Alimentary Pharmacology & Therapeutics最新文献

{"title":"Letter on “Inherited Genetic Risk of Liver Fibrosis in Lean Versus Nonlean Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)”","authors":"Di Chang, Yimeng Zhou","doi":"10.1111/apt.70555","DOIUrl":"10.1111/apt.70555","url":null,"abstract":"<p>We read with great interest the study by Tesfai et al. [<span>1</span>], which provides important insights into genetic fibrosis risk in lean versus non-lean metabolic dysfunction–associated steatotic liver disease (MASLD). Demonstrating that the cumulative burden of common variants (<i>PNPLA3</i>, <i>TM6SF2</i> and <i>HSD17B13</i>) confers a comparable fibrosis risk across BMI strata substantially advances our understanding. This aligns with broader epidemiological data highlighting global genetic variations [<span>2</span>]. Furthermore, while genetics are pivotal, acknowledging the intersection with environmental factors, such as social determinants of health, remains essential for a holistic view of disease susceptibility [<span>3</span>].</p><p>Building on these findings, we would like to offer several complementary considerations that may further refine risk stratification in lean MASLD.</p><p>First, lean MASLD cohorts may include a subset of patients with monogenic disorders of adipose tissue, particularly lipodystrophy syndromes. Current international guidelines recognise these conditions as distinct entities characterised by severe ectopic fat deposition, insulin resistance, and progressive liver disease despite a lean or near-normal BMI [<span>4</span>]. This perspective is strongly reinforced by the authors' data: notably, 82.5% of ‘lean’ participants exhibited an abnormal Waist-to-Hip Ratio. This specific phenotype, central adiposity with a lean periphery, is consistent with adipose tissue dysfunction and may help distinguish monogenic adipose failure from polygenic lean MASLD. While the current low-coverage sequencing was optimised for common variants, this striking phenotypic signal warrants targeted assessment of lipodystrophy-associated genes (e.g., <i>LMNA</i>, <i>PPARG</i>) in future high-depth sequencing or clinical screening efforts to distinguish these monogenic mimics.</p><p>Second, adipokine profiling offers mechanistic resolution. Leptin levels in conventional MASLD typically rise due to resistance [<span>5</span>]. In stark contrast, lipodystrophy is characterised by disproportionately low leptin due to adipose tissue failure. Identifying discordant leptin levels could thus serve as a non-invasive tool to unmask monogenic mimics. Furthermore, longitudinal data confirm that hypoadiponectinemia is a potent, early predictor of steatotic liver disease, warranting its inclusion in risk models [<span>6</span>].</p><p>Third, regarding biochemistry, the study focused on aminotransferases and alkaline phosphatase. However, γ-glutamyl transferase (GGT) may be a more sensitive indicator of metabolic stress, oxidative injury, and hepatic lipotoxicity, particularly in lean metabolic phenotypes. Prior analyses in lean populations highlight GGT as an independent marker of cardiometabolic and fibrotic risk, even when aminotransferase levels remain within the normal range [<span>7</span>]. Inclusion of GGT may therefore further enhance","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"63 8","pages":"1179-1180"},"PeriodicalIF":6.7,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70555","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146205012","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":"Comprehensive Risk Profile of Gastrointestinal and Extra Articular Comorbidities in Ehlers–Danlos Syndrome: A Propensity-Matched Analysis of 118,256 Individuals","authors":"Saqr Alsakarneh,&nbsp;Omar Al Ta’ani,&nbsp;Mahmoud Y. Madi,&nbsp;Wing-Kin Syn,&nbsp;James K. Ruffle,&nbsp;Qasim Aziz,&nbsp;Adam D. Farmer","doi":"10.1111/apt.70506","DOIUrl":"10.1111/apt.70506","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Ehlers–Danlos syndrome (EDS) comprises inherited connective tissue disorders characterised by joint hypermobility, skin hyperextensibility and tissue fragility. It links to systemic comorbidities, including gastrointestinal (GI) disorders, but hitherto large-scale data remain limited. We aimed to evaluate the prevalence of GI, systemic and psychological comorbidities in EDS patients versus propensity score-matched controls, using a comprehensive research network database.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Design</h3>\u0000 \u0000 <p>This was a retrospective, propensity-matched analysis (2005–2023) utilising the TriNetX network. We identified EDS patients (excluding Marfan's syndrome). Propensity score matching (1:1) generated balanced cohorts for age, sex and baseline characteristics. Comorbidities were analysed via prevalence rates and odds ratios (ORs) with 95% confidence intervals (CIs).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Matched cohorts included 59,128 pairs. Among GI disorders, gastroesophageal reflux disease was most common in EDS (18.4%, OR 1.5, 95% CI 1.4–1.5, <i>p</i> &lt; 0.001), followed by constipation (12.4%, OR 1.8, 95% CI 1.7–1.9, <i>p</i> &lt; 0.001), irritable bowel syndrome (7.3%, OR 2.6, 95% CI 2.5–2.8, <i>p</i> &lt; 0.001) and gastroparesis (4.7%, OR 8.2, 95% CI 7.3–9.2, <i>p</i> &lt; 0.001). Psychiatric conditions showed heightened prevalence of anxiety (26.1%, OR 1.8, 95% CI 1.7–1.8, <i>p</i> &lt; 0.001) and depression (18.7%, OR 1.3, 95% CI 1.2–1.3, <i>p</i> &lt; 0.001). Systemic comorbidities included postural orthostatic tachycardia syndrome (13.2%, OR 899.7, 95% CI 483.8–1673.0, <i>p</i> &lt; 0.001), chronic pain (7.9%, OR 7.0, 95% CI 6.4–7.6, <i>p</i> &lt; 0.001), migraines (19.7%, OR 2.5, 95% CI 2.4–2.6, <i>p</i> &lt; 0.001) and fibromyalgia (9.5%, OR 1.7, 95% CI 1.6–1.8, <i>p</i> &lt; 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>EDS patients exhibit heightened risk for GI, systemic and psychological comorbidities, highlighting the importance of multidisciplinary approaches for effective management.</p>\u0000 </section>\u0000 </div>","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"63 8","pages":"1151-1161"},"PeriodicalIF":6.7,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807674","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: Beyond Viral Eradication—Cardiometabolic Risk and Cardiovascular Outcomes After SVR in Chronic Hepatitis C. Authors' Reply","authors":"Pei-Chien Tsai,&nbsp;Jee-Fu Huang,&nbsp;Ming-Lung Yu","doi":"10.1111/apt.70567","DOIUrl":"10.1111/apt.70567","url":null,"abstract":"&lt;p&gt;We appreciate the insightful commentary by Wakabayashi et al. regarding the shifting paradigm in hepatitis C virus (HCV) care from a singular focus on viral clearance to the long-term management of residual intrahepatic and extrahepatic risks. Their editorial accurately underscores that the intersection of steatotic liver disease (SLD) and major adverse cardiovascular events (MACEs) has emerged as a critical frontier in post-SVR clinical care [&lt;span&gt;1&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Our study confirms a clear ‘dose–response’ relationship between the burden of cardiometabolic risk factors (CMRFs) and the incidence of MACE after viral eradication. Notably, our findings suggest that the predictive utility of CMRF burden for clinical outcomes may parallel or even exceed that of traditional liver-related risks in certain populations [&lt;span&gt;2&lt;/span&gt;]. This is consistent with recent Japanese data [&lt;span&gt;3&lt;/span&gt;], which highlights the superiority of CMRF burden in predicting MACE compared to HCC. This shift underscores that while virologic cure mitigates virus-induced injury, a persistent ‘metabolic scar’ continues to drive systemic and oncogenic risks [&lt;span&gt;4&lt;/span&gt;]. Recent findings link this ‘lipid rebound’ to restored SREBP1 and TM6SF2 expression, which correlated with elevated ASCVD and Framingham risk scores at 24 weeks post-treatment [&lt;span&gt;5&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Beyond systemic outcomes, the persistence of HCV-induced genetic and epigenetic ‘scars’ (e.g., H3K4Me3, TP53 mutations) maintains a pro-oncogenic environment in the liver even after SVR [&lt;span&gt;6&lt;/span&gt;]. Our findings highlight that CMRFs, particularly obesity and diabetes, function as catalysts that exacerbate this metabolic memory. Crucially, this risk is modifiable; for instance, metformin therapy has been shown to reduce 5-year HCC incidence by nearly 3-fold in diabetic patients after successful antiviral therapy [&lt;span&gt;7&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;In the post-SVR era, as non-liver-related events such as MACE become primary concerns [&lt;span&gt;4&lt;/span&gt;], the clinical significance of CMRF burden is most prominent in patients without advanced fibrosis, as they face fewer competing liver-related risks. This is corroborated by the OPERA-C study, showing that while liver-related death drives mortality in cirrhosis, MACE and extrahepatic cancers are significant contributors in older, non-cirrhotic patients, with diabetes doubling these risks [&lt;span&gt;8&lt;/span&gt;]. Consequently, we propose a stage-specific management framework: (1) For early-stage patients: The focus should shift toward aggressive metabolic optimisation (including the use of metformin and statins) to mitigate both systemic and long-term oncogenic threats. (2) For patients with advanced fibrosis: Rigorous HCC surveillance remains the indispensable priority.&lt;/p&gt;&lt;p&gt;We wholeheartedly agree that MASLD parameters are dynamic post-SVR. Potential risk factors for worsening metabolic status include elevated BMI, HbA1c and LDL-C levels [&lt;span&gt;9&lt;/span&gt;]. The ‘lipid paradox’ ","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"63 8","pages":"1175-1176"},"PeriodicalIF":6.7,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70567","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123085","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 on ‘Inherited Genetic Risk of Liver Fibrosis in Lean Versus Nonlean Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)’; Authors’ reply","authors":"Kaleb Tesfai,&nbsp;Luis Antonio Díaz,&nbsp;Veeral Ajmera","doi":"10.1111/apt.70577","DOIUrl":"10.1111/apt.70577","url":null,"abstract":"&lt;p&gt;We appreciate Chang and Zhou for their insight into risk stratification in lean MASLD [&lt;span&gt;1&lt;/span&gt;]. In our original research study, we prospectively recruited over 300 participants with MASLD and demonstrated that lean (BMI &lt; 25 kg/m&lt;sup&gt;2&lt;/sup&gt;) and non-lean (BMI ≥ 25 kg/m&lt;sup&gt;2&lt;/sup&gt;) MASLD patients have a comparable prevalence of significant and advanced fibrosis and share a similar effect of inherited risk on liver fibrosis [&lt;span&gt;2&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;First, we agree that a subset of patients with lean MASLD may be affected by monogenic drivers of disease. In a prospectively recruited cohort of lean and non-lean biopsy-proven MASLD patients, Zheng and colleagues reported two of six (33%) lean MASLD patients without visceral adiposity harboured monogenic disorders [&lt;span&gt;3&lt;/span&gt;]. Specifically, patient 1 had hereditary fructose intolerance due to a homozygous mutation in aldolase B, and patient 2 had familial hypobetalipoproteinaemia resulting from a heterozygous mutation in apolipoprotein B.&lt;/p&gt;&lt;p&gt;Based on previous research and our current study, we propose that lean MASLD may encompass at least two biologically distinct subtypes. Type 1 lean MASLD embodies patients with cardiometabolic comorbidities and a similar contribution from polygenic risk driven by common variants, whereas Type 2 lean MASLD includes those with low visceral adiposity and is enriched for rare monogenic drivers of disease [&lt;span&gt;4&lt;/span&gt;]. While our study demonstrated that elevated polygenic risk based on common MASLD- and fibrosis-associated variants is associated with increased liver fibrosis risk in lean MASLD, future studies are needed to comprehensively assess the contribution of monogenic variants in lean MASLD cohorts.&lt;/p&gt;&lt;p&gt;Secondly, we agree that adipokine profiling can provide additional mechanistic insight into lean MASLD. Given that metabolic imbalance drives adipokine dysregulation and a substantial proportion of lean MASLD patients have insulin resistance, hypertension and dyslipidaemia, adipokine profiling may be beneficial to differentiate between lean MASLD subtypes [&lt;span&gt;5&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Third, we appreciate the insight that γ-glutamyl transferase (GGT) influences fibrosis risk and completed additional analyses considering this variable. The median [IQR] GGT was similar between lean and non-lean MASLD, 33 (23–52) vs. 38 (24–67) U/L, &lt;i&gt;p&lt;/i&gt; = 0.395, with lean MASLD having a trend towards lower GGT, an effect seen in previous studies [&lt;span&gt;6, 7&lt;/span&gt;]. Given that GGT might reflect undisclosed alcohol intake, future incorporation of quantitative alcohol biomarkers, such as phosphatidylethanol, may also help to exclude hepatic steatosis driven by alcohol use [&lt;span&gt;8&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;In conclusion, we agree with Chang and Zhou that lean MASLD represents a biologically heterogeneous condition requiring refined phenotypic and mechanistic classification. Our findings support the concept that a substantial proportion of lean MASLD patients share cardi","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"63 8","pages":"1181-1182"},"PeriodicalIF":6.7,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70577","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146205014","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":"Characterisation and Prognostic Implication of Cholestasis After Burn Injury","authors":"Lorenz Semmler,&nbsp;Georg Semmler,&nbsp;Andreas Langa,&nbsp;Sebastian Rihl,&nbsp;Sebastian Hofstetter,&nbsp;Melissa-Patricia Mateas,&nbsp;Kevin Dilmen,&nbsp;Anton Borger,&nbsp;Paul Supper,&nbsp;Patrick Haselwanter,&nbsp;Emina Halilbasic,&nbsp;Christian Zauner,&nbsp;Albert Stättermayer,&nbsp;Gerald Ihra,&nbsp;Christine Radtke,&nbsp;Mathias Anselm Schneeweiss-Gleixner,&nbsp;Michael Trauner","doi":"10.1111/apt.70505","DOIUrl":"10.1111/apt.70505","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Cholestasis is a frequent phenomenon in patients with burn injury and linked with impaired outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>To explore longitudinal trajectories of cholestasis and validate the proposed definition of burn-associated cholestasis (BAC).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>532 patients admitted to an intensive care unit (ICU) for burn injury over a 10-year timeframe were included in this single-center, retrospective cohort study. Burn severity, ICU treatment, and laboratory parameters were longitudinally collected from admission to discharge or death.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Median total body surface area burned was 15% and 234 patients (44%) had severe burn (≥ 20%). 118 patients (22%) met the proposed criteria of BAC while 41%, 30%, and 68% developed elevated alkaline phosphatase, bilirubin, and gamma-glutamyl transferase, respectively. BAC was associated with burn severity, ketamine use, mechanical ventilation, and parenteral nutrition, and 85% of cases occurred in patients exposed to ketamine, mechanical ventilation, and parenteral nutrition. Hyperbilirubinemia (≥ 2× upper-limit-of-normal, i.e., BAC subtype B/C) was independently associated with mortality adjusting for burn severity, critical illness severity, and ICU-specific treatment. However, bilirubin alone provided better discrimination, especially regarding excess deaths after ≥ 7 days (Harrel's C: 0.80–0.83). Concordant increases in bilirubin and alkaline phosphatase/gamma-glutamyl transferase allow for early identification of an at-risk population. Developing hyperbilirubinemia until Day 14 identified a subgroup with severely impaired prognosis (survival at 90 days: 46% vs. 95%).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Cholestasis is frequent following burn injury. Prognosis is determined by bilirubin dynamics independently of disease and burn severity. Hyperbilirubinemia is associated with excess mortality ≥ 7 days after surviving burn injury.</p>\u0000 </section>\u0000 </div>","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"63 8","pages":"1140-1150"},"PeriodicalIF":6.7,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70505","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145961497","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: From Safety to Precision—Optimising the Use of GLP-1 Receptor Agonists in Gastroenterology","authors":"Joëlle St-Pierre,&nbsp;Brooke Maracle,&nbsp;Cynthia H. Seow","doi":"10.1111/apt.70538","DOIUrl":"10.1111/apt.70538","url":null,"abstract":"&lt;p&gt;The therapeutic landscape for glucagon-like peptide-1 receptor agonists (GLP-1 RAs) is rapidly expanding within gastroenterology, paralleling the epidemics of obesity, metabolic disease, and resulting in chronic disease sequelae. Pomenti et al. have provided a timely narrative overview of GLP-1 RA use with a focus on obesity-related gastrointestinal outcomes in individuals with steatotic liver disease, irritable bowel syndrome, and obesity-associated cancers [&lt;span&gt;1&lt;/span&gt;]. Distinct from the secondary effects of improved metabolic control on these disease outcomes, preliminary data on potential primary anti-inflammatory effects of GLP-1 RAs in the setting of inflammatory bowel disease (IBD) are cited. Complementing this perspective, a systematic review in the same issue synthesises evidence on the effectiveness, safety, and metabolic effects of these therapies in IBD, a population excluded from the GLP-1 RA pivotal trials [&lt;span&gt;2&lt;/span&gt;]. Collectively, these data reflect a maturation of the field, from initial concerns regarding gastrointestinal tolerability to growing reassurance, thereby establishing a scholarly framework for evidence-based integration of GLP-1-based therapies into clinical care.&lt;/p&gt;&lt;p&gt;While achieving consistent reductions in body weight and improvements of metabolic parameters, the most common gastrointestinal adverse effects of GLP-1 RA therapy including diarrhoea, abdominal pain and nausea appear similar in IBD and non-IBD cohorts, without an increased rate of disease flare or need for treatment escalation. In addition, several large registries report associations with improved IBD-related outcomes, including fewer hospitalisations and reduced corticosteroid exposure, although these observations are inherently limited by confounding and indication bias [&lt;span&gt;3-5&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;The hepatology literature provides efficacy data for GLP-1 RAs for metabolic dysfunction-associated steatohepatitis with robust primary end points including resolution of steatohepatitis without worsening of liver fibrosis and reduction in liver fibrosis without worsening of steatohepatitis. In contrast, GLP-1 RAs are not prescribed specifically for IBD. Hence, IBD-specific outcomes are obtained using proxies from administrative and pharmaceutical databases, with inconsistent and inadequate capture of objective markers of disease activity, namely inflammatory biomarkers, endoscopy or histology. Moreover, body mass index or total body weight changes are used as the primary metric of adiposity, overlooking heterogeneity in visceral fat distribution and metabolic phenotypes that may be more relevant to IBD biology and treatment response. Thus, current data remain insufficient to identify which patients with IBD may benefit from GLP-1-based therapies, through what mechanisms, and at what point in the disease course.&lt;/p&gt;&lt;p&gt;The next phase of research should focus on prospective, IBD-specific study designs that integrate metabolic and inflammatory endp","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"63 8","pages":"1183-1184"},"PeriodicalIF":6.7,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70538","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147483642","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":"Editorial: Personalising the Low FODMAP Diet to Achieve Therapeutic Benefit Whilst Reducing Burden and Maintaining Dietary Diversity in Irritable Bowel Syndrome. Authors' Reply","authors":"E. Coss‐Adame, M. F. Garcia‐Cedillo, M. F. Huerta‐de la Torre, J. S. Arenas‐Martinez","doi":"10.1111/apt.70631","DOIUrl":"https://doi.org/10.1111/apt.70631","url":null,"abstract":"","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"23 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147507942","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":"Barriers to Medical Care Are Frequently Reported by Patients With Cirrhosis","authors":"William Chai,&nbsp;Nicole E. Rich,&nbsp;Yan Liu,&nbsp;Juana Campos,&nbsp;Lisa Quirk,&nbsp;Jennifer R. Kramer,&nbsp;Jahna Anyanwu,&nbsp;Amanda Gibbons,&nbsp;Aaron Loewy,&nbsp;Dalal Youssef,&nbsp;Riya Malhorta,&nbsp;Hadley McGhee,&nbsp;Meena Tadros,&nbsp;Fasiha Kanwal,&nbsp;Amit G. Singal","doi":"10.1111/apt.70511","DOIUrl":"10.1111/apt.70511","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Patient-reported barriers to care can delay treatment and increase mortality. Addressing these barriers can improve clinical outcomes and reduce disparities, underscoring the importance to understand their prevalence in patients with cirrhosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We invited adults with cirrhosis at four US health systems (two tertiary care referral centres, one safety-net health system, and one Veterans Affairs medical center) to complete a survey assessing barriers to care. Questions for barriers to care were adapted from prior surveys as available. Responses were summarised using descriptive statistics, and Chi-square analysis was used to examine differences by study site and race/ethnicity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Of 5197 patients contacted by telephone, 1332 (25.6%) completed the survey and were eligible for analyses. The most frequent barriers to care included time to travel to clinic (22.7%), long wait times for appointments (21.6%), and difficulty scheduling visits (19.2%). Conversely, few patients reported competing demands or difficulty finding time for liver appointments, difficulty discussing concerns with their physicians, or lack of physician engagement with concerns. Several barriers to care significantly differed by study site but were generally consistent across racial and ethnic subgroups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Patients with cirrhosis report frequent barriers to medical care including limited access to clinic appointments, although barriers vary by healthcare system. Barriers to care serve as intervention targets to improve outcomes for patients with cirrhosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"63 8","pages":"1162-1168"},"PeriodicalIF":6.7,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70511","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145836123","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":"Editorial: Post Banding Ulcer Bleeding—Is There Scope for Prevention?","authors":"Rhys Williams,&nbsp;Keith Siau","doi":"10.1111/apt.70519","DOIUrl":"10.1111/apt.70519","url":null,"abstract":"&lt;p&gt;Post-banding ulcer bleeding (PBUB) is a potentially catastrophic complication of endoscopic band ligation (EBL) for portal hypertension–related varices. Despite its clinical relevance, PBUB has been inconsistently defined, variably reported, often difficult to distinguish from early rebleeding, and inadequately addressed in contemporary management algorithms.&lt;/p&gt;&lt;p&gt;In this issue, de Brito Nunes et al. provide important data clarifying the incidence, risk factors and prognostic implications of PBUB. In their Swiss cohort (&lt;i&gt;N&lt;/i&gt; = 206 patients) recruited over a 5-year period, PBUB was reported in 17.5% of patients, occurring after 6.8% of EBL procedures. Crucially, PBUB was associated with hepatic decompensation and a marked reduction in post-procedural survival [&lt;span&gt;1&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Urgent EBL and renal dysfunction emerged as the principal risk factors for PBUB-related morbidity and mortality [&lt;span&gt;1&lt;/span&gt;]. This is plausible because urgent EBL typically reflects advanced portal hypertension during acute variceal bleeding, while renal dysfunction is an established surrogate of circulatory failure and adverse outcomes in cirrhosis [&lt;span&gt;2&lt;/span&gt;]. In emergency settings, these factors are largely non-modifiable, as urgent EBL cannot be deferred. However, recognition of renal dysfunction as a predictor of PBUB may inform management in the elective setting.&lt;/p&gt;&lt;p&gt;The absence of robust, evidence-based preventative options for PBUB is a clear unmet clinical need. Pharmacological prophylaxis has been explored but remains contentious, with proton pump inhibitors (PPIs), sucralfate and non-selective beta blockers (NSBBs) among the most frequently studied agents. Data for PPIs are conflicting, ranging from improved bleeding-free survival compared with no PPI exposure [&lt;span&gt;3&lt;/span&gt;] to potential harm through increased infectious complications and hepatic decompensation [&lt;span&gt;4&lt;/span&gt;]. Sucralfate has shown more potential for benefit, with reported reduction in overall rebleeding events of approximately 10% [&lt;span&gt;5&lt;/span&gt;]. Adequately powered randomised trials with standardised dosing regimens remain necessary.&lt;/p&gt;&lt;p&gt;The only way to avoid a procedural complication is by not doing the procedure. Early initiation of NSBBs, as explored in the BOPP trial, may slow progression to high-risk varices and reduce the need for prophylactic or repeated EBL [&lt;span&gt;6&lt;/span&gt;]. This contrasts with current EASL recommendations, which suggest initiation of prophylaxis only in patients with advanced disease or large varices [&lt;span&gt;7&lt;/span&gt;]. Likewise, early transjugular intrahepatic portosystemic shunt placement for acute variceal bleeding, as endorsed by Baveno VII, may lessen reliance on EBL [&lt;span&gt;8&lt;/span&gt;]. Together, these have the potential to decrease the cumulative number of EBL procedures and, by extension, the risk of PBUB.&lt;/p&gt;&lt;p&gt;Future efforts should extend beyond pharmacological prevention. Procedural technique and inter-operator heterogeneity, for exa","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"63 8","pages":"1171-1172"},"PeriodicalIF":6.7,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70519","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145937840","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: Circulating CD4+PD-1+T Cell Ratio Predicts Response to Pegylated Interferon-Alpha Therapy in Chronic Hepatitis B.","authors":"Yonghong Wang,Bei Cai,Chengrun Song,Jiangnan Peng,Taoyou Zhou,Jiajie Lu,Xuezhong Lei,Enqiang Chen","doi":"10.1111/apt.70646","DOIUrl":"https://doi.org/10.1111/apt.70646","url":null,"abstract":"","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"191 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147518500","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}