Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) has become the most common chronic liver disease worldwide, and its core pathophysiological mechanism is closely related to insulin resistance. This literature review aims to systematically summarize the application progress of insulin resistance-related indicators in the clinical assessment of MASLD, points out the limitations of existing indicators in clinical application, and looks forward to future research directions, including the development of more accurate and non-invasive biomarkers, exploration of multi-omics integration models, and promotion of individualized diagnosis and treatment strategies, with the expectation of optimizing the clinical management of MASLD and improving patient prognosis.
BackgroundCocaine is the second most widely used illicit substance worldwide and exerts potent sympathomimetic effects by inhibiting the reuptake of norepinephrine, dopamine, and serotonin. While cardiovascular and neurological complications are well recognized, gastrointestinal (GI) manifestations are increasingly reported. These arise from multifactorial mechanisms including vasospasm, endothelial dysfunction, thrombosis, ischemia, and direct mucosal toxicity, often with severe clinical consequences.ObjectiveThis narrative review summarizes the mechanisms, pharmacokinetics, pharmacodynamics, routes of use, and spectrum of GI complications associated with cocaine exposure, with emphasis on ischemic, ulcerative, hemorrhagic, inflammatory, fibrotic, hepatobiliary, and pancreatic sequelae; provides a differential-diagnosis and diagnostic algorithm; and critically appraises the strength of the supporting evidence and its principal confounders.MethodsPubMed/MEDLINE, Embase, and Scopus were searched from January 1, 1987 through July 17, 2026, using the Boolean strings detailed in the Methods section. Case reports, case series, retrospective cohort/case-control studies, and systematic reviews published in English were eligible; both abstract and, where accessible, full text were screened. Reference lists of retrieved articles were hand-searched (snowballing) for additional citations.ResultsCocaine induces GI injury through vasoconstriction, pro-thrombotic effects, microvascular dysfunction, and direct cytotoxicity. Reported complications span ischemic/vascular disease (mesenteric ischemia/infarction, colonic ischemia, ischemic/hemorrhagic colitis, vascular thrombosis), ulcerative/perforative disease (peptic ulcer disease; gastric, duodenal, small-, and large-bowel perforation), inflammatory/fibrotic disease (enteritis, enterocolitis, strictures, retroperitoneal fibrosis), hepatobiliary and pancreatic injury, splenic infarction/hematoma/rupture, and other presentations including gastric antral vascular ectasia, an inflammatory bowel disease (IBD)-mimicking phenotype, and, rarely, acalculous cholecystitis. A systematic review of 53 studies (69 patients) found broadly similar mortality and surgical rates across routes of cocaine use, and two hybrid cohort/case-control studies of cocaine-associated ischemic colitis reported substantially higher mortality and surgical intervention rates than non-cocaine-related ischemic colitis. Polysubstance use — particularly concurrent alcohol (via the metabolite cocaethylene) and tobacco — and pre-existing vascular disease are common but incompletely characterized confounders. Notably, the evidence base underlying nearly every complication described here remains dominated by single case reports and small case series rather than comparative studies, a limitation that should temper the strength of any causal inference drawn from it.ConclusionCocaine use is a significant and under-recognized contributor to severe GI morbidity and mortality, with complications spanning ischemia and perforation to hepatopancreatic injury. The evidentiary foundation remains overwhelmingly derived from case reports and small series; only three comparative or aggregated studies provide quantitative risk data, two limited to ischemic colitis and one examining route of use across the wider intestinal-ischemia literature. Clinicians should maintain a high index of suspicion for cocaine-related GI disease in young patients presenting with abdominal pain or ischemic features, use the differential-diagnosis framework and algorithm proposed here to avoid diagnostic delay, and account for polysubstance use when interpreting presentations. Future research should prioritize registry-based or multicenter comparative studies to better quantify risk, outcomes, and the independent contribution of confounders.
IntroductionThe prevalence of obesity among patients with inflammatory bowel disease (IBD) continues to rise and is associated with adverse IBD outcomes and diminished treatment response. This study reviews the clinical safety and efficacy of glucagon-like peptide-1 receptor agonists (GLP-1RA) in patients with IBD and comorbid obesity and explores their theorized anti-inflammatory mechanisms.MethodsPublished articles through July 2026 were identified via a PubMed search for a narrative review using terms related to GLP-1RA, IBD, safety, effectiveness, and outcomes. Data extraction focused on GLP-1RA intervention details, IBD-related outcomes and inflammatory markers, and proposed anti-inflammatory mechanisms.ResultsGLP-1RA therapy promotes weight loss in patients with IBD comparable to the general population (about 16 pounds over 18 months). The most frequently reported adverse effects are gastrointestinal, often limiting treatment continuity. Most studies report no significant differences in hospitalization, surgery, steroid use or IBD medication adjustments, and some reported improvement in these outcomes. Data on endoscopic disease activity is limited. Inconsistent effects of GLP-1RA on inflammatory serum biomarkers were noted, with reductions in CRP but no consistent changes in fecal calprotectin.DiscussionAddressing obesity in patients with IBD is an emerging clinical priority. GLP-1RA therapy demonstrates efficacy in promoting weight loss, improving glycemic control, and reducing systemic inflammation, which may benefit IBD disease activity. Longitudinal studies are required to clarify the long-term impact of GLP-1RA on clinical and endoscopic outcomes in IBD.
BackgroundWe evaluated the safety of endoscopic procedures in cancer patients with neutropenia and/or thrombocytopenia.MethodsWe collected data on patients with neutropenia and/or thrombocytopenia who underwent endoscopy between 2012 and 2022 at Roswell Park Comprehensive Cancer Center. Neutropenia was defined as absolute neutrophil count (ANC) <1500 cells/µL, and thrombocytopenia was defined as platelet count <50 x 10³/µL. The development of infectious AEs (fever within 3 days or positive blood cultures within 7 days following endoscopy) in neutropenic patients and bleeding AEs (new overt GI bleeding within 3 days following endoscopy) in thrombocytopenic patients were the primary outcome measures; 30-day mortality was a secondary outcome measure. Univariate and multivariate analyses by logistic regressions were used to evaluate for risk factors.ResultsA total of 234 patients who underwent 329 endoscopic procedures were identified. In neutropenic patients, 7.8% (8/103) developed infectious AEs. In thrombocytopenic patients, 5.8% (12/208) developed bleeding AEs. Use of granulocyte colony-stimulating factor (G-CSF) was associated with increased risk of infectious AEs (OR 5.79, p = 0.02). The severity of neutropenia or thrombocytopenia and risk level of endoscopy were not associated with AEs. Multivariate analyses showed that poor performance status (PS) was the greatest risk factor for increased 30-day mortality (OR 4.69, p = <0.01).ConclusionsEndoscopy in patients with neutropenia and thrombocytopenia is relatively safe and does not lead to significant morbidity. A careful risk-benefit analysis in cancer patients with poor PS should be conducted prior to endoscopy.
BackgroundGallstone ileus is a rare cause of mechanical intestinal obstruction, predominantly affecting older adults. The ileum and ileocecal valve are the most common sites of impaction, whereas jejunal involvement is considerably less frequent. Contrast-enhanced computed tomography (CT) is the primary imaging modality for diagnosis; however, minimally calcified ectopic stones are prone to being overlooked, leading to delayed surgical intervention.Case presentationA 68-year-old woman presented with a 12-day history of abdominal pain, nausea, vomiting, and obstipation. She underwent two contrast-enhanced abdominal CT scans at different institutions, both of which demonstrated cholelithiasis, pneumobilia, and small bowel dilation, but failed to definitively identify an obstructive gallstone. Nevertheless, the combination of pneumobilia and small bowel obstruction—both components of Rigler’s triad—along with a visible cholecystoduodenal fistula, made gallstone ileus highly suspected. Emergency exploratory laparotomy revealed a 3.0 × 2.5 cm rim-calcified stone lodged in the jejunum, 80 cm distal to the ligament of Treitz. Simple enterolithotomy was performed without fistula repair. The patient recovered gradually, though she developed transient postoperative atrial fibrillation with hypotension on Day 21, which was managed medically. She was discharged on Day 30. Retrospective re-evaluation of the CT images confirmed the subtle rim-calcified stone.ConclusionsMinimally rim-calcified stones are easily missed on contrast-enhanced CT. In patients with intestinal obstruction exhibiting two of the three signs of Rigler’s triad, gallstone ileus should be strongly suspected even when no ectopic stone is clearly visible. Proactive clinician–radiologist communication and structured follow-up planning are essential to reduce diagnostic errors and manage recurrence risk.
Metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) have emerged as major global health challenges, particularly among individuals with obesity and metabolic dysfunction. Menopause represents a critical hormonal transition characterized by estrogen deficiency, visceral adiposity, insulin resistance, and chronic low-grade inflammation, all of which may accelerate MASH progression and hepatic fibrosis in women. This narrative review summarizes current evidence regarding the menopause-obesity axis in MASH progression, focusing on molecular mechanisms, histopathological alterations, diagnostic biomarkers, imaging modalities, and emerging therapeutic strategies. Estrogen deficiency contributes to metabolic dysregulation through impaired insulin signaling, increased visceral adiposity, lipotoxicity, oxidative stress, and adipose tissue inflammation, thereby promoting hepatic steatosis and progression toward fibrosis. Histopathological progression is characterized by steatosis, hepatocyte ballooning, chronic inflammation, and extracellular matrix deposition. Non-invasive diagnostic approaches, including serum biomarkers, transient elastography, controlled attenuation parameter (CAP), and magnetic resonance imaging proton density fat fraction (MRI-PDFF), have improved disease detection and risk stratification. Lifestyle modification and sustained weight reduction remain the cornerstone of management, while emerging pharmacologic therapies such as glucagon-like peptide-1 receptor agonists, tirzepatide, and resmetirom demonstrate promising metabolic and hepatic benefits. Hormone-based and anti-fibrotic therapies may offer additional therapeutic potential in postmenopausal women with obesity-associated MASH. Collectively, the menopause-obesity axis appears to play a central role in hepatic injury and fibrosis progression through interconnected hormonal, metabolic, and inflammatory pathways. Improved understanding of sex-specific mechanisms may facilitate the development of personalized diagnostic and therapeutic approaches for postmenopausal women with MASLD and MASH.
Critical illness is associated with a predictable ecological collapse of the gut microbiome. Within 48 hours of ICU admission, three convergent selective pressures-luminal oxygen enrichment from mucosal inflammation, nitrate provision by iNOS, and antibiotic-mediated niche clearance-drive a phase transition from obligate-anaerobe-dominated communities to pathogen-dominated monocultures, compromising barrier integrity and immune homeostasis. Multi-omics integration recasts this as a cross-kingdom phenomenon encompassing fungi, bacteriophages, and the metabolite networks linking them to host immunity. Whether this collapse directly causes organ dysfunction or merely marks disease severity remains the central unresolved question. This critical review examines evidence across six domains: the healthy microbiota as an ecological benchmark; patterns and temporal dynamics of ICU dysbiosis; molecular mechanisms across four gut-organ axes; clinical consequences including sepsis, nosocomial infection, acute gastrointestinal injury, and multiple organ dysfunction syndrome (MODS); biomarkers and machine-learning predictive models; and therapeutic strategies evaluated using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) framework. Only early enteral nutrition (GRADE: HIGH) and antimicrobial stewardship (GRADE: MODERATE-HIGH) have Phase III evidence supporting routine ICU use. The repeated failures of probiotic trials reflect design limitations-lack of patient stratification, strain mismatch, and soft endpoints-though biological efficacy limitations cannot be excluded. We conclude that ICU dysbiosis is best understood as ecosystem collapse driven by convergent selective pressures, not random taxonomic disturbance. Therapeutic strategies should target functional outputs-SCFAs, bile acids, indole derivatives-rather than species composition. The resilient minority (15-20% of patients who maintain diversity) holds keys to prevention science. A clinically actionable platform requires three components: rapid ecological risk assessment, endotype classification, and mortality-powered randomized controlled trials targeting functional restoration.
Inflammatory bowel diseases, encompassing Crohn’s disease and ulcerative colitis, are chronic inflammatory disorders of the gastrointestinal tract. The recent expansion in advanced therapy options has not dramatically altered the ceiling of treatment efficacy. Therapeutic drug monitoring (TDM) of the serum drug levels and anti-drug antibodies has the potential to optimise treatment efficacy through dose adjustment. TDM has shown benefit with purine analogues and anti-tumour necrosis factor (TNF) therapy. Less is known about the role of TDM in non-anti-TNF advanced therapies. This review summarises the current evidence base for TDM in non-anti-TNF advanced therapies.
BackgroundThe clinical role of endoscopic resection in the treatment of exophytic gastric schwannomas measuring ≥3 cm remains controversial owing to technical difficulties and a paucity of evidence.Case presentationA 58-year-old female patient was admitted for treatment after a gastric mass was discovered during routine physical examination. Endoscopic ultrasonography (EUS) revealed a well-demarcated, hypoechoic submucosal tumor measuring 40.9×32.3 mm. The patient subsequently underwent endoscopic submucosal dissection (ESD) under general anesthesia. Histopathological analysis confirmed the diagnosis of gastric schwannoma, with immunohistochemical staining showing strong S-100 protein positivity. The patient had an uneventful recovery with no procedure-related complications, and there has been no evidence of recurrence to date.ConclusionWhile this single-case experience indicates the technical feasibility of ESD for gastric schwannomas >3 cm, larger-scale prospective studies are required to establish its role in clinical practice.
ObjectiveLow anterior resection syndrome (LARS), a prevalent sequela following rectal cancer surgery, poses a substantial burden on patients’ quality of life (QOL), daily functioning, and psychological well-being, and its management remains an unmet clinical need due to the absence of specific therapeutic agents. Although traditional Chinese medicine (TCM) shows promise in supporting postoperative gastrointestinal recovery, high-quality evidence for its application in LARS is lacking. This trial is designed to assess the efficacy and safety of the investigational TCM formulation BL-1 in patients with LARS.Methods/designThe study will be conducted as a randomized, double-blind, placebo-controlled trial, comprising a 4-week intervention phase and a subsequent 2-week follow-up period. A total of 234 patients with LARS, aged 18 to 75 years, are planned to be enrolled in this study. Eligible participants will be randomized to receive either the BL-1 group or placebo group in a 1:1 ratio. Participants in the experimental group will receive BL-1 formulation, whereas those in the placebo group will receive an indistinguishable BL-1 placebo. The primary outcome measure is the change in LARS score from baseline to week 4. Secondary outcome measures encompass: (a) stool frequency and consistency (assessed via the Bristol Stool Scale); (b) severity of fecal incontinence (evaluated using the Wexner Anal Incontinence Scale); (c) QOL, measured with the European Organization for Research and Treatment of Cancer QOL questionnaire and the Karnofsky Performance Status score; and (d) other patient-reported outcomes. Safety will be monitored continuously throughout the treatment, with assessments including the incidence of adverse events and laboratory abnormalities.DiscussionBL-1 is the compound prescription of eleven traditional Chinese medicinal materials: Bupleuri Herba, Ginseng Radix et Rhizoma, Astragali Radix, Atractylodis Macrocephalae Rhizoma, Cimicifugae Rhizoma, Mume Fructus, and Aconiti Lateralis Radix Praeparata (patent number ZL 2024 1 1479878.8). In recent years, BL-1 has been applied to treat digestive system diseases, particularly defecation disorders, and may offer potential benefits for adults with LARS. The absence of robust clinical evidence has prompted the design of this randomized, double-blind, placebo-controlled trial to rigorously evaluate its therapeutic efficacy and safety. This trial is expected to yield critical data that will inform the clinical use of BL-1 formulation in the management of LARS.Ethics and disseminationEthical approval for this study was obtained from the Ethics Committee of West China Hospital, Sichuan University (Approval ID: 20241218). All participants must provide written informed consent before randomization. Subsequently, the trial results will be submitted for publication in a peer-reviewed academic journal.Clinical trial registrationhttps://www.chictr.org.cn, identifier ChiCTR2400087108.
IntroductionOptimised oral mesalazine therapy (4 or 4.8 g/day depending on the formulation) has been associated with better outcomes than lower doses in mild-to-moderate ulcerative colitis (UC). The aim of this post-hoc analysis of the IMPACT study was to provide a greater understanding of the influence of disease severity on the outcomes in patients with mild-to-moderate UC receiving oral mesalazine.MethodsIMPACT was a Dutch, phase 4, non-interventional, observational, 12-month prospective study that enrolled 151 adult patients with mild-to-moderate UC who received oral prolonged-release mesalazine de novo or had a dose escalation for an active episode (NCT02261636). The current analysis compared the outcomes in patients receiving mesalazine 4 g/day versus 2–3 g/day.ResultsOf 147 patients (median age = 46 years, 47.6% women), 139 (94.6%) received 4 g/day, mostly as prolonged-release mesalazine granules (74.2%). Recurrence was significantly reduced for patients on 4 g/day versus 2–3 g/day (26.6% vs. 62.5%, p = 0.03). There was a trend towards a longer disease-free interval for those on the optimised dose over the 12-month period (mean = 16.8 vs. 12.8 months, p = 0.49). Time to recurrence was similar (p = 0.241) for patients with milder [Ulcerative Colitis Disease Activity Index (UCDAI) scores ≤3] versus more moderately active disease (scores ≥4), with a significantly higher rate of combined oral plus topical therapy in the latter (23.2% vs. 46.1%, p = 0.004). Patients’ preferred formulation was granules (68.0%) given once daily (78.7%), with good adherence to all formulations (≥8.5/10, high = 10) irrespective of regimen (p = 0.873).DiscussionOptimised mesalazine treatment improved the clinical outcomes in patients across the spectrum of mild-to-moderate UC.
BackgroundCongenital hepatic fibrosis (CHF) is a rare disease associated with the polycystic kidney gene, and the initial symptoms are often associated with portal hypertension, such as splenomegaly and esophageal varices. While the basic clinical features and pathogenesis of isolated CHF have been thoroughly studied, patients frequently present variable combined phenotypes including autosomal dominant polycystic kidney disease (ADPKD) and Von Meyenburg complex (VMC). The pathogenic mechanisms driving these composite phenotypes require further exploration.Methods and resultsWe report a case of an adult female patient who was admitted due to unexplained upper gastrointestinal bleeding. Upon admission, the patient was diagnosed with congenital hepatic fibrosis in conjunction with VMC and ADPKD, based on findings from liver puncture biopsy, exome sequencing (ES), biochemical tests, and imaging examinations.ConclusionsThe PKD1 gene is the causative gene for this patient’s CHF combined with VMC and ADPKD.
BackgroundCrohn’s disease (CD) is a chronic inflammatory condition that affects the gastrointestinal tract. Currently, the diagnosis of CD is predominantly dependent on endoscopic procedures and histopathological tissue analysis. Endoscopy is an invasive procedure, patient compliance is poor, and the results are subject to the operator’s subjective judgment. Infliximab (IFX) and ustekinumab (UST) are two new biologics used for the treatment of CD, which are effective in reducing inflammatory markers. However, the correlation between blood metabolites and inflammatory markers has rarely been studied in the biologic agents employed in the management of CD, and their effects on metabolic processes remain inadequately understood. This study aimed to elucidate the effects of IFX and UST on the blood metabolites in patients with CD, investigate the correlations between metabolic variations and clinical indicators, and examine the relationship between the identified biomarkers and clinical efficacy.MethodsA total of 81 patients with CD who were receiving biologic therapy enrolled at week 16 between January 2022 and December 2023 (45 receiving IFX and 36 receiving UST) and 45 healthy controls were included. Metabolite profiling was performed using high-performance liquid chromatography–tandem mass spectrometry, followed by multivariate statistical and pathway enrichment analyses to identify differential metabolites and their correlations with clinical indicators.ResultDespite achieving clinical remission, both the IFX and UST groups exhibited significantly elevated C-reactive protein levels and erythrocyte sedimentation rate values compared with the control group (p < 0.05). IFX primarily influenced amino acid metabolism, including pathways involving arginine and glutamine, and glycolysis and the tricarboxylic acid cycle. UST impacted glutathione and purine metabolism. Pearson’s correlation analysis demonstrated that l-arginine, l-glutamine, and l-lysine were significantly negatively correlated with C-reactive protein. In the UST group, glutathione, adenosine, and hypoxanthine were primarily significantly negatively correlated with C-reactive protein and absolute lymphocyte count (p < 0.05).ConclusionWe identified two sets of diagnostic biomarkers: the biomarkers for the IFX group were l-arginine, l-glutamine, and l-lysine, while those for the UST group were glutathione and adenosine.
Background:IBS is a disorder of gut-brain interaction that is diagnosed positively but still requires a focused differential diagnosis and limited rule-out testing. IBS-Smart and Trio-Smart are commercially available serologic and breath tests that may alter diagnostic sequencing in clinical practice. Objective:To evaluate whether receipt of IBS-Smart and/or Trio-Smart was associated with differences in diagnostic resource utilization, captured diagnostic cost, chart-level diagnostic persistence, and medication use compared with contemporaneous control patients who did not receive these tests. Methods:This retrospective two-center cohort study included 219 adults with symptoms suggestive of IBS. Patients were grouped as IBS-Smart only (n=48), Trio-Smart only (n=43), both tests (n=11), or controls receiving neither test (n=117). Costs reflected a payer-proxy perspective in 2022 US dollars and included captured diagnostic tests and gastroenterology office visits. The archived study used propensity matching and an exploratory generalized linear model (GLM) for total diagnostic cost. Results:Colonoscopy rates were 50.0% in the IBS-Smart-only cohort, 53.5% in the Trio-Smart-only cohort, 27.3% in the combined-testing cohort, and 60.7% in controls; upper endoscopy rates were 31.3%, 41.9%, 0.0%, and 48.7%, respectively. Among patients first seen in 2018 or later, mean total captured diagnostic plus office-visit cost per patient per month was $366.85 for IBS-Smart only, $382.87 for Trio-Smart only, $361.83 for both tests, and $960.39 for controls. In the archived propensity-matched GLM, IBS-Smart testing was associated with lower total diagnostic cost (coefficient -0.22; P = 0.050), corresponding to an estimated incremental savings of $526 per patient. Stable chart-level diagnosis was observed in 79.2% of IBS-Smart-only patients, 90.7% of Trio-Smart-only patients, 72.7% of patients after IBS-Smart in the combined cohort, 90.9% after Trio-Smart in the combined cohort, and 25.6% of controls. Medication counts decreased descriptively in several tested subgroups at one year; drug-class-level aggregation could not be reconstructed reliably from the archived medication file and is therefore not overstated. Conclusions:In this observational study, receipt of IBS-Smart and/or Trio-Smart was associated with lower captured resource utilization and greater chart-level diagnostic persistence than standard care alone. These findings should be interpreted as real-world associations rather than causal proof and do not replace Rome IV-based evaluation, alarm-feature triage, or guideline-recommended rule-out testing.
Background:Metabolic dysfunction-associated steatohepatitis (MASH), formerly nonalcoholic steatohepatitis (NASH), is a progressive liver disease and a leading cause of cirrhosis and liver-related mortality worldwide, affecting approximately 3%-5% of the global adult population and up to 30%-40% of individuals with type 2 diabetes mellitus (T2DM) or those attending dedicated diabetes and endocrine centers. For decades, treatment was limited to lifestyle interventions. The years 2024 and 2025 marked a paradigm shift with the first-ever FDA approvals of pharmacologic agents for MASH. Scope:This comprehensive narrative review synthesizes the evidence for newly approved and emerging pharmacotherapies for MASH, addressing the mechanisms of action, pivotal clinical trial data, efficacy, safety profiles, and place in therapy for resmetirom and semaglutide. It also discusses key agents including pioglitazone, saroglitazar, and vitamin E, and evaluates the non-invasive testing (NIT) toolkit-including FIB-4, VCTE, shear wave elastography, MRE, and ELF-in the context of a structured, risk-stratified clinical algorithm. Findings:Resmetirom (Rezdiffra), a THR-β agonist, achieved MASH resolution in 26%-30% versus 10% placebo and fibrosis improvement in 24%-26% versus 14% placebo at 52 weeks in the MAESTRO-NASH trial. Semaglutide 2.4 mg (Wegovy) demonstrated a 28.7% delta over placebo in MASH resolution in the ESSENCE trial. Pioglitazone has additional evidence for reducing the FIB-4 index in real-world studies. Saroglitazar, a PPAR-α/γ dual agonist approved in India, has shown significant reductions in ALT, liver fat, and metabolic parameters in Phase 2 studies and is advancing to Phase 2b. Shear wave elastography is a clinically important alternative to VCTE for fibrosis staging, particularly in patients with obesity, and offers value in resolving discordant FIB-4/VCTE results. Conclusion:The approval of resmetirom and semaglutide marks a new era in MASH management. A risk-stratified algorithmic approach using NITs guides patient selection, with liver biopsy reserved for specific clinical scenarios. The therapeutic landscape is rapidly evolving, with saroglitazar and combination approaches representing key frontiers.
Early diagnosis of gastric cancer is critical for improving prognosis and increasing the 5-year survival rate. However, gastroscopy and pathological examination are invasive, resource-dependent, and associated with low adherence, while conventional serological and imaging screening methods have limited sensitivity for early lesions. In recent years, artificial intelligence (AI), especially deep learning, has improved the efficiency and accuracy of real-time endoscopic detection, digital pathological recognition, non-contrast CT-based opportunistic screening, and multimodal diagnostic decision support. This review summarizes recent advances in AI-assisted technologies for gastric cancer diagnosis and, in response to the need for a clearer methodological and quantitative framework, compares representative models according to data modality, model architecture, dataset size, validation strategy, and reported diagnostic performance, including AUC, accuracy, sensitivity, specificity, precision/positive predictive value (PPV), and F1 score when available. We further discuss how data size, modality diversity, annotation granularity, class imbalance, and missing modalities influence model performance in real-world multicenter settings. Finally, we propose a structured multimodal AI-clinical decision support system (AI-CDSS) framework integrating CT imaging, endoscopic images and videos, whole-slide pathological images, serological indicators, molecular biomarkers, and clinical reports. Although AI-assisted diagnosis has shown considerable promise, clinical translation still requires prospective multicenter validation, standardized reporting of performance metrics, interpretable model outputs, privacy-preserving data governance, and regulatory-compliant deployment.
Background:Helicobacter pylori infection is a major etiological factor for gastric cancer, but its prognostic relevance once invasive gastric cancer has developed remains uncertain in French Guiana. Methods:We conducted a retrospective hospital-based study including all patients diagnosed with histologically confirmed invasive gastric carcinoma at Cayenne Hospital Center between 2018 and 2023. H. pylori status was assessed by routine histopathology. Sociodemographic, clinicopathological, and histological characteristics, including associated gastric lesions, were collected. Overall survival was estimated using the Kaplan-Meier method and compared using the log-rank test according to H. pylori status and initial management strategy. Exploratory multivariable Cox regression analyses were performed. Results:Eighty-two patients were included, of whom 43 (52.4%) were H. pylori-positive. H. pylori positivity was significantly associated with non-active chronic gastritis, whereas H. pylori detection was uncommon in active chronic gastritis. H. pylori status was not associated with tumor location, histological subtype, differentiation, or preneoplastic lesions. Median follow-up was 25.7 months. Overall survival did not differ between H. pylori-positive and H. pylori-negative patients. In multivariable analyses, H. pylori status was not associated with survival, whereas initial management was strongly associated with outcome, likely reflecting disease stage at diagnosis rather than a causal treatment effect. Conclusion:Routine histology detected H. pylori in about half of gastric tumors, with an association with non-active chronic gastritis. H. pylori status was not associated with survival; differences by initial management likely reflected disease severity, with interpretation limited by incomplete TNM staging.
ObjectivesHelicobacter pylori infection is a major risk factor for gastric cancer, but evidence for predicting H. pylori status from endoscopic images in patients with established gastric cancer remains limited. We evaluated the performance of endoscopic image-based classification models for H. pylori status in a retrospective gastric cancer cohort.MethodsWe retrospectively collected 602 endoscopic images from 337 patients with gastric cancer treated at a tertiary cancer center. After preprocessing and quality control, 576 images from 329 patients were retained for model development and evaluation. Helicobacter pylori status was defined using routine clinical testing, including serum anti-H. pylori IgG and/or the 13C urea breath test. Endoscopic image classification models were evaluated across repeated stratified train, validation, and test splits. The primary performance metric was the area under the receiver operating characteristic curve (AUC).ResultsModel discrimination was limited. The best-performing approach achieved a median test AUC of 0.6255, with sensitivity of 0.7308, specificity of 0.3714, accuracy of 0.6092, and F1 score of 0.6800. Fine-tuning showed a higher median AUC than retraining, but discrimination remained limited in both strategies.ConclusionsIn this retrospective gastric cancer cohort, endoscopic image-based classification showed limited ability to discriminate H. pylori status. These findings suggest that image-based assessment of H. pylori status in patients with gastric cancer remains challenging and may require more rigorous phenotyping, larger datasets, and validation across clinically diverse populations.
