BMC Gastroenterology最新文献

Background: The incidence of lower gastrointestinal bleeding is on the rise, prompting the creation of various scoring systems to forecast patient's outcomes. But there is no single unified scoring system and these scoring systems clinical data are small and not worldwide.

Aims: To evaluate how different scoring systems predict mortality and prolonged hospital stay (≥ 10 days).

Methods: A retrospective review was conducted on the medical records of 4417 patients who presented with hematochezia at the emergency department from January 2016 to December 2022. We evaluated the predictive accuracy of various scoring systems for 30-day mortality and prolonged hospital stay (≥ 10 days) by analyzing the areas under the receiver-operating characteristic curves, taking into account factors such as patient age, laboratory findings, and comorbidities (ABC); AIMS 65; Glasgow-Blatchford; Oakland; Rockall(pre-endoscopy); SHA₂PE; and CHAMPS scores.

Results: We analyzed data from 1000 patients (mean age 66 years, 56.1% men, mean hospital stay 9.4 days) with lower gastrointestinal bleeding confirmed by any other means including DRE, colonoscopy and CT. The 30-day mortality rate was 3.7%. The primary etiologies of lower gastrointestinal bleeding were identified as ischemic colitis and diverticular bleeding, accounting for 18.8% and 18.5% of cases, respectively. In terms of forecasting 30-day mortality, the AIMS 65, CHAMPS, and ABC scoring systems demonstrated superior performance (p < 0.001). For predicting prolonged hospital stay, the SHA2PE score exhibited the highest accuracy among all evaluated systems (p < 0.001).

Conclusions: The newly developed scoring systems demonstrated superior accuracy in forecasting outcomes for patients with lower gastrointestinal bleeding, and the results of this study demonstrate that these scoring systems can be applied in clinical practice.

Background: Neuregulin (NRG) family is involved in energy metabolism, among which NRG1 is a neuregulin proved to play a protective role in MAFLD cells. But the presice echanism has not been fully illustrated. This study aimed to investigate the role of NRG1 via the ERK/SIRT1 signaling in the pathogenesis of MAFLD.

Methods: C57BL/6 mice were fed with high-fat diet for 8 weeks, and then injected with NRG1 (0.3 mg/kg/d) and PD98059 (0.3 mg/kg/d) via tail vein for 5 weeks. HepG2 cells induced by oleic acid and palmitic acid were treated with 20ng/mL NRG1 and 10µmol/L PD98059. The changes of histopathological, biochemical indexes, inflammatory factors, lipid metabolism, apoptosis and autophagy parameters were measured.

Results: The expressions of NRG1 in MAFLD cell and animal models were significantly lower than that in the control group. After the intervention of ERK inhibitor PD98059, the expression of NRG1 decreased significantly in vivo, but no significant change was observed in vitro. Moreover, NRG1 ameliorated hepatic steatosis, enhanced cell viability, reduced cell apoptosis, and attenuated liver injury both in vitro and in vivo. After NRG1 intervention, the expressions of ERBB2, ERBB3, p-ERK1/2, SIRT1 and p-FOXO1 as well as the LC3II/I ratio in MAFLD cells and liver tissues of MAFLD mice were significantly increased, while the expression of SREBP1c was decreased. The aforementioned therapeutic effect of NRG1 was lost after the intervention of PD98059.

Conclusion: NRG1 might play a protective role in the pathogenesis of MAFLD by activating the downstream ERK1/2 through ErbB2-ErbB3, which promotes the expression of SIRT1 and autophagy markers. This study might indicate a new therapeutic strategy for MAFLD.

Background: Colorectal cancer (CRC) is one common tumor with the high death rate, and badly affects the normal lives of CRC patients. Amarogentin (AG) has been found to exhibit regulatory roles and join into the progression of multiple diseases. However, the regulatory impacts and associated molecular mechanisms of AG in CRC progression keep unclear.

Methods and results: In this study, it was demonstrated that AG weakened CRC cell viability in a concentration- and time-dependent manner. In addition, AG accelerated cell apoptosis by triggering ferroptosis. The cell invasion and EMT process were restrained after AG treatment, but these impacts were reversed after Fer-1 addition. Moreover, it was uncovered that AG retarded Nrf2/HO-1/GPX4 activation. Additionally, AG modulated PTC cell viability and stimulated ferroptosis. At last, it was illustrated that AG suppressed tumor growth in vivo.

Conclusion: In conclusion, it was disclosed that AG suppressed cell proliferation and EMT process through inducing ferroptosis in CRC, and retarded Nrf2/HO-1/GPX4 activation. This discovery suggested that AG may be one effective drug for ameliorating CRC progression.

Background: The increased apoptosis of bile duct epithelial cells (BECs) due to some damage factors is considered the initiating factor in the occurrence and progression of biliary atresia (BA). Vitamin D receptor (VDR) is thought to play a crucial role in maintaining the intrinsic immune balance and integrity of bile duct epithelial cells (BECs). To investigate the role of VDRs in the pathogenesis and progression of BA using in vitro and in vivo models.

Materials and methods: The VDR expression levels in intrahepatic bile duct epithelial cells (IBDECs) in pediatric patients with BA were examined using immunohistochemical analysis. The correlation of the VDR levels with the incidence of refractory cholangitis after Kasai portoenterostomy (KPE) and the autologous liver survival time was analyzed. The levels of genes and proteins involved in related pathways were examined using quantitative real-time polymerase chain reaction and western blotting, respectively. The secretory levels of inflammatory factors were analyzed using enzyme-linked immunosorbent assay. A BA mouse model was established through the intraperitoneal sequential injection of rhesus rotavirus (RRV). The role of VDR in the pathogenesis and progression of BA was examined using in vitro and in vivo models. Retrospective analysis of patients with BA to examine the therapeutic efficacy of VDR activators on BA.

Results: 15 pediatric BA patients exhibiting VDR downregulation in IBDECs showed a higher incidence of refractory cholangitis after Kasai portoenterostomy (p = 0.037) and a lower native liver survival time compare to 23 BA patients without VDR downregulation (p = 0.032). 1,25-VD3 inhibited the degree of autophagy induction in HIBECs by poly(I: C) (p < 0.05), mitigated poly(I: C)-induced BEC damage and apoptosis by inhibiting autophagy (p < 0.05). 1,25-VD3 significantly suppressed the poly(I: C)-induced downregulation of SRC (p < 0.05) and ERK1/2 phosphorylation (p < 0.05). 1,25-VD3 exert a protective effect against RRV-induced BEC damage by inhibiting autophagy in BA mouse model. The incidence of cholangitis and the native liver survival time after surgery in the calcitriol-treated group was significantly lower than that in the control group. (p = 0.033, p = 0.035, respectively).

Conclusions: VDR activator mitigated dsRNA-induced BEC damage and apoptosis by inhibiting autophagy in vitro and in vivo. The 1,25-VD3/VDR/Src axis alleviated poly(I: C)-induced HIBEC damage and apoptosis through the PLA2/PKC/ERK pathway.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a primary cause of chronic liver disease, with potential progression to cirrhosis and hepatocellular carcinoma (HCC). Although systemic inflammatory biomarkers are associated with liver diseases, their specific role in MASLD remains unclear. This study examines the association between systemic inflammatory biomarkers and MASLD.

Methods: This cross-sectional study enrolled 6613 adults aged 20 years or older from the National Health and Nutrition Examination Survey (NHANES) spanning from 2017 to March 2020. Among these participants,, 34.67% were aged 40-59 years, 50.85% were female, and 63.26% were Non-Hispanic White. We investigated 10 inflammatory biomarkers: ALI, SIRI, SII, SIPS, IBI, NLR, PLR, CAR, LMR, and PNI. Logistic regression models were performed to assess the linear association between systemic inflammatory biomarkers and MASLD. Restricted cubic spline (RCS) regression was employed to explore potential nonlinear relationships between biomarkers and MASLD risk. Additionally, subgroup analyses were conducted to examine the influence of various demographic and clinical characteristics on the observed associations.

Results: After adjusting for key confounders, NLR and PLR exhibited negative association with MASLD risk, while ALI, CAR, and PNI exhibited the opposite association (P < 0.05). Most biomarkers, including ALI, SIRI, IBI, CAR, LMR, and PNI, exhibited significant non-linear correlations with MASLD (P < 0.05). Subgroup analyses revealed substantial age-related differences in the association between ALI and MASLD risk, as well as varying relationships between PNI and MASLD risk across various cardiovascular outcomes (P < 0.05).

Conclusion: Systemic inflammatory biomarkers are significantly associated with MASLD risk. Large-scale prospective studies are warranted to confirm these findings and elucidate the underlying mechanisms.

Background and aim: Remimazolam has proved to be a very promising sedative drug in randomized clinical trials for usage in a wide spectrum of patients, including critically ill ones. The purpose of our study was to verify efficacy and safety of remimazolam for procedural sedation during diagnostic and first level operative endoscopy in a real-world setting.

Methods: This single centre prospective study evaluated sedation regimen with remimazolam for EGDS and fentanyl and remimazolam for colonoscopy in consecutive ASA 1-3 patients.

Results: Seventy-one patients underwent 73 procedures (25 EGDS, 48 colonoscopies) with a total amount of 13.2 ± 8.7 mg and 10.2 ± 6.2 mg of remimazolam administered respectively. In 6 EGDS, rescue sedation with propofol was needed. Transient hypotension was frequent (37%) and no cases of hypoxia occurred. One case of suspected allergy (erythema of the trunk) without anaphylaxis was reported.

Conclusions: Procedural sedation can be applied with remimazolam without the use of propofol, obtaining effective sedation in colonoscopies while in EGDS remimazolam alone guarantees the result in a percentage of around 70-75% of cases.

Background: Gallstone disease (GSD) is associated with obesity. The Cardiometabolic Index (CMI), a metric that accurately assesses central adiposity and visceral fat, has not been extensively studied in relation to GSD risk. This study investigates the link between CMI and GSD incidence in U.S. adults.

Methods: This study utilized data from the National Health and Nutrition Examination Survey(NHANES)(2017-2020) to assess the association between CMI and GSD, adjusting for confounders such as age, sex, race, chronic diseases, and lifestyle factors. Multivariable logistic regression models and subgroup analyses were employed. Generalized Additive Models (GAM) and advanced curve fitting techniques were used to explore potential non-linear relationships, with threshold effects determined via piecewise linear regression if such relationships were identified. Receiver Operating Characteristic (ROC) curves evaluated and compared the predictive performance of CMI, Body Mass Index (BMI), and Waist Circumference (WC), establishing optimal cutoff values along with their sensitivity and specificity.

Results: This study included 3,706 participants, of whom 10.6% (392) had GSD. Participants with GSD showed significantly higher CMI values (0.57 vs. 0.44, P = 0.0002). The GSD group included more females and older adults, with increased risks for hypertension, diabetes, higher serum cholesterol and creatinine levels, and a higher risk of cancer. Logistic regression analysis revealed that higher CMI was significantly associated with greater GSD incidence (OR = 1.19, 95% CI = 1.02-1.38, P < 0.0001). The ROC curve demonstrated superior predictive performance (AUC = 0.778), outperforming conventional metrics like BMI and WC. GAM analysis indicated a non-linear positive correlation between CMI and GSD, with an optimal threshold of 0.996. Subgroup analysis found the strongest association among females, individuals aged 20-39, non-Hispanic Whites, those without a history of coronary heart disease, and alcohol consumers.

Conclusion: Our study reveals a nonlinear positive correlation between the CMI and the incidence of GSD among U.S. adults, with a threshold value of 0.996. Despite limitations in sample size that constrained the analysis of a fully adjusted model, after adjusting for confounding factors, the AUC for predicting GSD using CMI reached 0.778, surpassing traditional metrics. These findings underscore the importance of CMI as a critical risk factor and emphasize the necessity of targeted interventions for high-risk populations.

Objectives: Over 30% of people worldwide suffer from metabolic dysfunction-associated steatotic liver disease (MASLD), a significant global health issue. Identifying and preventing high-risk individuals for MASLD early is crucial. The purpose of our study is to investigate the factors related to the development of MASLD and develop a risk prediction model for its occurrence.

Methods: The study included 5107 subjects, divided into training and validation groups in a 7:3 ratio using a random number table method. Collinearity diagnosis and Cox regression were used to identify factors associated with MASLD incidence, and a risk prediction model was created. The model's accuracy, reliability, and clinical applicability were assessed.

Results: Our study indicated that male, body mass index (BMI), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), fasting plasma glucose (FPG), serum uric acid to creatinine ratio (SUA/Cr) and white blood cell (WBC) were associated with MASLD incidence. The elements were determined to be crucial for creating a risk prediction model. The model showed strong discriminative potential with a C-index of 0.783 and the time-dependent AUCs of 0.781, 0.789, 0.814 and 0.796 for 1-4 years in the training group, and a C-index of 0.788 and the time-dependent AUCs of 0.798, 0.782, 0.787 and 0.825 for 1-4 years in validation. Calibration curves confirmed the model's accuracy, and decision curve analysis (DCA) validated its clinical utility.

Conclusions: The model may provide clinical physicians with a reliable method for identifying high-risk populations for MASLD and serve as a guide for developing prediction models for other diseases.

Background & objectives: Differentiation of histologic subtypes of appendiceal mucoceles may prove to be difficult on computed tomography (CT). The main objective of this study was to identify the CT features of mucocele of the appendix and correlate the imaging findings with histopathology in inflammatory, benign, and malignant neoplastic lesions, and whether these entities can be accurately differentiated on CT imaging.

Materials and methods: CT scans of 31 patients with diagnosis of appendiceal mucocele were retrospectively reviewed and compared with histopathology. The appendix was evaluated for maximal luminal diameter, cystic dilatation, luminal attenuation, appendicolith, mural calcification and enhancement, periappendiceal fat stranding and fluid. CT findings were compared by use of Mann-Whitney U and Fisher's exact tests. Receiver operating characteristics analysis was performed to assess the diagnostic utility of appendiceal luminal diameter in differentiating different types of mucoceles.

Results: Patients were classified into three groups: those with inflammatory mucoceles (n = 10), benign mucoceles (simple mucocele, mucosal hyperplasia and low-grade appendiceal mucinous neoplasm (n = 17), and those with malignant mucinous adenocarcinoma (n = 4). The mean diameter was found to be significantly different in the three groups with the largest diameter in the benign subgroup. Soft tissue thickening (p-value 0.01), mural calcification (p-value < 0.01), internal septation (p-value 0.02) and fat stranding (p-value 0.05) was found to be of statistical significance among the various groups. The best cut-off diameter for diagnosis of inflammatory mucoceles to be ≤ 2.3 cm with a sensitivity of 71% and specificity of 90%.

Conclusion: Our study suggests that CT findings such as appendiceal diameter less than 2.3 cm, absence of soft tissue thickening, mural calcification and internal septation may be useful in preoperative diagnosis of inflammatory appendiceal mucocele.