Canadian Journal of Gastroenterology and Hepatology最新文献

Background and aims: Acute upper gastrointestinal (UGI) bleeding from variceal and nonvariceal sources is a leading cause of morbidity and mortality. Although current international guidelines recommend performing endoscopy within 24 h of presentation, the added value of very early ("urgent," < 6 h) versus "early" (6-24 h) endoscopy remains unclear. Therefore, this study aimed to analyze the impact of urgent versus early endoscopy on clinical outcomes.

Methods: In this retrospective cohort study, we reviewed the medical records of 599 patients admitted to the emergency or gastroenterology department who underwent UGI endoscopy. Patients were stratified by timing, urgent endoscopy within 6 h of specialist consultation and early endoscopy between 6-24 h postconsultation. The protocol was approved by the University of Rzeszów Ethics Committee and conducted in accordance with the Declaration of Helsinki.

Results: Compared to the early group, patients undergoing urgent endoscopy were younger (p = 0.013), predominantly male, and had higher baseline heart rates (p = 0.0371). Apart from more frequent hypertension in the early group (p = 0.0007), comorbiditiy profiles were otherwise similar. The urgent endoscopy group had longer hospital stays (6.88 vs. 5.95, p = 0.774), more frequent rebleeding within 7 days (p = 0.0213), and slightly higher 30-day all-cause mortality rates. Factors associated with poor prognosis included increases in Rockall's and GB's scores (42% and 19% higher risk per point, respectively) and the presence of active bleeding (105% higher odds).

Conclusions: In unadjusted analyses, urgent endoscopy (< 6 h) was associated with worse outcomes, likely reflecting the selection of more severely ill patients. After propensity-score matching for baseline risk factors, however, the timing of endoscopy (< 6 h vs. 6-24 h) was no longer an independent predictor of outcomes. These findings suggest that clinicians' decisions and outcome differences are driven by overall severity of presentation and comorbid burden, rather than the effect of ultra-early endoscopy itself.

Liver fibrosis is a pathological condition marked by excessive extracellular matrix accumulation, potentially leading to cirrhosis. Macrophages play a vital role in regulating inflammatory responses, facilitating tissue repair, and orchestrating extracellular matrix remodeling through their differentiation into proinflammatory and anti-inflammatory phenotypes. Hepatic stellate cell activation and the progression of fibrosis have been linked to ferroptosis, a controlled cell death process triggered by iron and characterized by lipid peroxidation. This review explores the interaction between ferroptosis and macrophage polarization in iron-overload-induced liver fibrosis. It examines how ferroptosis intensifies inflammatory and fibrotic processes through macrophage activity and identifies key macrophage marker proteins involved. Understanding this interplay offers novel therapeutic insights targeting macrophage polarization to mitigate liver fibrosis, particularly in conditions such as hemochromatosis and chronic transfusion-dependent disorders.

Introduction: Eosinophilic esophagitis (EoE) is a chronic immune-mediated disease and a leading cause of food impaction in pediatric populations, with potential functional and structural complications. Proton-pump inhibitors (PPIs) are widely used as first-line therapy, but the response rate in Colombian children remains unknown. This study aimed to determine the initial histologic response to PPI therapy and describe clinical, endoscopic, and histological characteristics in a sample of pediatric patients with EoE from Bogotá, Colombia.

Methodology: A retrospective observational longitudinal study of patients aged 2-18 years diagnosed with EoE at a tertiary care center between 2015 and 2022 was conducted. Patients underwent initial clinical and endoscopic assessment confirming esophageal eosinophilia (≥ 15 eosinophils per high-power field [eos/hpf]), followed by at least 8-week course of PPI therapy and a subsequent clinical-endoscopic re-evaluation. Treatment response was defined histologically as < 15 eos/hpf in follow-up esophageal biopsy. Demographic, clinical, endoscopic, and histological data were analyzed using descriptive and bivariate statistics.

Results: We included 34 patients (median age 11 years; 61.8% boys). Sixteen (47%) achieved histological remission with initial PPI therapy. Being esomeprazole preferred in 88%, with median dose 1.37 mg/kg/day. No significant differences were observed between responders and nonresponders in demographic variables, familial and personal atopic history, symptoms, or endoscopic findings. Histologically, responders demonstrated significant reductions in eosinophil counts, as well as improvements in basal zone hyperplasia, eosinophilic abscesses, and eosinophil surface layering (all p < 0.005).

Discussion: This is the first study to assess PPI response in Colombian pediatric EoE patients, demonstrating a response rate consistent with existing literature. Histologic evaluation was identified as the most reliable marker of treatment success, underscoring the critical role of histopathological follow-up in this disease.

Background: Due to poverty and the pervasive thin-body ideal, undernutrition poses a significant challenge in both developed and economically undeveloped nations. Maternal nutritional deprivation has been linked to negative outcomes for the health of the fetus, a higher chance of metabolic syndrome, and adult obesity.

Aim: Considering the functions of the liver, this study aims to assess the interface between maternal malnutrition and morphological changes of the liver in the first and second generations of aged offspring.

Methods: This experimental study conducted in the Department of Anatomy, Histology, and Anthropology involved 26 rats divided into 3 groups: a control group fed a standard diet, a group subjected to 50% dietary restriction before pregnancy, and a group experiencing 50% dietary restriction before and during pregnancy. Histopathological examination was conducted on the livers of both first- and second-generation rat offspring to assess the occurrence of hepatic steatosis, ballooning, inflammation, and fibrosis. Data comparisons were performed using the Kruskal-Wallis test.

Results: Both the first- and second-generation experimental groups displayed a more pronounced steatosis and ballooning index compared to the control group. In addition to this, both male and female progeny of the experimental groups exhibited higher levels of steatosis and ballooning. Offspring of mothers undernourished before pregnancy demonstrated a more severe case of steatosis, whereas offspring from mothers fed a low-calorie diet before and throughout pregnancy showed a higher ballooning index. In the second generation, these changes were less profound than those seen in the first generation. Notably, both experimental groups of the first generation exhibited significantly higher levels of steatosis compared to their equivalent second-generation counterparts.

Conclusions: According to this study, there is a link between maternal undernutrition and a higher risk of nonalcoholic steatohepatitis or nonalcoholic fatty liver disease in the offspring's later life.

Objective: This study investigates the prognostic significance of tumor budding and its association with E-cadherin expression in pancreatic ductal adenocarcinoma (PDAC) with a focus on a Turkish patient cohort.

Methods: A total of 76 patients who had undergone resection of PDAC were analyzed. Tumor budding was assessed according to Tumor Budding Consensus Conference (ITBCC) guideline and classified as low (1-4 buds), medium (5-9 buds), or high (≥ 10 buds). E-cadherin expression was assessed by immunohistochemistry and categorized as low, moderate, or high. The correlations between tumor budding, clinicopathological factors, and survival were statistically analyzed and examined, and p < 0.05 was considered significant.

Results: Tumor budding was detected in 42.1% of patients, significantly associated with advanced tumor stage (p < 0.001), perineural invasion (p = 0.015), and lymphatic invasion (p = 0.005). Reduced E-cadherin expression was strongly correlated with tumor budding, which occurred in 83.3% of patients with weak (+) expression. Kaplan-Meier survival analysis demonstrated a median survival of 7.03 months in patients with tumor budding, compared to 21.7 months in those without tumor budding (p < 0.001). Multivariate analysis confirmed tumor budding as an independent prognostic factor (HR = 6.594, 95% CI: 1.825-23.818, p = 0.004).

Conclusions: Tumor budding is a reliable prognostic marker in PDAC, demonstrating significant associations with poor clinical outcomes, including advanced tumor stage and reduced survival. These findings support the integration of tumor budding into clinical guidelines to enhance prognostic precision and guide treatment decision-making.

CA19-9 is one of the most widely applied tumor markers in clinical oncology, particularly in the diagnosis and prognostic evaluation of biliary tract and pancreatic cancers. However, its clinical utility is limited by biological variability, most notably the influence of the Lewis blood group system, which may result in false-negative findings. The Lewis system is composed of three major phenotypes, Le(a+b-), Le(a-b+), and Le(a-b-), with the less frequent Le(a+b+) also reported in certain populations. Current evidence indicates that CA19-9 expression occurs predominantly in Le(a+b-) or Le(a-b+) individuals, whereas it is largely absent in Le(a-b-) individuals. Insufficient consideration of this factor in clinical settings reduces diagnostic accuracy and complicates interpretation of CA19-9 results. This review summarizes the current understanding of the relationship between CA19-9 and the Lewis system, critically evaluates recent clinical studies, highlights existing limitations, and discusses the potential role of combined CA19-9 and Lewis typing in improving the diagnostic value of gallbladder cancer.

Objective: Except for liver transplantation, no definitive treatment exists for hepatocellular carcinoma (HCC) in individuals suffering from decompensated liver cirrhosis. This research evaluated the feasibility and outcomes of microwave ablation (MWA) treatment in this patient population.

Methods: This research involved individuals diagnosed with HCC and decompensated cirrhosis who underwent MWA between 2019 and 2022. The analysis examined complications associated with the procedure, the effectiveness of treatment, patient survival rates, and the variations in blood test results and liver function reserves before and after MWA.

Results: The 62 enrolled patients were predominantly male (n = 48), and the average age was 59.06 years. Fifty-one patients were diagnosed with HBV-related cirrhosis. The tumor characteristics varied: 47 patients had single lesions with diameters ranging from 8 to 57 mm. Following the MWA procedure, there was a notable rise in the levels of alanine transaminase, aspartate transaminase, total bilirubin, prothrombin time, and the Child-Pugh, albumin-bilirubin, and model for end-stage liver disease scores (p < 0.05). Analysis of survival data indicated that tumor diameter < 3 cm, complete response (CR), meeting the Milan criteria, and Barcelona Clinic Liver Cancer (BCLC) Stage 0-A were linked to a more favorable prognosis. Multivariable Cox regression analysis identified achieving a CR as the strongest independent predictor for improved overall survival (HR = 0.25, 95% CI [0.09, 0.66], p = 0.005). Furthermore, the Milan criteria were independently associated with reduced risk of tumor progression in both univariate and multivariate analyses.

Conclusion: MWA is a safe procedure for individuals with HCC and decompensated liver cirrhosis. CR is associated with a better prognosis.

Objective: Investigating the antialcoholic liver injury properties of Rabdosia rubescens and its effect on the expression of CYP7A1 and levels of autophagy.

Materials and methods: Male C57BL/6 mice were randomly divided into three groups, namely, the control group (Lieber-DeCarli standard diet), model group (Lieber-DeCarli ethanol diet), and treatment group (Rabdosia rubescens at concentrations of 50 mg/kg, 100 mg/kg, and 200 mg/kg). The mice were fed their respective diets for 10 days, with the treatment group receiving the corresponding concentration of Rabdosia rubescens. On the 11th day, all the mice except those in the control group were given 30% EtOH. Nine hours later, the mice were sacrificed and their blood serum and liver tissue were collected for analysis. The effect of Rabdosia rubescens on alcohol-induced liver damage was evaluated by testing serum biochemical indicators, liver bile acid content, liver tissue histopathological changes, liver LC3 and p62 immunohistochemical staining, liver inflammatory factors, and CYP7A1, SREBP, FAS, LC3, Beclin-1, ATG7, and p62 expressions.

Results: Compared with the model group, Rabdosia rubescens was found to significantly reduce the levels of ALT, AST, TG, TC, and TBA in the serum of mice with alcoholic liver injury (p < 0.05 or p < 0.01). Rabdosia rubescens was found to significantly reduce the level of apoptosis in H&E-stained liver tissue sections. Rabdosia rubescens also significantly reduced the levels of TNF-α and IL-1β in the livers of mice (p < 0.001). Rabdosia rubescens was found to induce the expression of LC3, Beclin-1, and ATG7 proteins and mRNA, while inhibiting the expression of CYP7A1, SREBP, FAS, and p62 proteins and mRNA (p < 0.05 or p < 0.01).

Conclusion: Rabdosia rubescens has been shown to relieve alcohol-induced liver damage in mice by reducing levels of CYP7A1, alleviating cholestasis and reducing inflammation. It can also reduce alcohol-induced liver damage by decreasing fat synthesis and inducing autophagy.

Celiac disease is an important yet often overlooked condition that, when left untreated, can lead to intestinal villous atrophy, resulting in malabsorption and nutritional deficiencies. The clinical presentation of celiac disease varies greatly and is not limited to gastrointestinal symptoms. The diverse clinical picture and nonspecific manifestations can lead to difficulties in the diagnostic process and a delay in diagnosis. In this article, we discuss two cases in which the diagnosis was established-but very late. The first case presents a woman who experienced symptoms for more than 10 years and was initially suspected of having cancer before finally receiving the correct diagnosis of celiac disease. The second case describes a former general practitioner who, at the age of 55 years, underwent transglutaminase antibody testing for celiac disease and only then realized that he could feel differently. Both cases presented early signs of micronutrient deficiencies and/or weight loss, despite maintaining an adequate dietary energy intake. These cases illustrate the challenges with diagnostic delay.

Background: Tetraspanin 7 (TSPAN7), a quadruple transmembrane glycoprotein, is involved in the growth, development, and energy metabolism of cells, particularly in tumor cells. Despite its recognized significance, the role of TSPAN7 in colorectal cancer (CRC) remains unexplored. The purpose of this study is to explore the antitumor activity of TSPAN7 through the STK11/AMPK/mTOR pathway. Methods: Analysis of differential genes in normal colon and CRC tissues was conducted using the Gene Expression Omnibus (GEO) database. Ten potential genes, including TSPAN7, were also identified through the database screening. Results: Assessment of TSPAN7 alterations in both CRC tissues as well as cell lines revealed reduced expression as compared to normal colon tissues. Based on the findings, modulation of TSPAN7 expression was performed through overexpression and downregulation in vitro within CRC cells. The findings indicated that TSPAN7 exerted a negative regulatory influence on the migration and proliferation of CRC cells. An examination of AMPK and mTOR phosphorylation levels revealed that TSPAN7 affected the phosphorylation of these proteins via STK11. Conclusion: In CRC, TSPAN7 exerts antitumor effects through the STK11/AMPK/mTOR axis.