Curr. Opin. Gastroenterol. [JOURNAL]
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200 papers
Endoscopic techniques to minimize gastroesophageal reflux during peroral endoscopic myotomy.
Miutescu B, Khashab M, El Abiad R
Curr Opin Gastroenterol · 2026 Jun · PMID 42267488 · Publisher ↗
PURPOSE OF REVIEW: Peroral endoscopic myotomy (POEM) is an established treatment for achalasia. Sacrificing the lower esophageal sphincter (LES) improves dysphagia but compromises the gastroesophageal junction (GEJ) barr...
PURPOSE OF REVIEW: Peroral endoscopic myotomy (POEM) is an established treatment for achalasia. Sacrificing the lower esophageal sphincter (LES) improves dysphagia but compromises the gastroesophageal junction (GEJ) barrier predisposing patients to acid reflux. RECENT FINDINGS: Indeed, 40-60% of patients experience abnormal esophageal acid exposure post-POEM, while clinically significant reflux esophagitis (Los Angeles grade ≥B) is observed in 20-35%. Symptom-reflux discordance is common, necessitating objective assessment with upper endoscopy and/or ambulatory reflux testing using Lyon Consensus 2.0 criteria. Critically, anatomical evaluation must exclude alternative causes of perceived gastroesophageal reflux disease (GERD), including candida esophagitis, failed myotomy or recurrent achalasia, peptic stricture, and blown-out myotomy. Proactive intra-procedural strategies during POEM to minimize reflux have included limiting myotomy length, selective circular-layer myotomy, sling fiber preservation, anterior versus posterior approach selection, and endolumenal functional lumen imaging probe (EndoFLIP)-guided refinement of myotomy, though none has demonstrated consistent reflux reduction in randomized trials. Hybrid procedures combining POEM with endoscopic fundoplication (POEM+F/POEM-F) offer same session approaches that can significantly lower objective reflux up to 3 years. SUMMARY: For proven post-POEM GERD, staged endoscopic options, transoral incisionless fundoplication, endoscopic full-thickness plication, and antireflux mucosectomy, offer symptom improvement and proton pump inhibitor (PPI) reduction in selected patients. A structured clinical pathway integrating proactive surveillance, objective confirmation, and individualized endoscopic intervention is proposed.
Postendoscopy esophageal adenocarcinoma and neoplasia: current status and future directions.
Goyal R, Codipilly DC, Iyer PG
Curr Opin Gastroenterol · 2026 Jul · PMID 42239986 · Publisher ↗
PURPOSE OF REVIEW: A substantial proportion of esophageal adenocarcinoma (EAC) and high-grade dysplasia (HGD) cases in Barrett's esophagus (BE) are diagnosed after a dysplasia-negative endoscopy before the next recommend...
PURPOSE OF REVIEW: A substantial proportion of esophageal adenocarcinoma (EAC) and high-grade dysplasia (HGD) cases in Barrett's esophagus (BE) are diagnosed after a dysplasia-negative endoscopy before the next recommended surveillance interval. These are classified as postendoscopy esophageal carcinoma (PEEC) or postendoscopy esophageal neoplasia (PEEN) and represent critical failures of BE surveillance. This review summarizes current definitions, epidemiology, potential etiologies, and evolving strategies to reduce PEEC/PEEN and improve the quality of BE surveillance. RECENT FINDINGS: High-quality endoscopic examination using high-definition white-light endoscopy (HD-WLE) and virtual chromoendoscopy (CE), adherence to the Seattle biopsy protocol, adequate inspection time, and training in the recognition of visible lesions harboring prevalent dysplasia/EAC, are critical in reducing PEEC/PEEN. Initial data on the use of adjunctive tools (wide-area transepithelial sampling) and molecular biomarkers (p53, DNA methylation panels, and Tissue Systems Pathology tests) demonstrate promising results for detecting prevalent dysplasia and for reducing PEEC and PEEN. BE surveillance quality metrics, such as cancer and neoplasia detection rates, have been shown to be inversely associated with PEEN. SUMMARY: PEEC and PEEN reflect critical gaps in the effectiveness of BE surveillance. Improving the quality of endoscopic surveillance is essential, including meticulous mucosal inspection, appropriate use of advanced imaging techniques, and adherence to systematic biopsy protocols, to minimize missed neoplasia.
The complement system in inflammatory bowel disease: from early observations to emerging frontiers.
Ramirez Reyes B, Kulkarni D
Curr Opin Gastroenterol · 2026 Jul · PMID 42239985 · Publisher ↗
PURPOSE OF REVIEW: The complement system is one of the most evolutionarily conserved arms of innate immunity and has re-emerged as an important regulator of intestinal inflammation in inflammatory bowel disease (IBD). Ea...
PURPOSE OF REVIEW: The complement system is one of the most evolutionarily conserved arms of innate immunity and has re-emerged as an important regulator of intestinal inflammation in inflammatory bowel disease (IBD). Early observations from the mid-1970 s such as complement deposition in diseased bowel tissue and elevated serum complement levels in patients with ulcerative colitis and Crohn's disease have evolved into a nuanced understanding of how individual complement components can exert both protective and pathogenic effects in IBD. This review highlights recent advances in complement biology and examines how complement shapes intestinal immune responses, particularly in the setting of ongoing inflammation. RECENT FINDINGS: The complement system consists of more than 60 proteins that act as rapid first responders to infection. Although traditionally considered primarily liver-derived circulating effectors, recent work has demonstrated local synthesis and activation of key complement components at mucosal sites, including the colon. In parallel, genome-wide association studies have identified variants in complement genes associated with severe IBD complications. Collectively, these findings reveal a dichotomous role for complement in IBD, whereby excessive activation promotes inflammation, while impaired function compromises host defense and worsens disease outcomes. SUMMARY: Complement-targeted therapies have been effective in other diseases but have not yet translated to IBD. A deeper understanding of context-dependent protective versus pathogenic complement functions will be essential for developing future therapeutic strategies.
Goblet cell-associated antigen passages in health and disease.
Cameron AJ, Rizzo GP, Newberry RD
Curr Opin Gastroenterol · 2026 Jul · PMID 42239984 · Publisher ↗
PURPOSE OF REVIEW: In the gut, the immune system is exposed to self and dietary antigens and antigens from microbes including potential pathogens. How the immune system distinguishes between this wide array of substances...
PURPOSE OF REVIEW: In the gut, the immune system is exposed to self and dietary antigens and antigens from microbes including potential pathogens. How the immune system distinguishes between this wide array of substances to mount appropriate responses that range from tolerance to immunity is not well understood. RECENT FINDINGS: Accumulating evidence suggests that intestinal goblet cells may play a central role in the ability of the immune system to mount appropriate responses and to discriminate between innocuous substances and potential pathogens. Intestinal goblet cells can form goblet cell-associated antigen passages (GAPs), which acquire luminal substances and deliver them to the immune system. GAPs are closely regulated to not only control where and when antigen delivery to the immune system occurs but also to shape downstream immune outcomes. More recent studies suggest roles for GAPs in health and for GAP dysregulation as a contributor to disease. SUMMARY: Here, we review emerging studies and concepts on the role of goblet cells and GAPs, highlighting implications of these observations on the pathogenesis of, and potential therapies for, disease.
Inflammatory bowel diseases 2026: form, function and therapeutic considerations for the epithelial barrier.
Ciorba MA
Curr Opin Gastroenterol · 2026 Jul · PMID 42239983 · Publisher ↗
Abstract loading — click title to view on PubMed.
Dietary protein as a regulator of colitis and colorectal cancer.
Thaker SD, Gogokhia L, Montrose DC
Curr Opin Gastroenterol · 2026 Jul · PMID 42165252 · Publisher ↗
PURPOSE OF REVIEW: Diet impacts the pathogenesis of gastrointestinal diseases including inflammatory bowel diseases (IBD) and colorectal cancer (CRC). Although dietary protein can influence physiologic health, its impact...
PURPOSE OF REVIEW: Diet impacts the pathogenesis of gastrointestinal diseases including inflammatory bowel diseases (IBD) and colorectal cancer (CRC). Although dietary protein can influence physiologic health, its impact on these diseases has not been adequately investigated. Consequently, clinical guidelines on optimal protein intake (i.e. amount and source) to help prevent or treat these conditions are limited. RECENT FINDINGS: Recent preclinical and clinical studies have examined how modifying dietary protein can impact the pathogenesis of intestinal inflammation. For example, work in mice reveals that higher protein intake worsens colitis and that different dietary protein sources can exert differential effects on colitis severity. Microbial populations and their metabolism were shown to play an important role in mediating these effects. Studies in humans have shown that high intake of red meat is associated with increased IBD incidence and decreased time to relapse in patients with ulcerative colitis; however, it is unclear which other protein sources may be more beneficial. Although a direct connection between dietary protein and CRC has not been established, multiple preclinical studies have shown that reducing dietary protein exerts anticancer effects, including improved response to therapy across multiple tumor types. These effects were shown to be predominantly mediated by restricting tumors of exogenous growth-promoting amino acids, resulting in tumor stress, and in certain cases, activation of antitumor immunity. SUMMARY: As a result of multiple studies, we have gained important insights into the role of dietary protein in mediating colonic inflammation and cancer. This work motivates clinical studies to directly test whether modifying source or amount of protein intake in patients with IBD or CRC will be beneficial for reducing disease severity and improving response to therapy.
Retrograde cricopharyngeus dysfunction: what the gastroenterologist should know.
Lechien JR, Bastian RW
Curr Opin Gastroenterol · 2026 Jul · PMID 42165231 · Publisher ↗
PURPOSE OF REVIEW: To review current literature about retrograde cricopharyngeus dysfunction (R-CPD) etiology, pathophysiology, clinical presentation and management. RECENT FINDINGS: R-CPD is a clinical condition charact...
PURPOSE OF REVIEW: To review current literature about retrograde cricopharyngeus dysfunction (R-CPD) etiology, pathophysiology, clinical presentation and management. RECENT FINDINGS: R-CPD is a clinical condition characterized by inability to burp that is often associated with a variety of other gastrointestinal symptoms. Limited data suggest that R-CPD may affect up to 22% of the general population, with 13% experiencing severely troublesome symptoms. Symptoms usually begin in childhood, though diagnosis typically occurs many years later after prolonged symptom burden. Gastroesophageal reflux disease (GERD) and laryngopharyngeal reflux disease (LPRD) are strongly associated with R-CPD, with prevalence rates ranging from 28 to 58% across studies, suggesting either that GERD and LPRD contribute to the development of R-CPD or vice versa , with R-CPD producing prolonged elevations in esophageal pressure and esophageal stretching that contribute to the development of GERD and LPRD. Family history is present in 28% of cases, suggesting possible genetic predisposition. Botulinum toxin injection (BTI) into the cricopharyngeal sphincter represents the primary therapeutic option, achieving up to 92.5% overall initial success rate using various approaches, including in-office transcervical (EMG-guided), transnasal, and operating room esophagoscopy techniques. Younger age, higher botulinum toxin doses, and operative esophagoscopy under general anesthesia have been associated with better treatment outcomes. Symptom recurrence occurs in 4-45% of patients, with mean recurrence intervals between 6 and 8 months. SUMMARY: R-CPD represents an underrecognized but potentially common condition with significant impact on quality-of-life. BTI demonstrates high efficacy with an acceptable safety profile. Standardized diagnostic criteria, treatment protocols, and comprehensive pediatric studies for R-CPD remain sorely needed.
Intestinal ultrasound in inflammatory bowel disease: current evidence and future directions.
Abu Hamad MR, Gergely M
Curr Opin Gastroenterol · 2026 Jul · PMID 42130307 · Publisher ↗
PURPOSE OF REVIEW: Intestinal ultrasound (IUS) as a noninvasive tool for assessment and longitudinal monitoring of inflammatory bowel disease (IBD) is gaining attention. This review examines current evidence supporting t...
PURPOSE OF REVIEW: Intestinal ultrasound (IUS) as a noninvasive tool for assessment and longitudinal monitoring of inflammatory bowel disease (IBD) is gaining attention. This review examines current evidence supporting the diagnostic performance and utility of IUS in IBD and explores expanding applications, use in special populations, and remaining gaps in knowledge. RECENT FINDINGS: Evidence supports its diagnostic accuracy in Crohn's disease (CD) and ulcerative colitis (UC). Bowel wall thickness (BWT) and vascularity through color Doppler signal (CDS) are among the most reliable markers of inflammation. IUS demonstrates utility for disease monitoring, assessment of treatment response, and prediction of long-term outcomes. Activity indices have been externally validated, demonstrating reproducibility. Beyond luminal assessment, transmural remission (TR) is emerging as a therapeutic target. Advanced techniques, including contrast-enhanced ultrasound (CEUS) and small-intestine contrast ultrasound (SICUS), may provide additional value in selected clinical scenarios, although their use remains limited to specialized settings. SUMMARY: IUS is an important practical tool in IBD, complementing endoscopy and biomarkers. Although diagnostic performance is well established, future work should focus on IUS-driven treatment strategies, validation of meaningful endpoints, and addressing barriers to implementation.
Roles for specialized secretory epithelial cells in inflammatory bowel disease.
Huang Z, Brown ME, Lau KS
Curr Opin Gastroenterol · 2026 Jul · PMID 42124523 · Full text
PURPOSE OF REVIEW: Current inflammatory bowel disease (IBD) therapies mainly target immune pathways, yet many patients fail to achieve durable remission, highlighting the need to understand epithelial-intrinsic drivers o...
PURPOSE OF REVIEW: Current inflammatory bowel disease (IBD) therapies mainly target immune pathways, yet many patients fail to achieve durable remission, highlighting the need to understand epithelial-intrinsic drivers of chronic inflammation and barrier defects. Recent single-cell, spatial, and functional studies have redefined secretory epithelial lineages as active regulators of mucosal immunity, microbial containment, and tissue recovery. RECENT FINDINGS: Goblet cells are increasingly recognized as heterogeneous barrier sentinels whose region-specific alterations in mucus organization, microbial sensing, and stress responses can influence disease location and variability. Tuft cells are chemosensory hubs that connect luminal cues to type-2 and neuroimmune circuits, with evidence linking tuft-cell programs to repair-associated remodeling in inflammatory settings. Paneth cell dysfunction in ileal Crohn's disease frequently reflects disrupted antimicrobial and stress-adaptation programs, while colonic ulcerative colitis can exhibit injury-associated Paneth-like remodeling within the regenerative epithelium. SUMMARY: Secretory epithelial lineages actively regulate mucosal immunity and barrier integrity through region-dependent programs that shift during chronic inflammation. Defining these lineage states and their signaling outputs can improve patient stratification and reveal epithelial-targeted therapeutic strategies that complement immunomodulatory treatment.
The end of 'leaky gut': pathway-specific mechanistic approaches to barrier restoration.
Sha Z, Bhardwaj A, Turner JR
Curr Opin Gastroenterol · 2026 Jul · PMID 41968935 · Publisher ↗
PURPOSE OF REVIEW: For over 50 years, increased intestinal permeability has been associated with diverse inflammatory and systemic diseases. Yet the oversimplified concept of 'leaky gut' as a singular phenomenon has limi...
PURPOSE OF REVIEW: For over 50 years, increased intestinal permeability has been associated with diverse inflammatory and systemic diseases. Yet the oversimplified concept of 'leaky gut' as a singular phenomenon has limited both mechanistic understanding and therapeutic development. RECENT FINDINGS: It is now recognized that intestinal permeability occurs via two molecularly distinct, differentially regulated trans-tight junction pathways, while a tight junction-independent unrestricted pathway allows flux at sites of epithelial damage. The pore pathway is a high-conductance, size-selective and charge-selective flux route that mediates ion and water flux. Its upregulation can be either protective, as in infectious enterocolitis, or pathogenic, as in immune-mediated disease or, as shown recently, in sepsis. Myosin light chain kinase activation enhances flux across the leak pathway, a low-conductance macromolecular flux route, that promotes progression of immune-mediated diseases. Recently developed molecularly targeted, pathway-specific approaches to barrier restoration are effective and can outperform current therapies without the complications of broad immunosuppression. SUMMARY: The evolving pathway-resolved framework transforms intestinal barrier biology from a descriptive science into mechanism-specific therapeutic approaches that have promise as independent agents and as complements to available immune-targeted therapies.
The Dallas Consensus for performing and interpreting functional lumen imaging probe panometry: what it means for the clinician.
Nguyen AD
Curr Opin Gastroenterol · 2026 Jul · PMID 41919517 · Publisher ↗
PURPOSE OF REVIEW: Functional lumen imaging probe (FLIP) panometry is being increasingly used to evaluate esophageal motility at the time of endoscopy. This review explains how the recently published Dallas Consensus pro...
PURPOSE OF REVIEW: Functional lumen imaging probe (FLIP) panometry is being increasingly used to evaluate esophageal motility at the time of endoscopy. This review explains how the recently published Dallas Consensus provides a standardized approach to FLIP protocol and interpretation with an updated motility classification scheme. RECENT FINDINGS: Performing a high quality upper endoscopy is paramount to optimally interpreting FLIP findings as it allows for exclusion of mechanical obstruction, which can contribute to abnormal FLIP findings. A normal FLIP classification with normal esophagogastric junction (EGJ) opening and normal contractile response makes a major motility unlikely, whereas a reduced EGJ opening with diminished or contractile response patterns makes an EGJ obstruction disorder such as achalasia or esophagogastric junction outflow obstruction likely on high resolution manometry (HRM). Findings of spastic contractile response or an indeterminant EGJ opening on FLIP may require further testing with HRM and/or timed barium esophagram with tablet. SUMMARY: Performing FLIP during endoscopy using the Dallas Consensus motility classification can help exclude or confirm an esophageal motility disorder with the potential to expedite the diagnostic workup and management for patients with esophageal symptoms.
Small bowel pathology - diet, pill or buzz?
Sidhu R
Curr Opin Gastroenterol · 2026 May · PMID 41912349 · Publisher ↗
Abstract loading — click title to view on PubMed.
Precision medicine in steatotic liver disease.
Prasitsumrit V, Chen VL
Curr Opin Gastroenterol · 2026 May · PMID 41912348 · Publisher ↗
PURPOSE OF REVIEW: Discuss advances in genomics, metabolomics, and proteomics in steatotic liver disease. RECENT FINDINGS: Common genetic variants in genes including PNPLA3, TM6SF2, and HSD17B13 are associated with risk...
PURPOSE OF REVIEW: Discuss advances in genomics, metabolomics, and proteomics in steatotic liver disease. RECENT FINDINGS: Common genetic variants in genes including PNPLA3, TM6SF2, and HSD17B13 are associated with risk of hepatic steatosis, metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD) cirrhosis, and hepatocellular carcinoma. In contrast, variants in other genes such as GCKR are strongly associated with steatosis but much more weakly associated with advanced liver disease. The cirrhosis-associated variants typically drive steatosis through reduction of lipid export from the liver, potentially highlighting this mechanism as a driver of fibrosis though not ruling out alternative pathways. Alterations in amino acids, lipids, bile acids, and other metabolites have been observed in both MASLD and ALD reflecting insulin resistance, altered bile acid metabolism, and increased fatty acid flux and de novo lipogenesis (for MASLD) or mitochondrial dysfunction (for ALD). Also seen are characteristic changes in serum/plasma protein levels reflecting fibrosis, systemic inflammation, and hepatic synthetic function are also seen with MASLD and ALD. Predictive models incorporating genomics, metabolomic, and proteomic biomarkers may improve upon existing clinical models, but nearly all studies on this topic have been retrospective or post hoc. SUMMARY: Genomics, metabolomics, proteomics, and multiomics may improve our understanding of disease pathophysiology. They may also have implications for clinical care, but further prospective studies are required to establish whether they provide sufficient benefit over clinical biomarkers to be routinely used.
The utility of albumin in cirrhosis: established benefits and unanswered questions.
Besir K, Rockey DC
Curr Opin Gastroenterol · 2026 May · PMID 41912347 · Publisher ↗
PURPOSE OF REVIEW: Albumin plays a central role in maintaining circulatory and endothelial homeostasis through its oncotic and nononcotic effects. In cirrhosis, reduced concentration and impaired function of albumin cont...
PURPOSE OF REVIEW: Albumin plays a central role in maintaining circulatory and endothelial homeostasis through its oncotic and nononcotic effects. In cirrhosis, reduced concentration and impaired function of albumin contribute to circulatory derangements, renal dysfunction, and infection risk. While albumin is firmly established in certain settings such as spontaneous bacterial peritonitis (SBP), hepatorenal syndrome (HRS), and large-volume paracentesis (LVP), its broader use in cirrhosis remains controversial and incompletely defined. We aim to integrate up to date guidance on the use of albumin in cirrhosis, and to highlight areas where evidence remains limited or evolving. RECENT FINDINGS: Evidence from randomized trials and meta-analyses highlights both established and emerging roles of albumin in cirrhosis. Albumin has demonstrated clear benefit after LVP, where it reduces postprocedural circulatory dysfunction, renal impairment, and hyponatremia compared with other plasma expanders. In HRS, albumin serves as an indispensable therapeutic backbone, enhancing the efficacy of vasoconstrictors and improving rates of renal reversal, yet its independent role remains incompletely defined. In SBP, co-administration of albumin with antibiotics reduces renal failure and improves short-term survival, establishing it as standard of care. In acute kidney injury (AKI) outside of HRS, current guidelines recommend the use of albumin as part of an initial volume challenge in many forms of AKI to aid diagnosis and potentially promote renal recovery, although the timing of its use differs among guidelines. SUMMARY: Albumin is a cornerstone therapy in the management of decompensated cirrhosis and its clinical complications. While its role is well defined in HRS, SBP, and post-LVP, higher-quality evidence is needed to refine its use in other settings, particularly in AKI.
The use of potassium-competitive acid blockers in the management of foregut disease.
Ghai MB, Sloan JA
Curr Opin Gastroenterol · 2026 Jul · PMID 41911485 · Publisher ↗
PURPOSE OF REVIEW: The purpose of this review is to explore the current clinical evidence evaluating the use of potassium-competitive acid blockers (PCABs) in the management of foregut diseases. RECENT FINDINGS: PCABs ha...
PURPOSE OF REVIEW: The purpose of this review is to explore the current clinical evidence evaluating the use of potassium-competitive acid blockers (PCABs) in the management of foregut diseases. RECENT FINDINGS: PCABs have been shown to have clinical superiority over proton pump inhibitors in the management of H. pylori and Los Angeles grade C/D erosive esophagitis. PCABs also are approved for use in nonerosive reflux disease, and data suggest a possible use in peptic ulcer disease. SUMMARY: There is utility of PCABs in the management of multiple foregut diseases. More data are required to understand the utility of PCABs in the management of Barett's esophagus and eosinophilic esophagitis.
The esophageal microbiome: mechanisms and clinical implications.
Ebigbo N
Curr Opin Gastroenterol · 2026 Jul · PMID 41866998 · Publisher ↗
PURPOSE OF REVIEW: Interest in the esophageal microbiome has expanded rapidly, yet its functional and clinical relevance remains incompletely defined. This review synthesizes emerging evidence on host-microbe interaction...
PURPOSE OF REVIEW: Interest in the esophageal microbiome has expanded rapidly, yet its functional and clinical relevance remains incompletely defined. This review synthesizes emerging evidence on host-microbe interactions in esophageal diseases, with a focus on mechanistic pathways and translational potential. RECENT FINDINGS: Recent studies demonstrate that esophageal microbes influence epithelial differentiation, barrier integrity, and inflammatory signaling in conditions such as eosinophilic esophagitis and Barrett's esophagus. Microbial metabolism, particularly bile acid transformation, links microbial composition to epithelial stress responses and neoplastic progression. In esophageal cancer, tumor-associated microbes modulate epigenetic regulation and suppress antitumor immunity. Integrative multiomics approaches have further identified microbial signatures associated with disease progression and treatment response. SUMMARY: The esophageal microbiome influences disease pathogenesis and has potential for risk stratification and therapeutic targeting. Future progress will depend on longitudinal studies, improved functional resolution, and integration of microbial data with epithelial and immune biology to enable clinical translation.
Glucagon-like peptide agonists and use in short bowel syndrome - what about the side effects?
Gorard L, Boucher M, Rutter C
Curr Opin Gastroenterol · 2026 May · PMID 41866997 · Publisher ↗
PURPOSE OF REVIEW: This review summarizes recent evidence on the use of glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) agonists in the management of short bowel syndrome (SBS), with a focus on emergi...
PURPOSE OF REVIEW: This review summarizes recent evidence on the use of glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) agonists in the management of short bowel syndrome (SBS), with a focus on emerging therapies and real-world experience. It evaluates their impact on intestinal adaptation, safety, and future clinical potential. RECENT FINDINGS: GLP-2 agonists such as teduglutide continue to demonstrate improvements in intestinal absorption resulting in reductions in parenteral support (PS) requirements and improved quality of life. Clinical trials report that newer long-acting agents, such as apraglutide and glepaglutide, allow less frequent dosing with a reduction in PS and structural intestinal changes on imaging. Safety profiles remain favourable, with gastrointestinal symptoms, fluid balance issues, gallbladder events and injection-site reactions reported most frequently. GLP-1 agonists show promise in slowing transit time and offer an area for further research. SUMMARY: While GLP-2 agonists shape the current landscape of SBS management, GLP-1 based therapies may complement future treatment strategies offering the potential to reduce or even eliminate dependence on PS. Continued long-term studies and registry data are essential to optimize patient selection, safety monitoring, and personalized use of GLP agonists.
Implementation science: a primer for hepatology research.
Verma M, Tahir H, Kalman R
Curr Opin Gastroenterol · 2026 May · PMID 41841669 · Publisher ↗
PURPOSE OF REVIEW: Despite significant progress in evidence-based therapies and models of care, hepatology continues to face challenges in translating proven interventions into routine clinical practice. Variability in a...
PURPOSE OF REVIEW: Despite significant progress in evidence-based therapies and models of care, hepatology continues to face challenges in translating proven interventions into routine clinical practice. Variability in adoption has contributed to ongoing gaps in quality, outcomes, and equity of care across diverse settings. Implementation science offers a systematic approach to understanding and improving how evidence-based interventions are delivered, adapted, and sustained in real-world environments. This review provides an overview of implementation science and discusses its increasing importance for advancing hepatology research and practice. RECENT FINDINGS: Recent studies in hepatology have applied implementation science frameworks to better understand why effective interventions fail to reach patients and how those barriers can be addressed. Work in areas such as viral hepatitis elimination, cirrhosis management, palliative care integration, hepatocellular cancer surveillance, and alcohol use disorder treatment illustrates the value of focusing on context, stakeholder engagement, and strategy selection. These studies commonly use established frameworks, pragmatic trial designs, and mixed methods to assess outcomes such as adoption, fidelity, and sustainability alongside clinical impact. SUMMARY: Implementation science offers a practical bridge between discovery and routine care in hepatology. Integrating implementation principles into research, quality improvement initiatives, and trainee education can accelerate the translation of evidence into practice, reduce unwarranted variation in care, and promote more equitable delivery of liver-related services.
Are we missing early pancreatic dysfunction? Expanding faecal elastase testing beyond pancreatic disease.
Cotton CEM, Hopper AD, Sanders DS
Curr Opin Gastroenterol · 2026 May · PMID 41782402 · Publisher ↗
PURPOSE OF REVIEW: Pancreatic exocrine insufficiency (PEI) has long been associated with intrinsic pancreatic disease, yet emerging evidence shows it is under-recognized in patients with nonspecific gastrointestinal symp...
PURPOSE OF REVIEW: Pancreatic exocrine insufficiency (PEI) has long been associated with intrinsic pancreatic disease, yet emerging evidence shows it is under-recognized in patients with nonspecific gastrointestinal symptoms. This review summarizes prevalence data, evaluates the performance and utility of faecal elastase-1 (FE-1), highlights the co-existence of PEI with other luminal conditions, and explores the presence of early pancreatic dysfunction among a subset of patients with irritable bowel syndrome (IBS)-type symptoms. Updates from the 2025 European guidelines are discussed. RECENT FINDINGS: Population studies estimate PEI prevalence at 11-21% in unselected gastroenterology cohorts. PEI is reported across coeliac disease, inflammatory bowel disease and functional gastrointestinal disorders, where overlapping symptoms can delay diagnosis. A 2025 meta-analysis of FE-1 performance demonstrated high sensitivity for moderate-severe PEI. Cohort data indicates repeat sampling can clarify borderline results. PEI may be an early marker of pancreatic dysfunction in a subset of patients with IBS-type symptoms. Identifying this group may offer opportunities for lifestyle modification with potential long-term benefit. SUMMARY: Collectively, these findings expand the relevance of PEI beyond classical pancreatic disease. Broader, proactive FE-1 testing may allow earlier recognition, which might allow intervention at a potentially modifiable stage of pancreatic dysfunction, accepting the limitations of the test.
Immune-related enteropathy.
Butler K, Penny HA, Tai FWD
Curr Opin Gastroenterol · 2026 May · PMID 41782401 · Publisher ↗
PURPOSE OF REVIEW: Immune-related enteropathies (IREs) represent a heterogeneous group of disorders characterised by immune-mediated small bowel injury. While coeliac disease is the most common cause, widespread use of s...
PURPOSE OF REVIEW: Immune-related enteropathies (IREs) represent a heterogeneous group of disorders characterised by immune-mediated small bowel injury. While coeliac disease is the most common cause, widespread use of small bowel endoscopy has expanded the recognition of rarer causes. This review aims to summarise recent advances in diagnosis, classification and management of IRE. RECENT FINDINGS: Significant overlap exists between coeliac disease, autoimmune enteropathy, collagenous sprue, drug-induced enteropathies, common variable immunodeficiency (CVID) associated enteropathy and other IRE. A recent meta-analysis supports a no-biopsy approach in selected adults with significantly elevated IgA tissue transglutaminase levels and suspected coeliac disease. Refractory coeliac disease type II is now recognised as a low-grade intraepithelial T-cell lymphoma with a high risk of progression to enteropathy-associated T-cell lymphoma (EATL). Drug-induced enteropathies, particularly olmesartan-associated enteropathy, are increasingly detected and may mimic autoimmune enteropathy histologically. Novel therapeutic approaches, including cladribine, JAK inhibitors and biologics, have shown promise in refractory disease, although evidence is limited to small studies. SUMMARY: IREs present substantial diagnostic and therapeutic challenges due to overlapping characteristics and variable disease course. A structured approach integrating clinical, serological and histopathological data is essential for accurate diagnosis. Early recognition and tailored management are crucial to prevent long-term complications.
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