中华肝脏病杂志最新文献

Objective: To investigate the prevalence status and the clinical characteristics of hepatitis D virus (HDV) among patients chronically infected with hepatitis B virus (HBV) in the Xinjiang region. Methods: A cross-sectional study was conducted. Serum samples from 1 830 patients with chronic HBV infection who visited the Traditional Chinese Medicine Hospital of Xinjiang Uygur Autonomous Region from December 2022 to October 2023 were collected. All sera were tested for anti-HDV IgG and IgM. Sera positive for anti-HDV IgG or IgM were selected for HDV RNA detection. HDV RNA-positive sera were sequenced to determine the HDV genotype. Age, gender, HBV course, and anti-HBV treatment status were used as scoring items based on the propensity score matching (PSM) method. Chronic HBV patients with negative anti-HDV were matched in a ratio of 1∶1. The clinical characteristics of anti-HDV -positive-patients were analyzed. The t-test was used for comparison between groups of normally distributed continuous data. The Wilcoxon signed-rank test was used for comparison between groups of skewness distribution. The χ² test was used for comparison between groups of enumeration data. Results: The positive detection rates of anti-HDV IgG, anti-HDV IgM, and HDV RNA in 1 830 cases with chronic HBV infection were 2.24% (41/1 830), 1.09% (20/1 830), and 1.69% (31/1 830), respectively. All HDV RNA-positive patients had HDV genotype 1. Two anti-HDV-positive patients had negative hepatitis B surface antigen (HBsAg). Gender, age, HBV course, and anti-HBV treatment status had no significant difference. The quantification of HBsAg, liver biochemical indexes (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and total bile acids), the proportion of patients with liver cirrhosis, and alpha-fetoprotein were significantly higher in the anti-HDV-positive group than in those in the anti-HDV-negative group (P<0.05). Conclusion: The prevalence rate of HDV in chronic HBV-infected patients at a single center in the Xinjiang region was 2.24%, with the primary genotype being 1. Furthermore, overlap infection should be paid attention to because it might aggravate liver damage.

The mortality rates are significantly elevated with the rapid progression of acute liver failure in the absence of timely diagnosis and treatment. Liver transplantation is an effective therapeutic approach that can halt disease progression, but transplantation timing is a crucial factor affecting prognosis. Patients with acute liver failure should be promptly transferred to hospitals equipped for liver transplantation while simultaneously preparing for the procedure during the course of treatment to avoid missing the opportunity to save lives when the condition suddenly worsens. Auxiliary liver transplantation preserves the patient's native liver while transplanting a new liver. Therefore, patients are expected to gradually reduce immunosuppressants following the regeneration of the autologous liver, so avoiding the problem of lifelong use of immunosuppressants. This is also a unique advantage, offering benefits to patients undergoing auxiliary liver transplantation therapy for acute liver failure, while simultaneously presenting challenges for clinicians in terms of technical skill and comprehensive management.

Portal hypertensive biliopathy is a secondary condition of intrahepatic and extrahepatic bile duct abnormalities caused by portal hypertension, especially in extrahepatic portal venous obstruction. Most patients may remain asymptomatic for a long time, while a few may present with symptomatic portal hypertensive biliopathy, such as obstructive jaundice, cholelithiasis with or without cholangitis, gastrointestinal bleeding, and others. Such disease is rare in clinical practice and is prone to misdiagnosis and missed diagnosis. Improper treatment can lead to serious adverse consequences. We report a case of unexpected discovery of bile duct dilation due to abdominal pain, which was ultimately diagnosed as portal hypertensive biliopathy based on the medical history, manifestations of portal hypertension, and imaging examinations, especially intraductal ultrasonography.

Hepatocellular carcinoma (hereinafter referred to as liver cancer) is the main indication for liver transplantation in China, but postoperative tumor recurrence and metastasis severely restrict the efficacy of liver transplantation. There exist significant differences between the traditional liver cancer research models due to the long-term immunosuppressive state of transplant recipients and the complex mechanism of tumor recurrence and metastasis, posing enormous challenges to existing theoretical system. Therefore, it is crucial to innovate the scientific research pattern and liver transplantation clinical management model for liver cancer. Herein, the author's team has innovatively proposed a 'Tumor-Donor Liver-Recipient' integrated research horizon for liver transplantation in liver cancer based on prior clinical practice and scientific exploration, with the aim to expand new concepts in basic research, explore new strategies for precise clinical intervention, and establish a refined recipient management system. This paper systematically elaborates on the research general situation and cutting-edge perspectives under the "tumor-donor liver-recipient" so as to classify HCC liver transplantation patients, pre-transplant downstaging therapy, scientific evaluation and application of donor livers, innovations in transplant surgical techniques, and individualized postoperative management.

Liver transplantation is the standard therapy for end-stage liver disease, but the long-standing shortage of donor livers has constrained its advancement. The use of standard donor criteria expansion partially alleviates the supply-demand imbalance but increases postoperative complication risks. Extracorporeal mechanical perfusion mitigates ischemia-reperfusion injury, extends preservation time, and enables functional assessment and partial repair of the liver under ex vivo settings. Current clinical evidence confirms that short-term mechanical perfusion positively improves outcomes, but it still has limitations in terms of functional evaluation and deep repair. Therefore, the exploration of prolonged mechanical perfusion has possibilities for the restoration of organ function. The concept of "organ medicine" has enabled the breakthrough application of mechanical perfusion technology, originating from organ transplantation, to multiple disciplines, such as organ research, education, and therapy. Additionally, advancements in transforming research results and industrial upgrading are anticipated to develop into a strategic technology for a new round of medical revolution and industrial transformation.

Liver transplantation techniques have made significant advances in recent years in surgical procedures, expanding liver donor sources and perioperative management, leading to markedly improved patient survival rates. This review focuses on key recent developments in the field of liver transplantation, summarizing practical achievements and technical breakthroughs in areas such as machine perfusion techniques and utilization of marginally viable donors, minimally invasive liver transplantation techniques, and the clinical application of small-and ultra-small-size grafts. Furthermore, it explores the current challenges encountered in clinical practice and analyzes future research priorities and developmental trends.

Objective: To explore the effects of quercetin on autophagy and proliferation in HBV-positive liver cancer HCCLM3 cells based on STING signaling and its underlying mechanism. Methods: HCCLM3 cells were treated with quercetin (50 μmol/L or 100 μmol/L), designated as the 50 μmol/L group and 100 μmol/L group, respectively. The inhibitory effect of quercetin on HCCLM3 cells was detected using the CCK-8 method. A scratch assay was conducted to assess the impact of quercetin on the migration ability of HCCLM3 cells. A CCK8 and ROS kit was used to detect the effect of quercetin on the levels of reactive oxygen species in HCCLM3 cells. Western blotting was employed to measure the effect of quercetin on the expression of STING signaling and autophagy-related proteins in HCCLM3 cells. RNA interference technology was used to assess the effects of STING signaling inhibition on the expression of autophagy-related proteins and reactive oxygen species levels in HCCLM3 cells. The combined effects of STING activators and quercetin on HCCLM3 cell proliferation and autophagy were evaluated. The t-test was used to detect data differences between two groups, while ANOVA was employed for comparisons among multiple groups, followed by the SNK-q test for further pairwise comparisons. Results: Compared with the control group, quercetin (50 μmol/L and 100 μmol/L groups) significantly inhibited HCCLM3 cell survival activity in a dose-dependent manner (control group: 100%; 50 μmol/L group: 75.25%; 100 μmol/L group: 50.36%, P<0.01 ). Quercetin inhibited HCCLM3 cell migration in a dose-dependent manner (>2 h, control group: 187.16 μm; 50 μmol/L group: 145.22 μm; 100 μmol/L group: 88.21 μm, P<0.01), which significantly increased intracellular reactive oxygen species (ROS) levels in HCCLM3 cells (control group: 1.00; 50 μmol/L group: 1.565; 100 μmol/L group: 2.175, P<0.01). The phosphorylation level of STING was significantly increased (P<0.01), and the expression of autophagy-related protein microtubule-related protein 1A/1B light chain 3 (LC3) protein was significantly promoted (P<0.01). Compared with the quercetin group, the cell viability of the small interfering-STING+quercetin group was increased (quercetin group: 56.3%; small interfering-STING+quercetin group: 85.7%, P<0.05), while the expression of autophagy-related protein LC3 was decreased. Compared with the quercetin group, the cell viability of the quercetin+STING activator group was further decreased (quercetin group: 56.7%; quercetin+STING activator group: 35.4%, P<0.01), and the expression levels of STING and autophagy protein LC3 were significantly increased (P<0.05). Conclusions: STING signaling-regulated cell autophagy mediates the inhibitory effect of quercetin on the proliferation of HCCLM3 cells, and this effect is enhanced after administration of the STING agonist.