PURPOSE OF REVIEW:Historically, enteral nutrition has been the preferred therapy due to its physiologic benefits, with parenteral nutrition selected if enteral nutrition was contraindicated or insufficient; however, recent advances in nutrition support have prompted reevaluation of this process. This review summarizes the current evidence regarding enteral nutrition and parenteral nutrition in gastrointestinal oncology, inflammatory bowel disease (IBD), critical care, and gastrointestinal surgery. RECENT FINDINGS:In gastric cancer, parenteral nutrition may improve the nutritional status and clinical outcomes of treatment-related gastrointestinal dysfunction. In IBD, exclusive enteral nutrition may be effective for inducing remission and promoting mucosal healing, whereas parenteral nutrition is preferred in intestinal failure and severe complications. Studies have shown the value of early parenteral nutrition when enteral nutrition is contraindicated or insufficient, specifically for improving nutrient delivery and reducing complications in critically ill and surgical patients. Additional areas of interest include caloric and protein dosing, indirect calorimetry, and the effect of nutrition support on the gut microbiome. SUMMARY:Current evidence supports a patient-centered approach to nutrition support with enteral nutrition remaining as the preference when the gastrointestinal tract can be utilized and parenteral nutrition as an important alternative or adjunct in select populations. Future research should focus on the refinement of supplemental parenteral nutrition practices and the development of evidence-based approaches for specific disease states.
PURPOSE OF REVIEW:Purpose of the review is provision of an up-to-date literature review on the growing importance of endoscopy in neurogastroenterology and its limitations. RECENT FINDINGS:Traditionally, the diagnostic role of endoscopy in neurogastroenterology lies in the initial suspicion of motility disorders and exclusion of important differential diagnoses. Endoscopy may serve also as a carrier for positioning examination devices such as the Bravo reflux-capsule to proof gastroesophageal reflux or the endoluminal functional lumen imaging probe (EndoFLIP). New interesting aspects are the resection-based and biopsy-based extraction of tissue for examination of the enteric nervous system by the full thickness resection device (FTRD) to detect structural gastrointestinal neuromuscular lesion and confocal laser endomicroscopy (CLE) to investigate potential correlations for food intolerance. Effectiveness of endoscopic therapy is dependent on whether the measured circumscribed dysfunction correlates with the symptoms and explains them. This is the case in esophageal achalasia and hypercontractile motility disorders. However, in gastropareses, the significance of endoscopic therapy is limited because of its complex pathophysiology. SUMMARY:There is an emerging role of endoscopy in neurogastroenetrology. However, effectiveness of endoscopic therapy is dependent on careful patient selection and evidence of a circumscribed dysfunction that correlates with the symptoms and explains them.
Purpose of review Eosinophilic esophagitis (EoE) is a chronic, type 2 inflammatory disease with a rapidly rising incidence and is a leading cause of solid-food dysphagia in young adults. While diagnosis has traditionally relied on esophageal eosinophilia, the central role of eosinophils in driving symptoms and disease activity has been increasingly questioned, as several non or low-eosinophilic EoE variants have recently been characterized. This review summarizes the current understanding of these emerging entities and their position within the EoE spectrum. Recent findings Current concepts support EoE as a Th2-mediated, multicellular disorder driven by genetic susceptibility, epithelial barrier dysfunction, and allergen-induced immune responses. Three EoE variants (EoE-like esophagitis, lymphocytic esophagitis, and nonspecific esophagitis) present with EoE-typical symptoms but fall below the diagnostic eosinophil threshold. Molecular and longitudinal data reveal distinct yet overlapping inflammatory signatures and demonstrate dynamic transitions between phenotypes, including progression to classical EoE in a subset of patients. Summary EoE variants demonstrate that clinically meaningful esophageal inflammation and structural remodeling can occur in the absence of significant tissue eosinophilia. Recognition of these entities has direct implications for biopsy strategy, histologic assessment beyond peak eosinophil counts, structured longitudinal monitoring and therapy to prevent fibrostenotic complications.
PURPOSE OF REVIEW:Colorectal polyps can be removed using cold or hot snare techniques, which differ primarily in their use of electrocautery, safety profile, and depth of resection. This review summarizes current evidence comparing cold and hot snare resection and provides a practical framework for technique selection. RECENT FINDINGS:Recent guidelines and randomized trials support cold snare polypectomy (CSP) for polyps 10 mm or less because of its favorable safety profile and low risk of delayed bleeding. For 10-19 mm lesions, technique selection should be guided by histology and morphology, with hot snare polypectomy (HSP) favored for pedunculated, bulky, fibrotic, or high-risk adenomatous lesions and CSP or cold EMR increasingly supported for nondysplastic sessile serrated lesions. For large adenomatous polyps at least 20 mm, in which advanced histology is more common, hot EMR with margin treatment remains standard, where as cold EMR reduces thermal injury at the cost of higher recurrence. SUMMARY:CSP is preferred for most diminutive and small polyps, while larger lesions require individualized selection according to histology, morphology, invasion risk, and the need for durable eradication. The goal is to choose the least injurious technique that still achieves complete and reliable resection. Long-term data are needed to define recurrence and subsequent colorectal cancer risk after different resection strategies.
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.
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.
Inflammatory bowel disease (IBD) has long been conceptualized as a disorder of dysregulated immunity, yet growing evidence highlights the intestinal epithelium as an active determinant of disease behavior and therapeutic response. This editorial synthesizes contributions in the current issue that collectively redefine IBD through a tissue-centric lens, emphasizing barrier integrity, epithelial lineage specialization, antigen sampling, innate immune amplification, and environmental modulation. While epithelial-targeted and gut-directed therapies are biologically compelling, their successful translation into clinical practice presents significant challenges related to disease selection, trial design, endpoint sensitivity, and expected effect size. Emerging approaches-including combination strategies, maintenance therapy, and enriched populations-offer pragmatic paths forward. Importantly, advances in non-invasive, localized monitoring and functional biomarkers may be as critical as the therapies themselves, enabling detection of incremental tissue-level responses that traditional endpoints often miss. Together, these themes underscore the need for context-aware therapeutic strategies and dynamic disease assessment to advance epithelial-focused innovation in IBD.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
