Raffaele Buono,1 Marzia La Franca,1 Paolo Girardi,2 Marco Di Pascoli11Unit of Internal Medicine and Hepatology (UIMH), Department of Medicine – DIMED, University of Padova, Padova, Italy; 2Department of Environmental Sciences, Informatics and Statistics, Ca’ Foscari University of Venice, Venice, ItalyCorrespondence: Marco Di Pascoli, Unit of Internal Medicine and Hepatology (UIMH), Department of Medicine – DIMED, University of Padova, Padova, Italy, Email marco.dipascoli@unipd.itBackground and Aims: While systemic arterial pressure typically declines with advancing cirrhosis, the relationship between arterial hypertension (AH) and clinical outcomes in compensated cirrhosis is not defined. We aimed to investigate the association between AH and non-invasive markers of portal hypertension and liver-related complications.Methods: We conducted a retrospective cohort study including 189 patients with compensated liver cirrhosis, stratified according to history of AH. Clinical, laboratory, endoscopic, and outcome data, including cirrhosis decompensation, liver transplantation, and mortality, were collected. Median follow-up time was 5 years, IQR 3.2– 5.0 years. Spleen diameter was assessed at baseline and serially during follow-up.Results: Of the 189 patients, 111 had a history of AH. Compared with non-hypertensive patients, those with AH were older, had higher platelet counts, smaller spleen diameter, and fewer indirect signs of portal hypertension, including esophageal varices, congestive gastropathy, and portosystemic shunts (all p < 0.05). During follow-up, spleen size remained stable in hypertensive patients, whereas a progressive increase in spleen diameter was observed in patients without AH. Despite these differences, no significant differences were found between groups in terms of cirrhosis decompensation or overall mortality. However, patients without AH had a significantly higher rate of liver transplantation (p = 0.008).Conclusion: In compensated cirrhosis, AH is associated with fewer indirect signs of portal hypertension, including smaller and stable spleen size. These findings support the concept that patients with AH exhibit a distinct hemodynamic phenotype, characterized by less pronounced portal hypertensive state and circulatory dysfunction.Keywords: liver cirrhosis, arterial hypertension, portal hypertension, splenomegaly
Colorectal cancer (CRC) remains a major global health concern, and experimental animal models continue to play a key role in understanding its development and in evaluating preventive and therapeutic strategies. Among these, the 1,2-dimethylhydrazine (DMH)-induced rat model is widely used; however, substantial variability in dosing regimens and study design has limited consistency across studies. The present systematic review aimed to synthesize existing evidence on DMH-induced colorectal carcinogenesis in rats, with particular attention to how dose, duration, and route of administration influence pathological outcomes. A comprehensive literature search was conducted across PubMed, Scopus, and Web of Science from January 2010 to December 2025. Eligible studies were screened and analyzed based on predefined inclusion criteria. Data were extracted on induction protocols, histopathological findings, and study characteristics. Across the 430 included studies, notable heterogeneity was observed in experimental protocols. Nevertheless, certain patterns emerged. Higher-dose, shorter-duration regimens were more frequently associated with early preneoplastic lesions such as aberrant crypt foci (ACF), whereas lower-dose, longer-duration protocols tended to be linked with more advanced tumor development. Subcutaneous administration appeared to provide more consistent results compared to other routes. These findings suggest that the choice of protocol should be guided by the intended stage of carcinogenesis under investigation. Importantly, the interpretation of these findings should be approached with caution. Many studies lacked detailed reporting of methodological parameters, and quantitative synthesis was limited by incomplete data. As such, the proposed framework should be viewed as a practical guide rather than a definitive standard. In conclusion, DMH-induced CRC models in rats remain valuable but highly sensitive to experimental design. Greater standardization and more rigorous reporting are needed to improve reproducibility and strengthen the translational relevance of future studies.
Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most prevalent chronic liver disease worldwide, reflecting the global epidemic of obesity, type 2 diabetes, and metabolic syndrome. However, MASLD is not a homogeneous condition; rather, it encompasses a broad clinical and biological spectrum ranging from simple steatosis to progressive steatohepatitis, advanced fibrosis, cirrhosis, and hepatocellular carcinoma. This heterogeneity is driven by complex interactions between metabolic dysfunction, genetic susceptibility, environmental exposures, and extrahepatic comorbidities. Recent advances have shifted the paradigm from a "one-size-fits-all" approach toward risk stratification and personalized care. Non-invasive tests (NITs), including FIB-4, transient and shear wave elastography, and novel biomarkers, have enabled scalable fibrosis assessment and prognostic stratification in real-world settings. At the same time, emerging therapies targeting metabolic pathways, inflammation, and fibrosis are paving the way for individualized treatment strategies. This review provides an updated and clinically oriented synthesis of MASLD by integrating clinical heterogeneity, phenotype-based disease trajectories, multidimensional risk stratification, and personalized management into a practical framework for precision hepatology. In addition, we summarize recent therapeutic advances, discuss current controversies and implementation challenges, and highlight future directions toward individualized care.
The spleen is usually viewed as a hematologic, vascular and immune organ, but rarely within lipid-associated disease. This review proposes splenic steatopathy as a provisional clinical and experimental framework rather than an established diagnosis or a splenic equivalent of fatty liver disease. Evidence is organized into pre-splenic drivers, intra-splenic pathology and post-splenic consequences. Upstream drivers include metabolic dysfunction-associated steatotic liver disease, obesity, severe hypertriglyceridemia, lysosomal storage disorders, drug-induced phospholipidosis, altered lymphatic lipid handling and portal-hemodynamic stress. Spleen-level findings include altered volume, attenuation, stiffness or metabolic activity; lipid-laden histiocytes; lysosomal or phospholipid storage; and immune-cell remodeling. Potential downstream relevance includes cytopenias, immune dysfunction, infection vulnerability, diagnostic redirection, cancer-associated immune biology and perioperative risk. Human evidence currently consists mainly of observational imaging studies and rare tissue reports; animal studies provide mechanistic support, while several proposed clinical links remain hypotheses. No validated diagnostic criteria, imaging thresholds or biomarkers currently exist. The framework may help distinguish unexplained splenomegaly from common mimics and, if validated, support long-term risk stratification for infection and malignancy in patients with metabolic liver disease. Future studies should prioritize spleen-specific imaging methods, tissue-imaging correlation, lipidomics, immune phenotyping and prospective outcome validation.
Background: Cardiac surgery with cardiopulmonary bypass (CPB) in young children is associated with systemic stress, gastrointestinal dysfunction, and impaired nutritional recovery. The role of gut microbiome disruption and short-chain fatty acid (SCFA) metabolism in these processes remains insufficiently studied. Objective: To evaluate changes in gut microbiome composition, SCFA profiles, and nutritional status in children aged 0-3 years after CPB, and to assess their association with postoperative feeding intolerance and impaired growth. Methods: This prospective observational study included 20 children undergoing cardiac surgery with CPB. Stool samples were collected preoperatively and during the early postoperative period. Microbiota composition was assessed using culture-based microbiological methods, and fecal SCFA concentrations were measured by gas chromatography. Clinical, anthropometric, and laboratory parameters were assessed, and their associations with CPB characteristics and microbiome alterations were analyzed. Results: The postoperative period was characterized by significant intestinal dysbiosis, including reduced abundance of beneficial bacteria (Bifidobacterium, Lactobacillus, Bacteroides) and decreased SCFA-producing taxa. Fecal butyrate and propionate levels were significantly reduced. These changes were associated with increased intestinal inflammation, feeding intolerance, impaired nutrient absorption, and insufficient weight gain. The severity of dysbiosis correlated with CPB duration. Conclusion: CPB in early childhood is associated with disruption of gut microbiota and reduced SCFA production, which are linked to postoperative feeding intolerance and impaired nutritional recovery. Targeted monitoring and modulation of the gut microbiome may improve clinical outcomes in pediatric cardiac surgery patients.
Background:Irritable bowel syndrome (IBS) and inflammatory bowel diseases (IBD) are characterized by features of abdominal pain and changes in bowel habits, making it hard to differentiate between the two. Early studies that estimated prevalence of IBS in IBD patients defined remission based only on clinical scores, potentially overestimating IBS symptoms and underestimating subclinical inflammation. The aim of this study was to determine prevalence of IBS in IBD patients who are treated with biologics and have reached clinical, biologic and endoscopic remission, thereby applying a more stringent definition of remission. Methods:This single-center cross-sectional study included 136 patients (68 patients with Crohn's disease and 68 with ulcerative colitis) who are treated with biologics from December 2022 to June 2023 and have reached clinical, biologic and endoscopic remission. Clinical remission was defined as Crohn's disease activity index (CDAI) ≤ 150 for patients with Crohn's disease (CD), and Mayo partial score ≤ 1 for patients with ulcerative colitis (UC). Biologic remission was defined as faecal calprotectin (FCP) ≤ 250 ug/g, and endoscopic remission was defined as the absence of ulcerations for CD and Mayo subscore ≤ 1 for UC patients. The presence of IBS was defined by Rome IV criteria. Results:A total of 28 (20.6%) patients in complete remission reported symptoms consistent with IBS, based on Rome IV criteria. The prevalence of IBS was higher in patients with Crohn's disease than in those with ulcerative colitis (CD 27.9% (19/68) vs UC 13.2% (9/68), p = 0.034). Females and smokers with Crohn's disease are more likely to report IBS symptoms. Conclusion:Prevalence of IBS symptoms in IBD patients varies according to how remission is defined. When using stringent clinical, biological and endoscopic remission criteria, 20% of patients present with IBS symptoms, more commonly in those with CD.
Sendzischew Shane MA, Ruddy J, Cline M, Rosenbaum DP, Edelstein S, Moshiree B. Clin Exp Gastroenterol. 2024;17:227–253. The authors have advised that they have identified errors in the reporting of the analysis of one of their previous studies, T3MPO-1, which did not adhere to the pre-specified Statistical Analysis Plan. As a result, secondary endpoints, in the “Tenapanor” section on page 246, should not be considered statistically significant due to the hierarchical testing procedure and edits are needed to Table 4 on page 242 of the published paper. Page 242, Table 4, Table caption, the text “Table 4 Key Efficacy Results from Pivotal Trials of FDA-Approved Treatments for IBS-C” should read “Table 4 Results from Pivotal Trials for FDA-Approved Treatments for IBS-C”. Page 244, Table 4, Outcomes column, the order of the two bullet points for “6/12-wk CSBM response rate” and “6/12-wk AP response rate” should be switched to align with the protocol-prespecified sequential testing procedure; a superscript “j” has been added to p-values p=0.008, p<0.001, p=0.014, p=0.02 and p The correct Table 4 is as follows. Table 4 Results from Pivotal Trials for FDA-Approved Treatments for IBS-C Page 246, Tenapanor section, second paragraph, last sentence, the text “Tenapanor significantly improved global and individual symptoms of IBS-C during the 12-week treatment period, as indicated by more patients in the tenapanor group achieving 6 of 12-week US FDA combined response rates, 6 of 12-week abdominal pain and CSBM rates, as well as 9 of 12-week and/or 13 of 26-week combined response rates (Table 4)” should read “Tenapanor improved global and individual symptoms of IBS-C during the 12-week treatment period, as indicated by higher percentages of patients in the tenapanor group achieving 6 of 12-week US FDA combined response rates, 6 of 12-week abdominal pain and CSBM rates, as well as 9 of 12-week and/or 13 of 26-week combined response rates (Table 4)”. The authors apologise for these errors and advise they do not change the primary findings or scientific conclusions of the study.
Background: Signet-ring cell carcinoma (SRCC) is a rare subtype of colorectal cancer, constituting 0.5-2.5% of all adenocarcinomas. It is characterized by signet ring cells as the dominant malignant cell type. Developing gastrointestinal (GI) second primary malignancies (SPMs) after SRCC is a rare event reported in the literature and insufficiently addressed. This study aimed to explore this gap and provide updated evidence about this rare cancer. Methods: Data were extracted from the Surveillance, Epidemiology, and End Results (SEER) database. Standardized incidence ratio (SIR) analyses with multiple outcome assessment were performed, applying a two-month latency exclusion period to evaluate the risk of GI SPMs in patients diagnosed with primary colorectal SRCC. The SIR was calculated as observed/expected (O/E), with excess absolute risk (EAR) per 10,000. Significance was achieved at 0.05 with a 95% confidence interval (CI). Results: There was an increased risk for GI SPMs after SRCC in the 2-11 months interval (O/E=2.49, P<0.05, EAR=37.31), and over 10 years of follow-up (O/E=3.08, P<0.05, EAR=59.20). Small intestine SPMs in the 2-11 months interval had an O/E of 4.17 (P<0.05, 95% CI: 0.11-23.26, EAR=1.97), with an overall O/E of 9.62 (P<0.05, EAR=6.32). No events of GI SPMs were observed among young patients during follow-up (O/E=1.05, P>0.05, EAR=0.12). Young patients had lack of observed events for GI SPMs (O/E=0.00, EAR=-0.15), compared to middle-aged (O/E=7.66, P<0.05) and elderly patients (O/E=2.36, P<0.05). Patients received chemotherapy showed a slightly higher observed incidence of SPMs (O/E=2.39, P<0.05, EAR=49.29); however, this finding should be interpreted cautiously given known limitations of chemotherapy data within the SEER database. Conclusion: Patients diagnosed with colorectal SRCC are at a significantly increased risk of developing GI SPMs. Given the poor overall prognosis of colorectal SRCC, early surveillance protocols must be carefully contextualized at short intervals (6-12 months) for early detection of GI SPMs. However, a reduced intensity surveillance is recommended beyond 3-5 years to integrate prevention with long-term follow-up. Recommendations should be tailored according to patients' risk profiles with individualized patient focused programs.
Objective:To explore the antibacterial effect of ginkgolic acid (GA) modified into liposome nanoparticles (TLM@GA) against Helicobacter pylori and investigate the antibacterial mechanism involved to provide a lead drug for radical clinical treatment. Methods:A new complex that improved GA stability and bioavailability was constructed using liposome nanoparticles (TLM@GA). The construction of the complex was verified by Fourier transform infrared spectroscopy, scanning electron microscopy, Zeta potential, and particle size detection, and its physicochemical properties were comprehensively evaluated. An acute gastritis model was also established using C57BL/6 mice, in which the in vivo therapeutic effect of TLM@GA was evaluated by detecting the colonization amount of the clinical multi-resistant strain HPBS001 in the gastric mucosa. Additionally, the pathological inflammation of the gastric mucosa was observed with H&E staining, apoptosis of gastric mucosal cells was observed with TUNEL staining, and the expression of serum inflammatory factors was detected with enzyme-linked immunosorbent assay. The in vivo safety of TLM@GA was evaluated by detecting its effect on mouse body weight and the damage to the stomach, liver, spleen, and kidneys. Results:The TLM@GA complex had excellent stability and dispersibility. The minimum inhibitory concentration of GA against H. pylori strains was 16-32 μg/mL, and that of TLM@GA was 0.25-0.5 μg/mL. After GA was modified into TLM@GA, its antibacterial activity was 32-128 times higher. After treatment with TLM@GA (28 mg/kg), the colonization of H. pylori in the gastric mucosa was significantly reduced, which was better than that in the omeprazole and amoxicillin (dual-therapy) and GA groups. Apoptotic and inflammatory cells in the gastric mucosa were significantly reduced, indicating alleviated inflammation. After treatment, the expression levels of major inflammatory factors were significantly decreased. There was no significant change in body weight when mice were intragastrically administered 140 mg/kg TLM@GA for 1 week, and no obvious pathological damage was found in the stomach, liver, spleen, or kidneys. Conclusion:TLM@GA had excellent stability, efficient release, and good loading capacity efficiency. It was significantly superior to GA in terms of in vitro antibacterial activity, had low toxicity, was not prone to drug resistance, and demonstrated high safety. TLM@GA demonstrated a good antibacterial effect in the in vivo acidic environment, effectively slowing the apoptosis of gastric mucosal cells and significantly reducing levels of inflammatory factors, alleviating the inflammatory response.
Background: Despite the similarities, Crohn's disease (CD) and ulcerative colitis (UC), the two major subtypes of inflammatory bowel disease (IBD), exhibit distinctions. The increasing burden of IBD necessitates discovering novel diagnostic markers. Considering the importance of distinguishing between CD and UC in selecting therapeutic strategies in clinical settings, this investigation focused on identifying subtype-specific blood biomarkers. Methods: The discovery set was formed by integrating five blood transcriptomic datasets, including GSE119600, GSE126124, GSE94648, GSE86434, and GSE71730, which incorporated samples from CD, UC, and controls. After determining DEGs in CD and UC, they were separately filtered according to WGCNA and then analyzed by LASSO and RF algorithms. Eventually, ROC analysis of the diagnostic performances was conducted independently in the datasets used for discovery. Moreover, ROC analysis was implemented in independent cohorts to assess the generalizability of findings. Results: Initially, the identified subtype-specific candidate biomarkers included INPPL1, TLR5, SLC9A8, IMPDH1, and GRK6 for CD, and IL4R, ACAA1, NARF, and RRM2 for UC. However, external validation only accentuated the promising diagnostic potential of TLR5 for CD. However, TLR5 was nonspecific for CD and also acts as a potential biomarker for UC. While this study did not unveil subtype-specific diagnostic markers capable of stratifying CD from UC, the upregulated TLR5 was identified as a shared biomarker for both subtypes. Conclusion: This integrative analysis of blood transcriptomes diverged from its initial purpose, the identification of subtype-specific biomarkers, and demonstrated that TLR5 exhibits reproducible diagnostic efficacy for IBD.
Purpose:A combination of bioinformatics methods including network pharmacology, molecular docking and molecular dynamics simulation was utilized to investigate the potential mechanism of Smilax glabra Roxb. (SG) in the treatment of ulcerative colitis (UC). Methods:We firstly used network pharmacology to screen out the major active components, targets and pathways. Secondly, the top 5 ingredients and the top 5 targets were docked with molecular docking technology respectively. Thirdly, the two protein-compound complexes with the lowest binding scores were subjected to molecular dynamics simulation (MDs). Results:A total of 15 bioactive compounds and 191 targets were identified, with the top 5 compounds being quercetin, beta-sitosterol, naringenin, stigmasterol and diosgenin, and the top 5 targets being AKT1, IL-6, TNF, TP53 and IL-1β. Predominant enrichment was observed in the PI3K-Akt signaling pathway, TNF signaling pathway, IL-17 signaling pathway, MAPK signaling pathway and apoptosis. Each set of molecular docking calculations was run 50 times and repeated 3 times for statistical analysis, with results showing that the majority of binding energies were less than -5 kcal/mol, indicating successful docking. Specifically, stigmasterol-TP53 (-9.10 ± 0.07 kcal/mol) and diosgenin-TP53 (-8.80 ± 0.73 kcal/mol) are the two complexes with the lowest binding energies for MDs. According to the MDs, the stig-masterol-TP53 and diosgenin-TP53 complex shows ideal conformational stability and interaction energy. Conclusion:Multiple components of SG may exert therapeutic effects on UC through multiple targets and various signaling pathways. Novelty of this study lies in linking SG compounds to UC-specific targets and confirming stable docking/MDs interactions with TP53. However, further validation through in vivo and in vitro experiments is required to provide reliable evidence for clinical application.
Purpose:With the global decline in Helicobacter pylori infection, upper gastrointestinal bleeding (UGIB) is increasingly driven by non-infectious, non-Nonsteroidal Anti-Inflammatory Drug (NSAID) mechanisms, particularly antithrombotic use and comorbidity-related mucosal injury. This study aimed to characterize the etiology, clinical profile, and in-hospital mortality predictors in patients with H. pylori-negative, non-variceal UGIB in a Colombian tertiary care setting. Patients and Methods:We conducted a retrospective cohort study at a quaternary hospital in Barranquilla, Colombia, including all adults (≥18 years) hospitalized with endoscopically confirmed non-variceal UGIB and negative H. pylori testing (rapid urease test and/or histology). Clinical, endoscopic, and medication data were analyzed. Results:Of 285 patients, the median age was 60 years (IQR: 39-73), and 54% were male. NSAID use was rare (2.8%), whereas antithrombotic exposure was prevalent (28.8%), including low-dose aspirin (18.2%) and dual antiplatelet therapy (4.9%). The most common endoscopic findings were erosive gastropathy (45%) and ulcers (12%). Overall in-hospital mortality was 5% (n=13). In multivariable analysis, age >60 years (aOR: 2.9; 95% CI: 1.7-10.2; p = 0.05), cardiovascular complications (aOR: 7.8; 95% CI: 1.9-32.0; p = 0.004), encephalopathy (aOR: 8.5; 95% CI: 2.2-33.0; p = 0.009), and antiplatelet plus anticoagulant therapy (aOR: 5.3; 95% CI: 1.6-17.5; p = 0.006) were independently associated with in-hospital mortality. Conclusion:In this cohort, in-hospital mortality in non-variceal UGIB patients without H. pylori infection was associated with systemic factors such as advanced age, cardiovascular complications, encephalopathy, and antiplatelet-anticoagulant combination therapy rather than bleeding lesions. These findings support risk stratification based on comorbidities and medication use in this growing population.
Background: Rectal prolapse is the protrusion of the rectum through the anal canal, commonly observed in older women with weakened pelvic floor muscles and anal sphincters. Clinical symptoms may include a painful, irreducible anal mass and rectal bleeding. Surgical intervention typically aims to restore normal anatomy through tumor resection and rectal fixation. The occurrence of colorectal cancer within rectal prolapse is rare and may present unique diagnostic and management challenges with distinct clinical implications. Case Series: We present three cases of rectal prolapse associated with colorectal cancer. The patients (aged 40, 79, and 79), one female and two males presented with rectal prolapse. One patient was seen in the outpatient clinic, while the other two presented to the emergency department with painful, strangulated prolapse. All patients underwent tailored surgical resections. Histological analysis revealed adenocarcinomas ranging from pT1 to pT2, all with N0Mx staging, two located in the rectum and one in the descending colon. These cases highlight the importance of preoperative imaging in identifying occult malignancies, particularly in atypical presentations of rectal prolapse. Conclusion: Patients presenting with rectal prolapse, especially without predisposing factors, should be evaluated for underlying malignancy. Preoperative assessment is critical for identifying concomitant tumors and optimizing management to prevent recurrence and complications.
Aberrant expression of the cytidine DNA deaminase AID in enterocytes within inflamed mucosa in ulcerative colitis (UC) patients has been proposed to be involved in progression of UC to colitis-associated colorectal cancer (CA-CRC). Here, we followed the expression of AID and other nuclear cytidine DNA deaminases of the APOBEC family through several stages of progression of UC in a CA-CRC case (UC progressor) and in a cohort of UC progressors and non-progressors. In inflamed and high-grade dysplastic mucosa, AICDA and APOBEC1 mRNAs, but not APOBEC3-family enzyme mRNAs, were overexpressed compared to non-inflamed tissue. Immunohistochemical staining did not show expression of AID or APOBEC3 enzymes in the enterocytes, neither in specimens from the CA-CRC case nor in biopsies from the progressor and non-progressor cohort. APOBEC1 was highly expressed in the enterocytes throughout the colorectum from the CA-CRC case and in most biopsies examined from the progressor and non-progressor cohort. The expression was not correlated with the histology of the mucosa or the progression status of the patients. In the CA-CRC case, we identified AID- and APOBEC3-associated mutation signatures in inflamed, high-grade dysplasia and cancer genomes. In conclusion, our findings suggest that AID or other nuclear APOBECs are unlikely to drive the progression of UC to CA-CRC late during course of UC. However, we cannot exclude the possibility that bursts of AID and nuclear APOBEC3 activity may contribute to formation of genome instability in early phases of disease development.
Purpose:Drug-induced liver injury (DILI) is an uncommon but potentially life-threatening condition. To date, the burden of DILI on a single, large healthcare system has not been investigated, preventing adequate resource allocation. This study aims to quantify DILI-related healthcare utilization within the Jefferson Health System (JHS) and identify case-related factors associated with high resource requirements; such information is crucial to focus efforts toward resource reduction. Patients and Methods:This study characterizes trends of 48 DILI cases within JHS, including demographics, payer status, causative agent, and DILI pattern. These variables were correlated with length of stay (LOS) and cost relating to the treatment encounter. Patient-level observed LOS and cost were then subtracted from their respective expected values from the Vizient Clinical Database, a platform that provides clinical outcome data from more than 1300 healthcare facilities in the United States. Results:Treatment of DILI cases at JHS required higher than expected cost compared to the Vizient Clinical Database. We found high resource utilization in females, those identifying as black, and in cases where the implicated agent was uncertain. Mixed pattern DILI required the highest healthcare utilization, whereas herbal and dietary supplements (HDS) cases were relatively resource minimal. Conclusion:This study indicates that high clinical suspicion of DILI in historically marginalized populations and improved causative agent identification are key to minimizing the healthcare burden of DILI.
Background:Artificial intelligence (AI) has emerged as a transformative force in gastrointestinal (GI) endoscopy, aiming to enhance diagnostic accuracy, detection rates, and workflow efficiency. With multiple AI-assisted systems now reaching clinical use, there is a growing need to consolidate evidence regarding their performance, applications, and limitations. Objective:To synthesize contemporary evidence from randomized trials, meta-analyses, and real-world studies to provide a clinically oriented overview of the effectiveness, limitations, and implementation challenges of artificial intelligence in gastrointestinal endoscopy, and to identify key translational gaps that justify the need for this updated review. Methods:A structured narrative synthesis of literature from PubMed, Scopus, Web of Science, and manual reference screening (2005-2025) was performed. Evidence was thematically analyzed across major domains including CADe, CADx, upper gastrointestinal neoplasia, capsule endoscopy, quality monitoring, implementation challenges, and real-world performance. Key lessons, translational barriers, and future research priorities were extracted. Quantitative performance estimates were derived from representative randomized controlled trials and meta-analyses and are presented as reported ranges rather than pooled analyses. Results:CADe systems have demonstrated a consistent 15-20% relative increase in adenoma detection rate (ADR) compared to conventional colonoscopy. CADx algorithms achieve >90% accuracy in differentiating neoplastic from non-neoplastic polyps, supporting "resect-and-discard" strategies. AI tools in upper GI endoscopy achieve diagnostic accuracies of 88-96% for early esophageal and gastric neoplasia, outperforming non-expert endoscopists. Despite these benefits, barriers persist-dataset bias, lack of generalizability, medicolegal ambiguity, and regulatory inconsistency. Conclusion:AI has proven efficacy in improving detection and diagnostic precision in GI endoscopy. Future progress requires multicenter validation, standardized datasets, ethical frameworks, and clinician training to enable equitable, safe, and evidence-based integration into routine clinical practice.
Integrated care refers to the coordinated delivery of health services across providers and settings, aimed at ensuring continuous, patient-centered care throughout the course of disease. Models of integrated care have demonstrated particular relevance in the management of gastrointestinal (GI) diseases, such as disorders of gut-brain interaction (DGBI) and inflammatory bowel disease (IBD), due to their multidimensional nature. Integrated care has the potential not only to alleviate symptom burden, but also to improve quality of life and mental health outcomes while reducing healthcare costs. Nevertheless, barriers to implementation persist, and despite growing recognition of its value, integrated care has not yet been systematically adopted for GI motility disorders. These disorders, thought to be multifactorial, exhibit considerable overlap with DGBI, rendering them clinically indistinguishable in some cases. Furthermore, while mental health problems are well recognized in DGBI, they are also commonly observed in individuals with GI motility disorders. In response, Maastricht University Medical Centre+ has developed a multidisciplinary, integrated, patient-centered care model for the diagnosis and management of neurogastroenterology and motility disorders. By presenting this approach, we aim to foster knowledge exchange and support the development of integrated care models adaptable to the specific needs of diverse healthcare settings.
Background:Gastric acid secretion by parietal cells depends on the trafficking and exocytosis of H⁺/K⁺-ATPase-rich tubulovesicles (TVs) to the apical membrane in response to histamine stimulation via cyclic AMP elevation. However, the role of parietal cell's protein sorting machinery [eg, coat protein (COP) II/COP I vesicle proteins, soluble NSF attachment protein receptors (SNAREs), Rab GTPases, clathrin-adaptor proteins, etc.] in the dysregulation of gastric acid homeostasis remains poorly understood. This review synthesizes available evidence on the role of protein sorting machinery in gastric proton pumpopathy, leading to dysregulation of gastric acid secretion. Methods:A thorough search was conducted on PubMed, with Wiley and African Journal Online as supplementary sources, and 15 original research articles published between January 1988 and July 2025 in English were included. Results:Misfolding of α- and β-subunits within the endoplasmic reticulum (ER) results in retention and degradation of the pump, leading to impaired acid secretion. Defective coat protein (COP) II/I vesicular transport disrupts Golgi processing and slows the delivery of proton pumps to tubulovesicles, while impaired Rab GTPase activity interferes with vesicle targeting toward the apical canalicular membrane. Also, dysregulation of SNARE complexes and adaptor proteins prevents effective vesicle docking and fusion, further compromising membrane insertion. In addition, abnormalities in endosomal recycling pathways hinder the retrieval and reinsertion of proton pumps, destabilizing long-term acid secretion. Conclusion:Defects in sorting machinery lead to gastric proton pumpopathy, causing impaired acid secretion. Thus, protein sorting regulators represent promising therapeutic targets to restore proper pump localization, which is a paradigm shift toward disease-modifying therapies that act upstream of the pump, potentially offering solutions for proton pump inhibitor (PPI)-resistant cases and congenital gastric acid disorders.
Introduction:Among patients with rectal cancer undergoing abdominoperineal resection (APR), parastomal hernia (PSH) is the most common long-term complication. Although extraperitoneal colostomy (EPC) has been proposed as an effective surgical method to prevent PSH, its efficacy remains controversial. To effectively reduce the incidence of PSH after APR, we report a new surgical technique-extraperitoneal rectus abdominis anterior sigmoid colostomy (ERASC). Objective:To preliminarily explore the feasibility of extraperitoneal rectus abdominis anterior sigmoid colostomy (ERASC) and its effectiveness in preventing parastomal hernia after abdominoperineal resection (APR). Methods:A retrospective analysis was conducted on the clinical data of patients diagnosed with rectal cancer at the First Affiliated Hospital of Chongqing Medical University from 2022 to 2025, who underwent APR and ERASC. Operative duration, stoma-related complications, re-hospitalizations, and re-operations were recorded and preliminarily analyzed. Results:A total of eight patients met the criteria (six males and two females). Two patients developed incomplete intestinal obstruction during the postoperative hospital stay, both of whom improved after conservative treatment. During a median follow-up of 501 days (IQR 338-618), no stoma-related complications (including but not limited to postoperative stoma obstruction, prolapse, or necrosis) were observed, and none of the eight patients developed a parastomal hernia. Conclusion:Extraperitoneal rectus abdominis anterior sigmoid colostomy (ERASC) has preliminarily demonstrated technical feasibility and long-term effectiveness in preventing PSH in this study.
