Canadian Journal of Gastroenterology and Hepatology

Purpose. The aim of the study was to investigate the effect of hyperthermic intraperitoneal perfusion chemotherapy (HIPEC) combined with radical surgery and capecitabine on stage III gallbladder cancer. Method. Seventy-eight patients with stage III gallbladder cancer treated in our hospital between December 2015 and April 2019 were retrospectively enrolled. Depending on the treatment approach, the patients were divided into the control group (radical surgery and capecitabine) and the HIPEC group (hyperthermic intraperitoneal perfusion chemotherapy combined with radical surgery and capecitabine). The patients were followed up by outpatient or through telephone until April 1, 2020. SPSS 19.0 software was applied for data analysis. Survival analysis was performed using the Kaplan–Meier method and parallel log-rank test. Results. There were 43 cases in the control group and 35 cases in the HIPEC group. There were no significant differences in operation time, lymph node metastasis, microvascular infiltration, and nerve invasion; there was no significant difference in postoperative complications between the two groups (). The average hospitalization time of the HIPEC group was 23.0 ± 6.9 days, which was longer than the 20.0 ± 5.8 days of the control group (). The body temperatures of HIPEC group patients at 0 h and 6 h after operation were higher than those of patients in the control group (); however, the body temperature of the two groups gradually became the same at 12–24 h after operation. There was no liver and kidney damage in the two groups after surgery. The platelets in the HIPEC group were less than those in the control group (). The median survival time of HIPEC was 19.2 months, which was longer than 15.3 months in the control group. The 1-year survival rates of the two groups were 91.43% vs. 76.71%, and the 2-year survival rates were 26.29% vs. 17.53%, respectively (). Conclusion. HIPEC combined with radical surgery and capecitabine for stage III gallbladder cancer can effectively prolong survival time without increasing surgery-related complications.

Background. The role of liver function tests (LFT) as prognostic factors in patients admitted with COVID-19 has not been fully investigated, particularly outside resource-rich countries. We aimed at evaluating the prognostic value of abnormal LFT on admission and during hospitalization of patients with COVID-19. Methods. We performed a retrospective study that included 298 adult patients hospitalized for COVID-19, between 05/2020 and 02/2021, in 6 hospitals from 5 countries in South America. We analyzed demographic and comorbid variables and laboratory tests on admission and during hospitalization. LFT over twice the upper limit of normal (ALEx2) were also evaluated in relation to a variety of factors on admission and during hospitalization. De novo-ALEx2 was defined as the presence of ALEx2 at one week of hospitalization in patients without ALEx2 on admission. Patients were followed until hospital discharge or death. Multivariable analysis was used to evaluate the association between ALEx2 on admission and during hospitalization and mortality. Results. Of the total of 298 patients, 60% were male, with a mean age of 60 years, and 74% of patients had at least one comorbidity. Of those, 137 (46%) patients were transferred to the intensive care unit and 66 (22.1%) patients died during hospitalization. ALEx2 on admission was present in 87 (29.2%) patients and was found to be independently associated with 1-week mortality (odds ratio (OR) = 3.55; 95% confidence interval (95%CI) 1.05–12.05). Moreover, 84 (39.8%) out of 211 patients without ALEx2 at admission developed de novo-ALEx2, which was independently associated with mortality during second week of hospitalization (OR = 6.09; 95%CI 1.28–29) and overall mortality (OR = 2.93, 95%CI 1.05–8.19). Conclusions. A moderate elevation of LFT during admission was associated with a poor short-term prognosis in patients hospitalized with COVID-19. In addition, moderate elevation of LFT at one week of hospitalization was an independent risk factor for overall mortality in these patients.

Objectives. Alcohol-related liver disease is an increasing public health burden in China, but there is a lack of models to predict its prognosis. This study established a nomogram for predicting the survival of Chinese patients with alcohol-related liver disease (ALD). Methods. Hospitalized alcohol-related liver disease patients were retrospectively enrolled from 2015 to 2018 and followed up for 24 months to evaluate survival profiles. A total of 379 patients were divided into a training cohort (n = 265) and validation cohort (n = 114). Cox proportional hazard survival analysis identified survival factors of the patients in the training cohort. A nomogram was built and internally validated. Results. The 3-month, 6-month, 12-month, and 24-month survival rates for the training cohort were 82.6%, 81.1%, 74.3%, and 64.5%, respectively. The Cox analysis showed relapse (), cirrhosis (), liver cancer (), and a model for end-stage liver diseases score of ≥21 () as independent prognostic factors. A nomogram was built, which predicted the survival of patients in the training cohort with a concordance index of 0.749 and in the internal validation cohort with a concordance index of 0.756. Conclusion. The long-term survival of Chinese alcohol-related liver disease patients was poor with a 24-month survival rate of 64.5%. Relapse, cirrhosis, liver cancer, and a model for end-stage liver disease score of ≥21 were independent risk factors for those patients. A nomogram was developed and internally validated for predicting the probability of their survival at different time points.

Introduction. Acute Physiology and Chronic Health Evaluation (APACHE) II and III and Sequential Organ Failure Assessment (SOFA) are prognostic scores commonly used in the intensive care unit (ICU). Their accuracy in predicting mortality has not been adequately evaluated in comparison to prognostic scores commonly used in critically ill cirrhotic patients with acute decompensation (AD) or acute-on-chronic liver failure (ACLF). Aims. This study was conducted to evaluate the performance of prognostic scores, including APACHE II, SOFA, Chronic Liver Failure Consortium (CLIF-C) SOFA, Child–Turcotte–Pugh (CPS), Model for End-Stage Liver Disease (MELD), MELD-Na, MELD to serum sodium ratio (MESO) index, CLIF-C organ failure (CLIF-C OF), CLIF-C ACLF, and CLIF-C AD scores, in predicting mortality of cirrhotic patients admitted to the ICU. Patients and Methods. A total of 382 patients (280 males, mean age 67.3 ± 10.6 years) with cirrhosis were retrospectively evaluated. All prognostic scores were calculated in the first 24 hours of ICU admission. Their ability to predict mortality was measured using the analysis of the area under the receiver operating characteristic curve (AUC). Results. Mortality was observed in 31% of the patients. Analysis of AUC revealed that CLIF-C OF (0.807) and CLIF-SOFA (0.776) had the best ability to predict mortality in all patients, but CLIF-C OF (0.749) had higher prognostic accuracy in patients with ACLF. CLIF-SOFA, SOFA, and CLIF-C AD had the highest AUC values in patients with AD, with no statistical difference (). Conclusions. When compared to other general or liver-specific prognostic scores, CLIF-C OF, CLIF-SOFA, SOFA, and CLIF-C AD have good accuracy to predict mortality in critically ill patients with cirrhosis and patients with AD. According to the clinical scenario, different scores should be used to provide prognosis to patients with cirrhosis in the ICU.

Background/Objectives. Liver fibrosis is the inevitable end result of chronic hepatitis C (HCV) infection and is responsible for almost all liver-related complications. After the big advancement in therapeutics of HCV, liver fibrosis would expectedly improve after viral clearance. Many studies showed significant improvement of liver fibrosis shortly after successful treatment with direct acting antiviral agents (DAAs); however, the long-term changes have been scarcely addressed in the literature. We aimed to trace dynamical changes in liver stiffness 1, 3, and 5 years after HCV eradication. Methods. Liver stiffness measurements (LSM) have been serially assessed 1, 3, and 5 years after HCV clearance in 655 patients who have been treated with DAAs. Results. The mean age was 51.44 ± 10 years. 73% of patients were males. 48% were cirrhotics. In noncirrhotics, the mean LSM was significantly decreased from 8.29 ± 2.3 kPa to 4.03 ± 1.0 kPa at the end of the follow-up. Likewise, LSM decreased in cirrhotics from 29.66 ± 14.25 kPa to 22.50 ± 11.16 kPa . The proportions of F1, F2, F3, and F4 patients at the baseline were 17.7%, 17.9%, 16.6%, and 47.8%, which became 56.5%, 4.1%, 4.9%, and 34.5%, respectively, with a substantial reversal of cirrhosis in 87 patients (27.7%) at the end of follow-up. Conclusions. There was an overall significant regression of liver stiffness in all patients after sustained HCV eradication. Liver stiffness reflecting mild fibrosis (F0–F2) usually improves shortly after treatment, while measurements reflecting advanced fibrosis (F3–F4) take a longer time to regress to lower fibrosis stages.

Long noncoding RNAs (lncRNAs) have been substantially reported to have critical roles in regulating tumorigenesis in recent years. However, the expression pattern and biological function of SNHG17 in hepatocellular carcinoma (HCC) remain unclear. Bioinformatics analysis and qRT-PCR were performed to detect the expression pattern of SNHG17 in HCC tissues, adjacent nontumorous tissues, and cell lines. The effect of SNHG17 on proliferation, migration, and apoptosis of HCC was investigated by knockdown and overexpressing SNHG17 in HCC cell lines. RNA sequencing was utilized to explore the underlying mechanism. Utilizing publicly available TCGA-LIHC, GSE102079 HCC datasets, and qRT-PCR, we found SNHG17 was significantly upregulated in HCC tissues and cell lines and was notably associated with larger tumor size, poorly differentiation, presence of vascular invasion, and advanced TNM stage. Furthermore, gain- and loss-of-function studies demonstrated that SNHG17 promoted cell proliferation and migration and inhibited apoptosis of HCC. By employing RNA sequencing, we found knockdown of SNHG17 caused 1037 differentially expressed genes, highly enriched in several pathways, including metabolic, PI3K-Akt, cell adhesion, regulation of cell proliferation, and apoptotic pathway; among them, 92 were overlapped with SNHG17-related genes in the TCGA-LIHC dataset. Furthermore, ERH, TBCA, TDO2, and PDK4 were successfully validated and found significantly dysregulated in HCC tissues. Moreover, HCC patients with higher SNHG17 expression had a relatively poor overall survival and disease-free survival, and ERH and PDK4 also played a marked role in the prognosis of HCC. Broadly, our findings illustrate that SNHG17 acts as a noncoding oncogene in HCC progression, suggesting its potential value as a novel target for HCC therapy.