two patient representatives was assembled. A total of 466 statements on definitions and response to therapy of stricturing Crohn's disease on intestinal ultrasound were generated from a systematic review and from expert opinion, with subsequent rating for appropriateness. Two rounds of voting with an interposed survey result discussion were performed. Statements were classified as inappropriate, uncertain, or appropriate based on the median panel rating and degree of disagreement. Appropriateness was rated using a nine-point Likert scale (1 being inappropriate, 9 being highly appropriate).<h3>Findings</h3>A naive or anastomotic small bowel Crohn's disease stricture on intestinal ultrasound is defined by the combination of bowel wall thickening, luminal narrowing, and pre-stenotic dilation. Bowel wall thickness is defined as being more than 3 mm. Luminal narrowing is defined as either a luminal diameter reduction of more than 50% in the narrowest area and relative to a normal adjacent bowel loop, or a luminal diameter of less than 1 cm. Pre-stenotic dilation is defined as more than 2·5 cm or an increase in bowel diameter relative to a normal adjacent bowel loop. Definitions for grading hyperaemia, inflammatory fat, wall stratification, intestinal ultrasound machine technical parameters, and image acquisition were also devised. Treatment response of strictures was defined as reduction in stricture length, bowel wall thickening, luminal narrowing, pre-stenotic dilation, and motility abnormalities.<h3>Interpretation</h3>To our knowledge, this is the first intestinal ultrasound appropriateness rating exercise conducted for defining, diagnosing, and measuring response to therapy in small bowel stricturing Crohn's disease and informs future clinical use and intestinal ultrasound index development for clinical trials.<h3>Funding</h3>Leona M and Harry B Helmsley Charitable Trust.","PeriodicalId":56028,"journal":{"name":"Lancet Gastroenterology & Hepatology","volume":"33 1","pages":""},"PeriodicalIF":35.7,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142452524","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}
Pub Date : 2024-10-22DOI: 10.1016/s2468-1253(24)00354-6
Rob Brierley
Section snippets
Cendakimab for eosinophilic oesophagitis
Cendakimab, a monoclonal antibody that inhibits IL-13 binding to both IL-13Rα1 and IL-13Rα2, improved 24-week outcomes in patients with eosinophilic oesophagitis, according to data presented by Alain M Schoepfer (Lausanne, Switzerland). In a phase 3 trial, adults and adolescents with active eosinophilic oesophagitis were randomly assigned to receive subcutaneous cendakimab at 360 mg every week for 48 weeks (n=143), cendakimab 360 mg every week for 24 weeks followed by the same dose every other
TUSCANY-2
RO7790121, an anti-TL1A monoclonal antibody, could improve outcomes for patients with moderately to severely active ulcerative colitis who have failed previous treatment, according to results from the phase 2B TUSCANY-2 trial, presented by Silvio Danese (Milan, Italy). In this dose-ranging trial, patients were randomly assigned to receive RO7790121 subcutaneously once a month at 50 mg, 150 mg, or 450 mg, or placebo once a month for a 12-week induction period; in the 40-week treat-through
SHINE-1
In the phase 2 SHINE-1 trial, paediatric patients (2 to <18 years) with moderate-to-severe ulcerative colitis who had an inadequate response, loss of response, or intolerance to previous treatment, or who had corticosteroid-dependent colitis, were treated with mirikizumab at a dose determined by bodyweight. Patients with a clinical response per modified Mayo score at week 12 entered a maintenance period, receiving subcutaneous mirikizumab every 4 weeks (with dose again determined by patient
Partially hydrolysed guar gum for chronic constipation
Partially hydrolysed guar gum, a water-soluble fibre derived from guar seed, resulted in greater improvements in frequency of spontaneous bowel movements than did placebo after 6 weeks among patients with functional constipation or IBS-constipation. In a double-blind randomised trial presented by Sílvia Delgado-Aros (Vervey, Switzerland), participants were randomly assigned to receive partially hydrolysed guar gum (10 g/day) or placebo (80 patients in each group). At 6 weeks, patients in the
{"title":"UEG Week 2024","authors":"Rob Brierley","doi":"10.1016/s2468-1253(24)00354-6","DOIUrl":"https://doi.org/10.1016/s2468-1253(24)00354-6","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Cendakimab for eosinophilic oesophagitis</h2>Cendakimab, a monoclonal antibody that inhibits IL-13 binding to both IL-13Rα1 and IL-13Rα2, improved 24-week outcomes in patients with eosinophilic oesophagitis, according to data presented by Alain M Schoepfer (Lausanne, Switzerland). In a phase 3 trial, adults and adolescents with active eosinophilic oesophagitis were randomly assigned to receive subcutaneous cendakimab at 360 mg every week for 48 weeks (n=143), cendakimab 360 mg every week for 24 weeks followed by the same dose every other</section></section><section><section><h2>TUSCANY-2</h2>RO7790121, an anti-TL1A monoclonal antibody, could improve outcomes for patients with moderately to severely active ulcerative colitis who have failed previous treatment, according to results from the phase 2B TUSCANY-2 trial, presented by Silvio Danese (Milan, Italy). In this dose-ranging trial, patients were randomly assigned to receive RO7790121 subcutaneously once a month at 50 mg, 150 mg, or 450 mg, or placebo once a month for a 12-week induction period; in the 40-week treat-through</section></section><section><section><h2>SHINE-1</h2>In the phase 2 SHINE-1 trial, paediatric patients (2 to <18 years) with moderate-to-severe ulcerative colitis who had an inadequate response, loss of response, or intolerance to previous treatment, or who had corticosteroid-dependent colitis, were treated with mirikizumab at a dose determined by bodyweight. Patients with a clinical response per modified Mayo score at week 12 entered a maintenance period, receiving subcutaneous mirikizumab every 4 weeks (with dose again determined by patient</section></section><section><section><h2>Partially hydrolysed guar gum for chronic constipation</h2>Partially hydrolysed guar gum, a water-soluble fibre derived from guar seed, resulted in greater improvements in frequency of spontaneous bowel movements than did placebo after 6 weeks among patients with functional constipation or IBS-constipation. In a double-blind randomised trial presented by Sílvia Delgado-Aros (Vervey, Switzerland), participants were randomly assigned to receive partially hydrolysed guar gum (10 g/day) or placebo (80 patients in each group). At 6 weeks, patients in the</section></section>","PeriodicalId":56028,"journal":{"name":"Lancet Gastroenterology & Hepatology","volume":"2 1","pages":""},"PeriodicalIF":35.7,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142452525","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}
Pub Date : 2024-10-11DOI: 10.1016/s2468-1253(24)00306-6
Sven M Francque, Luisa Vonghia
The treatment of metabolic dysfunction-associated steatohepatitis (MASH) has proven challenging, with many compounds failing during development for various reasons. However, with the recent accelerated approval of resmetirom by the US Food and Drug Administration for the treatment of individuals with fibrotic MASH,1 there is renewed enthusiasm in the field. MASH pathophysiology is complex, and progressive disease results from an imbalance between the driving metabolic inflammatory mechanisms (many of which are extrahepatic; eg, the dysfunctional adipose tissue) and intrahepatic defence and repair mechanisms.2 Many of the compounds currently considered to be the most promising mainly improve the cardiometabolic environment, subsequently (with or without additional direct intrahepatic effects) improving MASH. Many drugs targeting specific intrahepatic metabolic or fibroinflammatory mechanisms have proven unsuccessful in clinical trials, despite preclinical evidence.3 Resmetirom, a liver-targeted thyroid hormone β receptor agonist, showed that a more isolated liver-directed approach, with little or no effect on the extrahepatic drivers of MASH, is also capable of not only improving MASH but inducing the regression of fibrosis.1
{"title":"Expanding the armamentarium for metabolic dysfunction-associated steatohepatitis","authors":"Sven M Francque, Luisa Vonghia","doi":"10.1016/s2468-1253(24)00306-6","DOIUrl":"https://doi.org/10.1016/s2468-1253(24)00306-6","url":null,"abstract":"The treatment of metabolic dysfunction-associated steatohepatitis (MASH) has proven challenging, with many compounds failing during development for various reasons. However, with the recent accelerated approval of resmetirom by the US Food and Drug Administration for the treatment of individuals with fibrotic MASH,<span><span><sup>1</sup></span></span> there is renewed enthusiasm in the field. MASH pathophysiology is complex, and progressive disease results from an imbalance between the driving metabolic inflammatory mechanisms (many of which are extrahepatic; eg, the dysfunctional adipose tissue) and intrahepatic defence and repair mechanisms.<span><span><sup>2</sup></span></span> Many of the compounds currently considered to be the most promising mainly improve the cardiometabolic environment, subsequently (with or without additional direct intrahepatic effects) improving MASH. Many drugs targeting specific intrahepatic metabolic or fibroinflammatory mechanisms have proven unsuccessful in clinical trials, despite preclinical evidence.<span><span><sup>3</sup></span></span> Resmetirom, a liver-targeted thyroid hormone β receptor agonist, showed that a more isolated liver-directed approach, with little or no effect on the extrahepatic drivers of MASH, is also capable of not only improving MASH but inducing the regression of fibrosis.<span><span><sup>1</sup></span></span>","PeriodicalId":56028,"journal":{"name":"Lancet Gastroenterology & Hepatology","volume":"25 1","pages":""},"PeriodicalIF":35.7,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142404972","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}
Pub Date : 2024-10-11DOI: 10.1016/s2468-1253(24)00246-2
Rohit Loomba, Pierre Bedossa, Katharine Grimmer, George Kemble, Eduardo Bruno Martins, William McCulloch, Marie O'Farrell, Wen-Wei Tsai, Jose Cobiella, Eric Lawitz, Madhavi Rudraraju, Stephen A Harrison
<h3>Background</h3>Denifanstat, an oral fatty acid synthase (FASN) inhibitor, blocks de-novo lipogenesis, a key pathway driving progressive lipotoxicity, inflammation, and fibrosis in metabolic dysfunction-associated steatohepatitis (MASH). This study aimed to examine the safety and efficacy of denifanstat for improving liver histology in individuals with MASH and moderate to advanced fibrosis.<h3>Methods</h3>This multicentre, double-blind, randomised, placebo-controlled, phase 2b trial was conducted at 100 clinical sites in the USA, Canada, and Poland. After a screening period of up to 90 days, participants aged 18 years and older with biopsy-confirmed MASH and stage F2 or F3 fibrosis were randomly assigned (2:1) to receive either 50 mg oral denifanstat or placebo once per day for 52 weeks. Participants were dynamically allocated to treatment groups via a centrally administered interactive web-based response system and stratified by type 2 diabetes, region, and fibrosis stage. Investigators, patients, and the sponsor were masked to group allocation until database lock. The primary efficacy endpoints were a 2-point or greater improvement in non-alcoholic fatty liver disease activity score (NAS) without a worsening of fibrosis or MASH resolution with a 2-point or greater improvement in NAS without a worsening of fibrosis at week 52, assessed by intention to treat. Safety was assessed in all participants who received at least one dose of study drug. This trial is registered with <span><span>ClinicalTrials.gov</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span>, <span><span>NCT04906421</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span>, and is closed for enrolment.<h3>Findings</h3>Of the 1087 individuals screened between June 2, 2021, and June 28, 2022, 168 eligible participants were randomly assigned to receive a dose of 50 mg denifanstat once per day (n=112) or placebo (n=56). All 168 participants (100 female, 68 male) received at least one dose of study treatment. In the ITT population, 42 (38%) of 112 participants in the denifanstat group had a 2-point or greater improvement in NAS without a worsening of fibrosis versus nine (16%) of 56 participants in the placebo group (common risk difference 21·0%, 95% CI 8·1–33·9; p=0·0035). 29 (26%) of 112 participants in the denifanstat group showed MASH resolution with a 2-point or greater improvement in NAS without a worsening of fibrosis compared with six (11%) of 56 participants in the placebo group (common risk difference 13·0%, 0·7–25·3; p=0·0173). The most common treatment-emergent adverse events were COVID-19 (19 [17%] of 112 in the denifanstat group <em>vs</em> six [11%] of 56) in th
{"title":"Denifanstat for the treatment of metabolic dysfunction-associated steatohepatitis: a multicentre, double-blind, randomised, placebo-controlled, phase 2b trial","authors":"Rohit Loomba, Pierre Bedossa, Katharine Grimmer, George Kemble, Eduardo Bruno Martins, William McCulloch, Marie O'Farrell, Wen-Wei Tsai, Jose Cobiella, Eric Lawitz, Madhavi Rudraraju, Stephen A Harrison","doi":"10.1016/s2468-1253(24)00246-2","DOIUrl":"https://doi.org/10.1016/s2468-1253(24)00246-2","url":null,"abstract":"<h3>Background</h3>Denifanstat, an oral fatty acid synthase (FASN) inhibitor, blocks de-novo lipogenesis, a key pathway driving progressive lipotoxicity, inflammation, and fibrosis in metabolic dysfunction-associated steatohepatitis (MASH). This study aimed to examine the safety and efficacy of denifanstat for improving liver histology in individuals with MASH and moderate to advanced fibrosis.<h3>Methods</h3>This multicentre, double-blind, randomised, placebo-controlled, phase 2b trial was conducted at 100 clinical sites in the USA, Canada, and Poland. After a screening period of up to 90 days, participants aged 18 years and older with biopsy-confirmed MASH and stage F2 or F3 fibrosis were randomly assigned (2:1) to receive either 50 mg oral denifanstat or placebo once per day for 52 weeks. Participants were dynamically allocated to treatment groups via a centrally administered interactive web-based response system and stratified by type 2 diabetes, region, and fibrosis stage. Investigators, patients, and the sponsor were masked to group allocation until database lock. The primary efficacy endpoints were a 2-point or greater improvement in non-alcoholic fatty liver disease activity score (NAS) without a worsening of fibrosis or MASH resolution with a 2-point or greater improvement in NAS without a worsening of fibrosis at week 52, assessed by intention to treat. Safety was assessed in all participants who received at least one dose of study drug. This trial is registered with <span><span>ClinicalTrials.gov</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>, <span><span>NCT04906421</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>, and is closed for enrolment.<h3>Findings</h3>Of the 1087 individuals screened between June 2, 2021, and June 28, 2022, 168 eligible participants were randomly assigned to receive a dose of 50 mg denifanstat once per day (n=112) or placebo (n=56). All 168 participants (100 female, 68 male) received at least one dose of study treatment. In the ITT population, 42 (38%) of 112 participants in the denifanstat group had a 2-point or greater improvement in NAS without a worsening of fibrosis versus nine (16%) of 56 participants in the placebo group (common risk difference 21·0%, 95% CI 8·1–33·9; p=0·0035). 29 (26%) of 112 participants in the denifanstat group showed MASH resolution with a 2-point or greater improvement in NAS without a worsening of fibrosis compared with six (11%) of 56 participants in the placebo group (common risk difference 13·0%, 0·7–25·3; p=0·0173). The most common treatment-emergent adverse events were COVID-19 (19 [17%] of 112 in the denifanstat group <em>vs</em> six [11%] of 56) in th","PeriodicalId":56028,"journal":{"name":"Lancet Gastroenterology & Hepatology","volume":"6 1","pages":""},"PeriodicalIF":35.7,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142404971","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}
Pub Date : 2024-10-09DOI: 10.1016/s2468-1253(24)00321-2
Holly Baker
<h2>Section snippets</h2><section><section><h2>Cabozantinib for advanced neuroendocrine tumours</h2>Cabozantinib shows promise for patients with neuroendocrine tumours, according to the <span><span>CABINET phase 3 trial</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span>. Jennifer A Chan and colleagues randomly assigned patients with previously treated, progressive advanced extrapancreatic or pancreatic neuroendocrine tumours to receive either cabozantinib 60 mg or placebo daily. Among patients with pancreatic neuroendocrine tumours, a significant improvement in progression-free survival was observed in the cabozantinib group compared with the placebo</section></section><section><section><h2>Preoperative chemoradiotherapy for gastric cancer</h2>Preoperative chemoradiotherapy did not improve outcomes for patients with resectable gastric cancer in the <span><span>TOPGEAR phase 3 trial</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span>. Trevor Leong and colleagues randomly assigned patients with resectable adenocarcinoma of the stomach or gastro-oesophageal junction to receive either preoperative chemoradiotherapy plus perioperative chemotherapy (n=286) or perioperative chemotherapy alone (standard of care; n=288). 36 (17%) of 214 patients in the preoperative chemoradiotherapy group had a</section></section><section><section><h2>Peg-interferon after bepirovirsen for chronic hepatitis B</h2>Sequential therapy with pegylated interferon-alfa-2b after bepirovirsen might reduce relapse rates seen in earlier trials of bepirovirsen alone in patients with chronic hepatitis B, according to the <span><span>B-Together trial</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span>. Maria Buti and colleagues randomly assigned patients on stable nucleoside or nucleotide analogue therapy to receive bepirovirsen 300 mg once weekly for 24 weeks (n=55) or 12 weeks (n=53), followed by pegylated interferon-alfa-2b 180 μg once weekly for up to 24 weeks, with up to 36</section></section><section><section><h2>Terlipressin in decompensated cirrhosis</h2>Long-term <span><span>terlipressin therapy</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span> might improve cardiac reserve in patients with decompensated cirrhosis, according to new research. Ryma Terbah and colleagues enrolled 22 patients to receive home continuous terlipressin infusion for 12 wee
{"title":"Research in Brief","authors":"Holly Baker","doi":"10.1016/s2468-1253(24)00321-2","DOIUrl":"https://doi.org/10.1016/s2468-1253(24)00321-2","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Cabozantinib for advanced neuroendocrine tumours</h2>Cabozantinib shows promise for patients with neuroendocrine tumours, according to the <span><span>CABINET phase 3 trial</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>. Jennifer A Chan and colleagues randomly assigned patients with previously treated, progressive advanced extrapancreatic or pancreatic neuroendocrine tumours to receive either cabozantinib 60 mg or placebo daily. Among patients with pancreatic neuroendocrine tumours, a significant improvement in progression-free survival was observed in the cabozantinib group compared with the placebo</section></section><section><section><h2>Preoperative chemoradiotherapy for gastric cancer</h2>Preoperative chemoradiotherapy did not improve outcomes for patients with resectable gastric cancer in the <span><span>TOPGEAR phase 3 trial</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>. Trevor Leong and colleagues randomly assigned patients with resectable adenocarcinoma of the stomach or gastro-oesophageal junction to receive either preoperative chemoradiotherapy plus perioperative chemotherapy (n=286) or perioperative chemotherapy alone (standard of care; n=288). 36 (17%) of 214 patients in the preoperative chemoradiotherapy group had a</section></section><section><section><h2>Peg-interferon after bepirovirsen for chronic hepatitis B</h2>Sequential therapy with pegylated interferon-alfa-2b after bepirovirsen might reduce relapse rates seen in earlier trials of bepirovirsen alone in patients with chronic hepatitis B, according to the <span><span>B-Together trial</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>. Maria Buti and colleagues randomly assigned patients on stable nucleoside or nucleotide analogue therapy to receive bepirovirsen 300 mg once weekly for 24 weeks (n=55) or 12 weeks (n=53), followed by pegylated interferon-alfa-2b 180 μg once weekly for up to 24 weeks, with up to 36</section></section><section><section><h2>Terlipressin in decompensated cirrhosis</h2>Long-term <span><span>terlipressin therapy</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> might improve cardiac reserve in patients with decompensated cirrhosis, according to new research. Ryma Terbah and colleagues enrolled 22 patients to receive home continuous terlipressin infusion for 12 wee","PeriodicalId":56028,"journal":{"name":"Lancet Gastroenterology & Hepatology","volume":"23 1","pages":""},"PeriodicalIF":35.7,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142397760","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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