Gastroenterology Research and Practice

Patients with end-stage renal disease (ESRD) have a five times higher risk of gastrointestinal bleed (GIB) and mortality than the general population. Aortic stenosis (AS) has been associated with GIB from intestinal angiodysplasia. In this retrospective analysis, we obtained data from the 2012 and 2019 National Inpatient Sample. The primary outcome of interest was all-cause in-hospital mortality and risk factors of mortality in patients with ESRD with GIB with aortic valve disorders especially AS. We identified all patients (≥18 years of age) with ESRD () and analyzed based on discharge diagnosis of valvular heart disease () in patients with GIB compared with those without GIB (). Survey statistical methods accounting for strata and weighted data were used for analysis using survey packages in R (version 4.0). Baseline categorical data were compared using Rao-Scott chi square test, and continuous data were compared using Student’s t-test. Covariates were assessed using univariate regression analysis, and factors with value less than 0.1 in the univariate analysis were entered in the final model. The univariate and multivariable associations of presumed risk factors of mortality in ESRD with GIB patients were performed by Cox proportional hazards model censored at length of stay. Propensity score matching was done using MatchIt package in R (version 4.3.0). 1 : 1 nearest neighbour matching was done with propensity scores estimated through logistic regression, in which occurrence of GIB, valvular lesions, and AS was regressed according to other patient characteristics. Among patients with ESRD with valvular heart diseases, AS was found to be associated with increased risk of GIB (; 95% CI 1.003–1.008; ). ESRD patients with AS showed increased risk of lower GIB (; 95% CI 1.01–1.06; ), colonic angiodysplasia (; 95% CI 1.01–1.05; ), stomach and duodenal angiodysplasia (; 95% CI 1.02–1.06; ), need for blood transfusion add pressors as compared to those without AS. However, there was no increased risk of mortality (; 95% CI 0.95–0.99; ).

Inflammatory bowel disease (IBD) is a complex chronic immune disease with two subtypes: Crohn’s disease and ulcerative colitis. Considering the differences in pathogenesis, etiology, clinical presentation, and response to therapy among patients, gastroenterologists mainly rely on endoscopy to diagnose and treat IBD during clinical practice. However, as exemplified by the increasingly comprehensive ulcerative colitis endoscopic scoring system, the endoscopic diagnosis, evaluation, and treatment of IBD still rely on the subjective manipulation and judgment of endoscopists. In recent years, the use of artificial intelligence (AI) has grown substantially in various medical fields, and an increasing number of studies have investigated the use of this emerging technology in the field of gastroenterology. Clinical applications of AI have focused on IBD pathogenesis, etiology, diagnosis, and patient prognosis. Large-scale datasets offer tremendous utility in the development of novel tools to address the unmet clinical and practice needs for treating patients with IBD. However, significant differences among AI methodologies, datasets, and clinical findings limit the incorporation of AI technology into clinical practice. In this review, we discuss practical AI applications in the diagnosis of IBD via gastroenteroscopy and speculate regarding a future in which AI technology provides value for the diagnosis and treatment of IBD patients.

Aims. To evaluate the value of endoscopic screening during endoscopic submucosal dissection (ESD) in the detection of synchronous multiple early gastric cancer (SMEGC) and the risk factors for missed diagnosis of SMEGC. Methods. We conducted gastric endoscopic screening during ESD operation in 271 patients with early gastric cancer (EGC) referred for ESD, and endoscopic follow-up within 1 year after the operation. The detection and characteristics of SMEGC were analyzed in three stages: before ESD, during ESD operation, and within 1 year after ESD. Results. SMEGC was detected in 37 of 271 patients (13.6%). Among them, 21 patients with SMEGC (56.8%) were diagnosed before ESD, 9 (24.3%) were diagnosed with SMEGC by endoscopic screening during ESD operation, and 7 (18.9%) were found to have EGC lesions in the stomach during postoperative endoscopic follow-up within 1 year. The preoperative missed detection rate of SMEGC was 43.2%, and the rate of missed detection could be reduced by 24.3% (9/37) with endoscopic screening during ESD operation. Missed SMEGC lesions were more common in flat or depressed type and smaller in size than the lesions found before ESD. The presence of severe atrophic gastritis and age ≥60 years were significantly correlated with SMEGC (), while multivariate analysis showed that age ≥60 years was an independent risk factor (OR = 2.63, ) for SMEGC. Conclusions. SMEGC lesions are apt to be missed endoscopically. Special attention should be paid to small, depressed, or flat lesions in detecting SMEGC, especially in elderly patients or (and) patients with severe atrophic gastritis. Endoscopic screening during ESD operation can effectively reduce the missed diagnosis rate of SMEGC.

Background. Necrotizing enterocolitis (NEC) is often associated with exaggerated activation of inflammatory response. Astaxanthin has been shown in studies to have a positive and advantageous effect on anti-inflammatory response. Hence, it is of great significance to study the protective effect of astaxanthin in NEC disease and its molecular mechanism. Objective. The present study was to investigate whether astaxanthin attenuates NEC rats and to explore its potential mechanism. Material and Methods. Hematoxylin-eosin staining was used to observe the pathological change of the intestinal tissue in NEC rats. Subsequently, we determined the anti-oxidative stress, anti-apoptosis, and anti-inflammation in astaxanthin with enzyme-linked immunosorbent assay kits, TUNEL staining, western blot, and immunohistochemistry assay. Furthermore, we added nucleotide-binding oligomerization domain 2 (NOD2) inhibitor to certify the molecular pathway of the astaxanthin in NEC rats. Results. Astaxanthin improved the pathological changes of the intestinal tissues. It restrained inflammation, oxidative stress, and protected cells from apoptosis in the intestinal tissue and serum of the NEC rats. Moreover, astaxanthin enhanced NOD2, whereas it suppressed toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB) pathway-related proteins. Apart from that, the NOD2 inhibitor offset the protective effect of the astaxanthin towards the NEC rats. Conclusion. The present study indicated that astaxanthin alleviated oxidative stress, inflammatory response, and apoptosis in NEC rats by enhancing NOD2 and inhibiting TLR4 pathway.

Liver fibrosis is a wound-healing response to chronic injury, which may result in cirrhosis and liver failure. Studies have been carried on the mechanisms and pathogenesis of liver fibrosis. However, the potential cell-specific expressed marker genes involved in fibrotic processes remain unknown. In this study, we combined a publicly accessible single-cell transcriptome of human liver with microarray datasets to evaluate the cell-specific expression patterns of differentially expressed genes in the liver. We noticed that EMP1 (epithelial membrane protein 1) is significantly active not only in CCl₄ (carbon tetrachloride)-treated mouse liver fibrosis but also in BDL (bile duct ligation)-induced liver fibrosis and even in human fibrotic liver tissues such as alcoholic hepatitis, NASH (nonalcoholic steatohepatitis), and advanced stage liver fibrosis. Furthermore, we demonstrated that EMP1 is a specific fibrotic gene expressed in HSCs (hepatic stellate cells) and endothelial cells using the Protein Atlas single-cell transcriptome RNA-sequencing clustering. Its expression was significantly elevated in fibrotic HSCs or CCl₄ and NASH-induced fibroblasts. Previous research revealed that EMP1 plays a role in proliferation, migration, metastasis, and tumorigeneses in different cancers via a variety of mechanisms. Because HSC activation and proliferation are two important steps following liver injury, it would be interesting to investigate the role of EMP1 in these processes. All of this information suggested that EMP1 could be used as a novel fibrotic liver marker and a possible target in the future.

Background. On September 5, 2019, British Columbia announced a new policy (the Biosimilars Initiative) to switch from originator to biosimilar infliximab for patients with inflammatory bowel diseases. Objective. To monitor the impacts of the policy on the use of medications and health services during the first year of the policy. Methods. In this population-based cohort study, we used administrative health data to construct three historical cohorts and one policy cohort of patients with inflammatory bowel diseases who used the originator infliximab. We then monitored the cumulative incidence of medications and health services. Log-likelihood ratios were used to quantify differences between the policy cohort and the average of the historical cohorts. Results. The cohorts included 1839–2368 users of the originator infliximab, ages 4–90 years, mean age 43 years. During the first year of follow-up, we found: (1) a 0.9% increase in the first dispensation of infliximab, biosimilar, or originator; (2) a 16.2% increase in infliximab dose escalation; (3) a decrease of 2.4% in the dispensation of antibiotics and a 2.6% decrease in new use of prednison; (4) an anticipated increase in visits to physicians and gastroenterologists to manage switching to biosimilars (24.0%); (5) a 4.0% decrease in discharges from hospital; and (6) a 2.9% decrease in emergency admissions to hospital. Conclusion. British Columbia’s Biosimilars Initiative for nonmedical switching from originator to biosimilar infliximab for inflammatory bowel diseases was not associated with harmful impacts on medications and health services use. An increase in dose escalation was accompanied by an improvement in health status proxies.