Vol.42 No.6 (308 in total) Jun. 2026
Theme Issue: New Advances in the Clinical Management of Liver Cirrhosis: From Recompensation to Multisystem Intervention
Executive Chief Editor: XU Xiaoyuan
Peking University First Hospital
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2026, 42(6): 1241-1245.
DOI: 10.12449/JCH260601
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Abstract:
Liver cirrhosis is the end-stage of various chronic liver diseases， and hepatic fibrosis caused by persistent inflammation is the core mechanism of the development and progression of liver cirrhosis. With the evolution of disease spectrum and a deeper understanding of the reversal of hepatic fibrosis， dual antiviral-antifibrotic therapy initially applied in the treatment of hepatitis B cirrhosis has gradually evolved into a broad-sense dual therapy for liver cirrhosis， which integrates etiological treatment with antifibrotic and/or anti-inflammatory interventions. This article systematically reviews the conceptual evolution of dual therapy for liver cirrhosis and related research advances.
Liver cirrhosis is the end-stage of various chronic liver diseases， and hepatic fibrosis caused by persistent inflammation is the core mechanism of the development and progression of liver cirrhosis. With the evolution of disease spectrum and a deeper understanding of the reversal of hepatic fibrosis， dual antiviral-antifibrotic therapy initially applied in the treatment of hepatitis B cirrhosis has gradually evolved into a broad-sense dual therapy for liver cirrhosis， which integrates etiological treatment with antifibrotic and/or anti-inflammatory interventions. This article systematically reviews the conceptual evolution of dual therapy for liver cirrhosis and related research advances.
2026, 42(6): 1246-1252.
DOI: 10.12449/JCH260602
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Liver cirrhosis recompensation refers to the process in which patients with decompensated cirrhosis achieve the disappearance of decompensated complications and restoration of liver function and clinical phenotype to a compensated state after etiological treatment or symptomatic treatment. In recent years， with effective control of the etiology of cirrhosis and treatment or prevention of decompensated complications， the clinical significance of recompensation has gained increasing attention. This article elaborates on recompensation from the aspects of definition， diagnostic criteria， influencing factors， mechanisms affecting long-term prognosis， and clinical management strategies， and with reference to the latest research evidence， this article also discusses the core value of recompensation in improving quality of life and reducing the risk of end-stage events， in order to provide a basis for optimizing the comprehensive management of liver cirrhosis.
Liver cirrhosis recompensation refers to the process in which patients with decompensated cirrhosis achieve the disappearance of decompensated complications and restoration of liver function and clinical phenotype to a compensated state after etiological treatment or symptomatic treatment. In recent years， with effective control of the etiology of cirrhosis and treatment or prevention of decompensated complications， the clinical significance of recompensation has gained increasing attention. This article elaborates on recompensation from the aspects of definition， diagnostic criteria， influencing factors， mechanisms affecting long-term prognosis， and clinical management strategies， and with reference to the latest research evidence， this article also discusses the core value of recompensation in improving quality of life and reducing the risk of end-stage events， in order to provide a basis for optimizing the comprehensive management of liver cirrhosis.
2026, 42(6): 1253-1259.
DOI: 10.12449/JCH260603
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Patients with liver cirrhosis often experience a reduction in bone mineral density （BMD） or even osteoporosis （OP） due to long-term chronic liver dysfunction and systemic metabolic disorders， and this condition has become one of the major complications affecting their quality of life and long-term prognosis. This article systematically reviews the epidemiological characteristics of reduced BMD associated with liver cirrhosis， summarizes the incidence of reduced BMD in liver cirrhosis patients with different etiologies， and analyzes its association with disease severity. This article further discusses the main pathophysiological mechanisms of reduced BMD induced by liver cirrhosis （including calcium/phosphorus metabolism disorders， sex hormone imbalance， chronic inflammatory response， and bone metabolism dysregulation）， reviews the clinical manifestations， fracture risk， and adverse outcomes associated with reduced BMD， and summarizes current prevention and treatment strategies for cirrhosis-related OP. This review aims to integrate recent research advances in this field and to provide a reference for future mechanistic studies and standardized clinical management.
Patients with liver cirrhosis often experience a reduction in bone mineral density （BMD） or even osteoporosis （OP） due to long-term chronic liver dysfunction and systemic metabolic disorders， and this condition has become one of the major complications affecting their quality of life and long-term prognosis. This article systematically reviews the epidemiological characteristics of reduced BMD associated with liver cirrhosis， summarizes the incidence of reduced BMD in liver cirrhosis patients with different etiologies， and analyzes its association with disease severity. This article further discusses the main pathophysiological mechanisms of reduced BMD induced by liver cirrhosis （including calcium/phosphorus metabolism disorders， sex hormone imbalance， chronic inflammatory response， and bone metabolism dysregulation）， reviews the clinical manifestations， fracture risk， and adverse outcomes associated with reduced BMD， and summarizes current prevention and treatment strategies for cirrhosis-related OP. This review aims to integrate recent research advances in this field and to provide a reference for future mechanistic studies and standardized clinical management.
2026, 42(6): 1260-1265.
DOI: 10.12449/JCH260604
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Pancreatic portal hypertension （PPH） is a type of regional portal hypertension secondary to pancreatic diseases and their complications. Unlike portal hypertension caused by liver cirrhosis， PPH is confined to the splenic venous system， and most patients tend to have normal liver function. Splenic vein obstruction and impaired blood return are the core mechanisms underlying the development of PPH， and isolated gastric fundal varices represent a characteristic manifestation of PPH. For patients with pancreatic diseases， it is necessary to establish early warning and risk stratification strategies， and high-quality studies are needed to further confirm the safety and efficacy of anticoagulation， surgical approaches， and interventional therapies in patients with PPH. This article systematically reviews the pathogenesis， etiological classification， clinical features， and key diagnostic points of PPH and discusses the current status of PPH treatment and existing challenges.
Pancreatic portal hypertension （PPH） is a type of regional portal hypertension secondary to pancreatic diseases and their complications. Unlike portal hypertension caused by liver cirrhosis， PPH is confined to the splenic venous system， and most patients tend to have normal liver function. Splenic vein obstruction and impaired blood return are the core mechanisms underlying the development of PPH， and isolated gastric fundal varices represent a characteristic manifestation of PPH. For patients with pancreatic diseases， it is necessary to establish early warning and risk stratification strategies， and high-quality studies are needed to further confirm the safety and efficacy of anticoagulation， surgical approaches， and interventional therapies in patients with PPH. This article systematically reviews the pathogenesis， etiological classification， clinical features， and key diagnostic points of PPH and discusses the current status of PPH treatment and existing challenges.
2026, 42(6): 1266-1269.
DOI: 10.12449/JCH260605
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Hepatic encephalopathy （HE） is a major complication of liver cirrhosis associated with a poor prognosis， imposing a heavy burden on patients， families， and the healthcare system. In recent years， although significant advances have been made in the diagnosis and management strategies for HE， many issues remain to be resolved. In 2026， the American College of Gastroenterology released a clinical guideline on HE， covering recommendations on the diagnosis， management， and prevention of HE， which provides guidance for clinical practice. This article gives an excerpt of the recommendations and key views from this guideline.
Hepatic encephalopathy （HE） is a major complication of liver cirrhosis associated with a poor prognosis， imposing a heavy burden on patients， families， and the healthcare system. In recent years， although significant advances have been made in the diagnosis and management strategies for HE， many issues remain to be resolved. In 2026， the American College of Gastroenterology released a clinical guideline on HE， covering recommendations on the diagnosis， management， and prevention of HE， which provides guidance for clinical practice. This article gives an excerpt of the recommendations and key views from this guideline.
2026, 42(6): 1270-1274.
DOI: 10.12449/JCH260606
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Recently， Gastroenterological Society of Australia convened a multidisciplinary group and applied a modified Delphi process to develop the first Australian consensus statement on the application of transjugular intrahepatic portosystemic shunt （TIPS） in portal hypertension. To address the current issues of insufficient application and a lack of standardized protocols for TIPS in Australia， this consensus provides evidence-based recommendations across the key domains of preoperative preparation and assessment for TIPS， surgical standards， postoperative care and follow-up， and specific clinical indications， in order to provide standardized guidance for the comprehensive management of TIPS in liver disease patients with portal hypertension. This article gives an excerpt of the key statements in the consensus.
Recently， Gastroenterological Society of Australia convened a multidisciplinary group and applied a modified Delphi process to develop the first Australian consensus statement on the application of transjugular intrahepatic portosystemic shunt （TIPS） in portal hypertension. To address the current issues of insufficient application and a lack of standardized protocols for TIPS in Australia， this consensus provides evidence-based recommendations across the key domains of preoperative preparation and assessment for TIPS， surgical standards， postoperative care and follow-up， and specific clinical indications， in order to provide standardized guidance for the comprehensive management of TIPS in liver disease patients with portal hypertension. This article gives an excerpt of the key statements in the consensus.
2026, 42(6): 1275-1278.
DOI: 10.12449/JCH260607
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Sinusoidal obstruction syndrome/veno-occlusive disease （SOS/VOD） after hematopoietic stem cell transplantation （HSCT） in children has high incidence and mortality rates， and missed diagnosis of jaundice-free cases is common. In addition， there are still controversies over the efficacy of prophylactic defibrotide （DF） use， and the European Medicines Agency does not recommend the prophylactic use of DF， whereas clinical needs remain urgent. In 2026， by integrating controversial research evidence and focusing on specific prophylaxis for high-risk children， the European Society for Blood and Marrow Transplantation established a weighted cumulative scoring system to quantify risks and accurately identify the populations who may benefit from DF prophylaxis， in order to provide evidence-based support for the prophylactic use of DF， reduce the incidence and mortality rates of SOS/VOD in children， and improve the prognosis of patients. This article gives an excerpt of the key points in the consensus guidelines.
Sinusoidal obstruction syndrome/veno-occlusive disease （SOS/VOD） after hematopoietic stem cell transplantation （HSCT） in children has high incidence and mortality rates， and missed diagnosis of jaundice-free cases is common. In addition， there are still controversies over the efficacy of prophylactic defibrotide （DF） use， and the European Medicines Agency does not recommend the prophylactic use of DF， whereas clinical needs remain urgent. In 2026， by integrating controversial research evidence and focusing on specific prophylaxis for high-risk children， the European Society for Blood and Marrow Transplantation established a weighted cumulative scoring system to quantify risks and accurately identify the populations who may benefit from DF prophylaxis， in order to provide evidence-based support for the prophylactic use of DF， reduce the incidence and mortality rates of SOS/VOD in children， and improve the prognosis of patients. This article gives an excerpt of the key points in the consensus guidelines.
2026, 42(6): 1279-1286.
DOI: 10.12449/JCH260608
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Objective To investigate the association of hepatic steatosis with the level of viral replication and the progression of hepatic fibrosis in patients with chronic hepatitis B （CHB） through a real-world study， and to determine the independent influencing factors for hepatic fibrosis. Methods A total of 887 CHB patients who attended the outpatient service and inpatient ward of Hepatology in The First Affiliated Hospital of Dalian Medical University from July 2021 to March 2025 were enrolled as subjects， and according to the presence or absence of metabolic dysfunction-associated steatotic liver disease （MASLD）， they were divided into CHB group with 560 patients and CHB+MASLD group with 327 patients. The association between hepatic steatosis and HBV load in CHB patients was analyzed， as well as the impact of varying degrees of hepatic steatosis on hepatic fibrosis. The t-test or the Mann-Whitney U test was used for comparison of continuous data between groups； the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups； a Spearman correlation analysis was performed； a Logistic regression analysis was used to investigate influencing factors. Results The patients enrolled received antiviral therapy according to viral load； of all patients， 275 （31%） received nucleos（t）ide analogue combined with pegylated interferon-α， 532 （60%） received nucleos（t）ide analogue monotherapy， and 80 （9%） did not receive antiviral therapy. A total of 44 patients （5.0%） who were receiving PEG-IFN-α therapy and had marked thrombocytopenia were excluded， and finally 843 patients were included for comparison of aspartate aminotransferase-to-platelet ratio index （APRI） and fibrosis-4 index （FIB-4）. Compared with the CHB group， the CHB+MASLD group had a significantly higher proportion of male patients （χ2=5.917， P<0.05） and a significant increase in CAP value （t=21.646， P<0.05）. The median values of liver function parameters for the population enrolled were within the normal range， and no significant inflammatory activity was observed. The virological analysis showed that compared with the CHB group， the CHB+MASLD group had significantly lower serum level of pregenomic RNA （Z=-2.894， P<0.05） and HBeAg positivity rate （χ2=8.725， P<0.05）， and CAP was significantly negatively correlated with pgRNA （r=-0.117， P<0.05）. In the HBeAg-negative subgroup， compared with the CHB group， the CHB+MASLD group had a significantly lower level of hepatitis B surface antigen （Z=-0.765， P<0.05）； in the HBeAg-positive subgroup， the CHB+MASLD group had a significantly higher level of HBV DNA than the CHB group （Z=-2.509， P<0.05）. The analysis of hepatic fibrosis showed that the CHB+MASLD group had significantly lower values of APRI （Z=-3.418， P<0.05） and FIB-4 （Z=-6.237， P<0.05）. Compared with the CHB group， the CHB+MASLD S1 group had a significantly higher proportion of patients without fibrosis and a significantly lower proportion patients with liver cirrhosis （χ2=7.935， P<0.05）； in the CHB+MASLD S2 group， there was no significant difference in the proportion of patients with different fibrosis stages； the CHB+MASLD S3 group had a significantly lower proportion of patients without fibrosis and a significantly higher proportion of patients with early-stage fibrosis （χ2=9.101， P<0.05）. The Logistic regression analysis showed that an increase in CAP （odds ratio ［OR］=1.08， 95% confidence interval ［CI］： 1.03 — 1.13， P<0.05）， an increase in age （OR=1.02， 95%CI： 1.01 — 1.04， P<0.05）， male sex （OR=1.77， 95%CI： 1.19 — 2.64， P<0.05）， an increase in HBV DNA （OR=1.35， 95%CI： 1.15 — 1.57， P<0.001）， an increase in aspartate aminotransferase （OR=1.02， 95%CI： 1.01 — 1.03， P<0.001）， and an increase in gamma-glutamyl transpeptidase （OR=1.00， 95%CI： 1.00 — 1.01， P=0.028） were independent influencing factors for hepatic fibrosis. The risk of hepatic fibrosis in S3 patients was higher than that in patients without steatosis （OR=5.05， 95%CI： 2.48 — 10.29， P<0.001）. Conclusion There is a lower level of HBV replication in CHB patients comorbid with MASLD. Hepatic steatosis is associated with HBV-related virological markers and the progression of hepatic fibrosis， and severe fatty liver disease may promote the progression of hepatic fibrosis in CHB patients.
2026, 42(6): 1287-1293.
DOI: 10.12449/JCH260609
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Objective To investigate the efficacy and safety of simplified diagnosis and treatment strategies and regimens in the treatment of patients with human immunodeficiency virus （HIV）/hepatitis C virus （HCV） co-infection. Methods This multicenter prospective real-world study was conducted among 198 patients with HIV/HCV co-infection who received hepatitis C treatment in 10 designated primary hospitals for hepatitis C in Yuxi， China from July 2023 to June 2024， and according to whether genotype detection was performed， they were divided into genotype detection group with 122 patients and non-genotype detection group with 76 patients. The patients were observed in terms of sustained virologic response at 12 weeks （SVR12）， safety， and liver biochemical parameters. Propensity score matching was used to match the two cohorts， using caliper matching （caliper value = 0.02） at a ratio of 1∶1. The independent-samples t test or the Wilcoxon signed-rank test was used for comparison of continuous data between two groups， and the chi-square test was used for comparison of categorical data between groups. Results Among the 122 patients in the genotype detection group， 63.11% （77/122） had genotype 3， while the non-genotype detection group had 76 patients； both groups achieved an SVR12 rate of 100%. From baseline to 12 weeks after treatment， both groups had a significant increase in the serum level of albumin， significant reductions in the serum levels of total bilirubin， alanine aminotransferase， aspartate aminotransferase， and alpha-fetoprotein， and a significant reduction in FibroScan value （all P<0.05）. A total of 54 patients （27.27%） experienced at least one adverse reaction， and anemia was the most common adverse reaction （38 patients， 19.19%）， with an incidence rate of 50.00% （33/66） in patients with liver cirrhosis. HIV viral load remained <50 IU/mL before and after treatment， and there was no significant change in CD4+ T lymphocyte count after treatment （Z=-0.969， P=0.202）. Compared with the genotype detection group， the non-genotype detection group had a significantly shorter time from positive HCV RNA testing to treatment initiation （4±2 days vs 19±4 days， t=5.321， P<0.05） and significantly lower testing costs （618±97 yuan vs 789±129 yuan， t=3.661， P<0.05）. Conclusion For patients with HIV/HCV co-infection， the simplified diagnosis and treatment strategies can achieve a relatively high SVR12 rate， improve biochemical indicators， and effectively reduce time cost and economic burden， with a favorable safety profile.
2026, 42(6): 1294-1300.
DOI: 10.12449/JCH260610
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Objective To perform metabolic associated fatty liver disease （MAFLD） screening among individuals attending community health institutions， to identify the patients at a low， moderate or high risk of advanced liver fibrosis based on fibrosis-4 index （FIB-4） and liver stiffness measurement （LSM） measured by liver transient elastography， and to implement stratified management. Methods A cross-sectional study was conducted among 630 individuals attending Beijing Baizhifang Community Health Service Center from January to July 2024， and they were divided into MAFLD group and non-MAFLD group. According to body mass index （BMI）， the MAFLD group was further divided into lean MAFLD group （BMI<23 kg/m2） and non-lean MAFLD group （BMI≥23 kg/m2）. The above groups were compared in terms of demographic features， laboratory markers， hepatic steatosis， and LSM. Fibrosis risk stratification was performed for MAFLD patients based on FIB-4 and LSM， and a closed-loop management system involving referral to tertiary hospitals and follow-up at community health institutions was implemented. The Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups， and the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. Results There were 445 individuals （70.6%） in the MAFLD group and 185 individuals （29.4%） in the non-MAFLD group. Compared with the non-MAFLD group， the MAFLD group had a significantly lower proportion of male individuals （χ2=4.299， P<0.05）， a significant reduction in the level of high-density lipoprotein cholesterol （Z=3.484， P<0.05）， and significant increases in body weight （Z=-7.366， P<0.05）， BMI （Z=-9.740， P<0.05）， waist circumference （Z=-6.397， P<0.05）， hip circumference （Z=-6.935， P<0.05）， alanine aminotransferase （ALT） （Z=-2.765， P<0.05）， fasting blood glucose （Z=-3.646， P<0.05）， triglyceride （TG） （Z=-6.569， P<0.05）， total cholesterol （Z=-2.033， P<0.05）， low-density lipoprotein cholesterol （Z=-2.935， P<0.05）， controlled attenuation parameter （CAP） （Z=-19.784， P<0.05）， and LSM （Z=-5.703， P<0.05）. Within the MAFLD group， there were 124 individuals （27.9%） in the lean MAFLD group and 321 individuals （72.1%） in the non-lean MAFLD group. Compared with the non-lean MAFLD group， the lean MAFLD group had significantly lower body weight （Z=-12.414， P<0.05）， BMI （Z=-16.363， P<0.05）， waist circumference （Z=-7.733， P<0.05）， hip circumference （Z=-8.595， P<0.05）， ALT （Z=-2.835， P<0.05）， aspartate aminotransferase （Z=-1.972， P<0.05）， TG （Z=-2.407， P<0.05）， CAP （Z=-4.429， P<0.05）， degree of steatosis （χ2=16.588， P<0.05）， and LSM （Z=-3.908， P<0.05）. Based on the results of FIB-4 and LSM， 76 patients at a moderate or high risk of liver fibrosis should be referred to a higher-level hospital for further management. Conclusion The detection rate of MAFLD reaches 70.6% among the individuals attending community health institutions， among whom 76 （17.1%） should be referred to a higher-level hospital. Establishing a liver fibrosis risk stratification and management system based on FIB-4 and LSM among MAFLD individuals in communities provides a practical pathway for chronic disease management and referral system construction in community health institutions.
2026, 42(6): 1301-1309.
DOI: 10.12449/JCH260611
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Objective To investigate whether there exists an independent association beyond shared risk factors between colorectal space-occupying lesions and metabolic associated fatty liver disease （MAFLD）， and to provide new ideas for early identification of colorectal space-occupying lesions in the MAFLD population. Methods A retrospective analysis was performed for 12 252 patients who were hospitalized in The First Affiliated Hospital of Shandong First Medical University （Shandong Provincial Qianfoshan Hospital） and underwent both colonoscopy and abdominal imaging （abdominal ultrasound， magnetic resonance imaging， or computed tomography） from September 1， 2018 to August 31， 2023. According to colonoscopy findings， the patients were divided into colorectal space-occupying lesion group with 6 545 patients and non-colorectal space-occupying lesion group with 5 707 patients. Baseline data were compared between the two groups. The univariate and multivariate Logistic regression analyses were used to identify influencing factors for colorectal space-occupying lesions， and further analysis was performed to investigate the association of MAFLD and liver fibrosis （assessed by fibrosis-4 ［FIB-4］， nonalcoholic fatty liver disease fibrosis score ［NFS］， and aspartate aminotransferase-to-platelet ratio index） with colorectal space-occupying lesions. The Mann-Whitney U test was used for comparison of continuous data with skewed distribution between groups， and the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. Results The univariate analysis showed that compared with the non-colorectal space-occupying lesion group， the colorectal space-occupying lesion group had significantly higher age （Z=-95.628， P<0.001）， proportion of male patients （χ2=406.910， P<0.001）， body weight （Z=-24.928， P<0.001）， body mass index （BMI） （Z=-21.367， P<0.001）， diastolic blood pressure （Z=-15.527， P<0.001）， systolic blood pressure （Z=-16.965， P<0.001）， proportion of patients with history of coronary heart disease （χ2 =28.112， P<0.001）/hypertension （χ2 =152.993， P<0.001）/diabetes （χ2 =52.175， P<0.001）/cerebral infarction （χ2 =14.097， P<0.001）， white blood cell count （WBC） （Z=-12.801， P<0.001）， hemoglobin （HGB） （Z=-19.258， P<0.001）， aspartate aminotransferase （Z=-6.673， P=0.001）， alanine aminotransferase （Z=-10.375， P<0.001）， alkaline phosphatase （Z=-10.496， P<0.001）， gamma-glutamyl transpeptidase （GGT） （Z=-18.893， P<0.001）， blood urea nitrogen （Z=-13.291， P<0.001）， creatinine （Z=-16.798， P<0.001）， uric acid （Z=-16.822， P<0.001）， triglyceride （Z=-10.186， P<0.001）， and fasting blood glucose （Z=-15.761， P<0.001）. The multivariate Logistic regression analysis showed that age （odds ratio ［OR］=1.052， 95% confidence interval ［CI］： 1.045 — 1.057， P<0.001）， sex （OR=0.523， 95%CI： 0.466 — 0.587， P<0.001）， BMI （OR=1.031， 95%CI： 1.018 — 1.046， P<0.001）， history of hypertension （OR=1.140， 95%CI： 1.019 — 1.276， P=0.022）， WBC （OR=1.057， 95%CI： 1.028 — 1.087， P<0.001）， GGT （OR=1.001， 95%CI： 1.000 — 1.002， P=0.021）， Alb （OR=0.982， 95%CI： 0.969 — 0.995， P=0.008）， and HGB （OR=1.004， 95%CI： 1.001 — 1.008， P=0.019） were independent influencing factors for colorectal space-occupying lesions. In the MAFLD population， after adjustment for age， sex， BMI， history of hypertension， WBC， HGB， GGT， and Alb， intermediate-to-high risk of advanced liver fibrosis assessed by FIB-4 and NFS was still an influencing factor for colorectal space-occupying lesions （FIB-4： OR=1.457， 95%CI： 1.176 — 1.810， P<0.05； NFS： OR=1.499， 95%CI： 1.244 — 1.809， P<0.05）. Liver fibrosis degree based on FIB-4 was not significantly associated with the pathological type， location， size， or number of colorectal space-occupying lesions （all P>0.05）. While intermediate-to-high risk of advanced liver fibrosis based on NFS was not associated with pathological type， location， or size， it might be associated with the number of lesions （χ2=9.770， P<0.05）. Conclusion Age， sex， BMI， history of hypertension， WBC， HGB， GGT， and Alb are independent influencing factors for colorectal space-occupying lesions. Intermediate-to-high risk of advanced liver fibrosis assessed by FIB-4 or NFS is independently associated with colorectal space-occupying lesions， and liver fibrosis assessed by NFS might be associated with the increase in the number of lesions.
2026, 42(6): 1310-1320.
DOI: 10.12449/JCH260612
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Objective To investigate the effect of SU056， an azo-podophyllotoxin derivative， on carbon tetrachloride （CCl4）-induced liver fibrosis in mice and related mechanisms of action. Methods A total of 12 mice were randomly divided into control group， model group （CCl4+normal saline）， and treatment group （CCl4+SU056）， with 4 mice in each group. Mice were given intraperitoneal injection of CCl4 to establish a model of liver fibrosis， and during the middle stage of modeling， the mice in the treatment group were given daily intraperitoneal injection of SU056. Liver histopathological injury， collagen deposition， and liver function were assessed based on HE staining， Masson staining， Sirius Red staining， the content of hydroxyproline in liver tissue， and the serum levels of alanine aminotransferase and aspartate aminotransferase， and immunofluorescence assay was used to measure the expression levels of smooth muscle actin α （α-SMA）， collagen type Ⅰ， and Y-box binding protein 1 （YB1）. The human hepatic stellate cell （HSC） line LX-2 and primary mouse HSC were used， and CCK-8 assay was used to measure cell proliferation； Transwell assay was used to observe cell migration； quantitative reverse transcription-polymerase chain reaction and Western Blot were used to measure the expression levels of collagen type Ⅰ， collagen type Ⅲ， YB1， phosphorylated mammalian target of rapamycin （mTOR）， and phosphorylated S6K， so as to validate the function of the YB1/mTOR signaling axis. The one-way or two-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups. Results In the mouse model of liver fibrosis induced by CCl4， compared with the model group， the treatment group had significant alleviation of inflammatory cell infiltration， collagen deposition， and pseudolobule formation in liver tissue and significant reductions in the serum levels of alanine aminotransferase and aspartate aminotransferase and the content of hydroxyproline in liver tissue （all P<0.01）. Immunofluorescence assay showed that SU056 significantly inhibited the abnormal high expression of α-SMA， collagen type I， and YB1 in liver tissue （all P<0.01）. In vitro experiments showed that SU056 inhibited the transforming growth factor-β1-induced proliferation of LX-2 cells （P<0.01）， the migration of LX-2 cells （P<0.05）， and the transcriptional up-regulation of collagen type Ⅰ and collagen type Ⅲ （all P<0.05） in a dose-dependent manner， and SU056 could inhibit the spontaneous activation of primary HSC in vitro. Mechanistic studies revealed that transforming growth factor-β1 simultaneously upregulated the expression levels of YB1， phosphorylated mTOR， and phosphorylated S6K in LX-2 cells， and treatment with SU056 （10 and 20 µmol/L） could downregulate the protein expression levels of collagen type I， YB1， phosphorylated mTOR， and phosphorylated S6K. Specific knockdown of YB1 or administration of the mTOR inhibitor rapamycin exerted a similar effect as SU056. SU056 also inhibited the co-upregulation of α-SMA and phosphorylated mTOR in liver tissue of model mice （P<0.01）. Conclusion SU056 can effectively inhibit HSC activation， proliferation， migration， and extracellular matrix production both in vivo and in vitro and thus delay the progression of liver fibrosis， by disrupting the YB1/mTOR positive feedback signaling axis.
2026, 42(6): 1321-1326.
DOI: 10.12449/JCH260613
Abstract:
Objective To investigate the potential differences in cardiac lesions between the patients with viral， alcoholic or biliary cirrhosis. Methods A retrospective analysis was performed for the clinical data of 512 patients who were hospitalized in Hunan Provincial People’s Hospital due to liver cirrhosis from January 2020 to December 2023， and according to the etiology， the patients were divided into viral cirrhosis group with 275 patients， alcoholic cirrhosis group with 70 patients， and biliary cirrhosis group with 167 patients. A one-way analysis of variance was used for comparison of normally distributed continuous data between multiple groups， and the least significant difference t-test or the Tamhane’s T2 test was used based on homogeneity of variance for further comparison between two groups； the Kruskal-Wallis H test was used for comparison of non-normally distributed continuous data between multiple groups； the chi-square test was used for comparison of categorical data between groups. Results There was a significant difference in sex distribution between the three groups， and the male patients accounted for 71.3% in the viral cirrhosis group and 95.7% in the alcoholic cirrhosis group， while the female patients accounted for 64.7% in the biliary cirrhosis group. The biliary cirrhosis group had an age of 61.67±9.59 years， which was significantly higher than that in the other two groups （P<0.05）. Compared with the viral cirrhosis group and the biliary cirrhosis group， the alcoholic cirrhosis group had significantly higher Child-Pugh score （H=30.598， P<0.05）， globulin （H=13.350， P<0.05）， and QTc interval （F=9.956， P<0.05） and significantly lower hemoglobin （F=4.529， P<0.05）， prothrombin activity （F=36.293， P<0.05）， and albumin （F=15.744， P<0.05）. There were no significant differences in each echocardiography parameter between the viral cirrhosis group and the alcoholic cirrhosis group （P>0.05）； compared with the biliary cirrhosis group， the viral cirrhosis group and the alcoholic cirrhosis group had significantly larger left atrial anterior-posterior diameter （H=19.197， P<0.05）， left ventricular end-diastolic diameter （LVEDD） （H=15.660， P<0.05）， right atrial transverse diameter （H=22.854， P<0.05）， mid-right ventricular transverse diameter （H=10.936， P<0.05）， interventricular septal thickness in diastole （IVSd） （H=13.539， P<0.05）， and left ventricular posterior wall thickness in diastole （LVPWd） （H=14.139， P<0.05）； compared with the biliary cirrhosis group， the viral cirrhosis group had a significantly higher mitral ratio of peak early to late diastolic filling velocity （E/A） （P<0.05）. Left ventricular diastolic dysfunction was observed in 170 patients （61.8%） in the viral cirrhosis group， 45 patients （64.3%） in the alcoholic cirrhosis group， and 125 patients （74.9%） in the biliary cirrhosis group， with a significant difference between the three groups （χ2=8.074， P=0.018）. The patients were divided into grade A， B， and C groups based on Child-Pugh score， and comparisons of echocardiography findings between the three groups showed no significant differences in LVEDD， IVSd， LVPWd， E/A， and left ventricular ejection fraction （all P>0.05）. Conclusion There are differences in cardiac structure and function between patients with different etiologies of liver cirrhosis， and in clinical practice， individualized cardiac assessment and intervention should be performed based on different etiologies.
2026, 42(6): 1327-1334.
DOI: 10.12449/JCH260614
Abstract:
Objective To investigate the independent risk factors for decompensation in patients with liver cirrhosis， to construct a nomogram-based risk assessment model， and to assess its risk assessment performance and clinical value by comparing it with Model for End-Stage Liver Disease （MELD）， MELD combined with serum sodium concentration （MELD-Na）， and MELD 3.0 scoring system. Methods A retrospective analysis was performed for 514 patients with liver cirrhosis who attended The First Hospital of Shanxi Medical University from January 2020 to May 2025， and related data were collected， including demographic data and laboratory markers. According to the presence or absence of decompensation， the patients were divided into compensation group with 275 patients and decompensation group with 239 patients. The Mann-Whitney U test was used for comparison of continuous data between two groups， and the chi-square test was used for comparison of categorical data between two groups. The least absolute shrinkage and selection operator regression analysis was used for screening of variables， and the multivariate logistic regression analysis was used to identify independent risk factors for decompensated liver cirrhosis and construct a nomogram model. The receiver operating characteristic （ROC） curve， calibration curve， and decision curve analysis were used to assess the discriminatory ability， calibration， and net clinical benefit of the model. Results The multivariate logistic regression analysis showed that low hemoglobin （odds ratio ［OR］=0.984， 95% confidence interval ［CI］： 0.969 — 0.999， P<0.05）， low lymphocytes （OR=0.564， 95%CI： 0.383 — 0.830， P<0.05）， high international normalized ratio （OR=3.131， 95%CI： 1.242 — 7.891， P<0.05）， and low serum sodium （OR=0.922， 95%CI： 0.872 — 0.975， P<0.05） were independent risk factors for decompensation events in patients with liver cirrhosis. Construct the prediction model equation： Logit（P）=intercept value－0.016×hemoglobin－0.573×lymphocytes+1.141×INR－0.081×serum sodium. The nomogram constructed based on these factors had a good discriminatory ability， with an area under the ROC curve （AUC） of 0.787， a specificity of 77.8%， and a sensitivity of 67.4%， and it had significantly better predictive performance than MELD score （AUC=0.718）， MELD-Na score （AUC=0.719）， and MELD 3.0 score （AUC=0.725）. The calibration curve showed good consistency between the probability of risk assessed by the model and the observed probability. The decision curve analysis showed that compared with the MELD-based scores， this model provided higher net clinical benefit across a wide range of risk thresholds. Conclusion This study successfully constructed and validated a nomogram risk assessment model incorporating hemoglobin， international normalized ratio， lymphocytes， and serum sodium. This model has good clinical practicability and can help to achieve early identification of high-risk patients with decompensated liver cirrhosis and optimize intervention strategies in clinical practice.
2026, 42(6): 1335-1341.
DOI: 10.12449/JCH260615
Abstract:
Objective To investigate the efficacy and safety of lenvatinib combined with sintilimab versus atezolizumab combined with bevacizumab in patients with unresectable hepatocellular carcinoma （uHCC）， aims to provide real-world evidence for clinical personalized treatment. Methods A retrospective analysis was performed for 78 patients with uHCC who were admitted to Beijing Ditan Hospital， Capital Medical University， from January 1， 2023， to May 31， 2025， and according to the treatment modality， they were divided into lenvatinib+sintilimab group （L+S group with 49 patients） and atezolizumab+bevacizumab group （A+T group with 29 patients）. The primary endpoints were progression-free survival （PFS） and overall survival （OS）， and the secondary endpoints included objective response rate （ORR）， disease control rate （DCR）， and the incidence rate of adverse events. The independent-samples t test was used for comparison of normally distributed continuous data between groups， and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between groups； the chi-square test was used for comparison of categorical data between groups. The Kaplan-Meier method was used for survival analysis， and the log-rank test was used for comparison between groups. Results The 78 patients had a median PFS of 9 months and a median OS of 15 months. The median PFS was 11 months in the L+S group and 7 months in the A+T group， with no significant difference between the two groups （χ2=0.247， P=0.619）； the median OS was 19 months in the L+S group and 12 months in the A+T group， with a significant difference between the two groups （χ2=6.565， P=0.010）. There were no significant differences between the two groups in complete remission， partial remission， stable disease， disease progression， DCR， and ORR （all P>0.05）. The L+S group had a significantly higher incidence rate of adverse events than the A+T group （95.9% vs 75.9%， P=0.007）， and there was a significant difference in the incidence rate of grade ≥3 adverse events between the L+S group and the A+T group （65.3% vs 34.5%， P=0.008）. Conclusion Compared with atezolizumab combined with bevacizumab， lenvatinib combined with sintilimab can improve the OS of patients with uHCC， while atezolizumab combined with bevacizumab has a better safety profile.
2026, 42(6): 1342-1348.
DOI: 10.12449/JCH260616
Abstract:
Objective To investigate the association of the serum levels of Golgi protein 73 （GP73）， hypoxia-inducible factor-1α （HIF-1α）， and matrix metalloproteinase-9 （MMP-9） before and after transcatheter arterial chemoembolization （TACE） with the treatment outcome of patients with hepatitis B virus （HBV）-related hepatocellular carcinoma （HCC）. Methods A total of 135 patients with HBV-related HCC who received TACE for the first time in The First Affiliated Hospital of Xinjiang Medical University from January 2023 to October 2025 were enrolled as subjects， and the serum levels of GP73， HIF-1α， and MMP-9 were measured before TACE and at 1 month after TACE. According to the treatment outcome after TACE， the patients were divided into remission group and non-remission group. The two groups were compared in terms of general information and the serum levels of GP73， HIF-1α， and MMP-9 before and after treatment. The Logistic regression analysis was used to investigate the influencing factors for the efficacy of TACE， and the receiver operating characteristic （ROC） curve was used to assess the value of the serum levels of GP73， HIF-1α， and MMP-9 before treatment used alone or in combination in predicting the efficacy of TACE. The independent-samples t test was used for comparison of continuous data between two groups， and the chi-square test was used for comparison of categorical data between two groups. Results Among the 135 patients after treatment， 78 （57.78%） were enrolled in the remission group and 57 （42.22%） were enrolled in the non-remission group. Before treatment， the remission group had significantly lower serum levels of GP73， HIF-1α， and MMP-9 than the non-remission group （all P<0.05）； after treatment， both groups had reductions in the serum levels of GP73， HIF-1α， and MMP-9， and the remission group had significantly lower levels than the non-remission group （all P<0.05）. The binary Logistic regression analysis showed that increases in the serum levels of GP73， HIF-1α， and MMP-9 before treatment were independent influencing factors for the efficacy of TACE （all P<0.05）. The ROC curve analysis showed that the serum levels of GP73， HIF-1α， and MMP-9 before treatment used alone had an area under the ROC curve （AUC） of 0.799， 0.835， and 0.777， respectively， in predicting the efficacy of TACE， among which HIF-1α showed the highest predictive value， and the combination of these three indicators had an AUC of 0.950， a Youden index of 0.787， an optimal cut-off value of 0.39， a sensitivity of 87.72%， and a specificity of 91.03%. Conclusion TACE can reduce the serum levels of GP73， HIF-1α， and MMP-9 in patients with HBV-related HCC， and patients with a good outcome tend to have greater reductions. The high serum levels of GP73， HIF-1α， and MMP-9 before treatment are independent risk factors for poor short-term efficacy of TACE， and the combination of these three indicators has a relatively high value in predicting the efficacy of TACE.
2026, 42(6): 1349-1357.
DOI: 10.12449/JCH260617
Abstract:
Objective To investigate the efficacy and safety of Shuganning injection in the treatment of liver injury by observing the clinical outcome of patients with liver injury after treatment with Shuganning injection and comparing it with reduced glutathione （GSH）. Methods This study was conducted among 175 patients with liver injury who attended 6 hospitals in China （Beijing YouAn Hospital， Capital Medical University； Nanyang First People’s Hospital； The Second Affiliated Hospital of Xi’an Jiaotong University； The Fifth Medical Center of Chinese PLA General Hospital； The Third Hospital of Hebei Medical University； The Affiliated Hospital of Guizhou Medical University） from April 25， 2019 to February 28， 2022. The patients were divided into experimental group （89 patients treated with Shuganning injection） and control group （86 patients treated with GSH）， and the course of treatment was 4 weeks for both groups. Related indicators were recorded before treatment， after treatment， and after drug withdrawal for 8 weeks， including liver function parameters， blood biochemical parameters， blood lipids， coagulation profiles， liver fibrosis markers， traditional Chinese medicine （TCM） syndrome score， and ultrasound findings， as well as adverse events during treatment. The Wilcoxon rank-sum test was used for comparison of continuous data between two groups， and the chi-square test was used for comparison of categorical data between two groups. The Wilcoxon signed-rank test was used for comparison of observation indicators before treatment， at week 4 of treatment， and after drug withdrawal for 8 weeks. When the efficacy evaluation of TCM syndromes was used as the outcome， a pooled analysis was performed for the effective cases and the markedly effective cases， and a Logistic regression model was used to calculate the odds ratio （OR） and its 95%CI. Results After 4 weeks of treatment with Shuganning injection， the patients showed significant reductions in TCM syndrome score （P<0.001） and the levels of aspartate aminotransferase， alanine aminotransferase， total bilirubin， and direct bilirubin （all P<0.001） and a significant increase in the level of albumin （P=0.002）， and these significant improvements persisted after drug withdrawal for 8 weeks. Furthermore， compared with the control group， the experimental group had a significantly higher proportion of patients assessed as effective or markedly effective cases （48.31% vs 32.56%， P=0.033）. Compared with the control group， the experimental group had a significantly greater change in TCM syndrome score at weeks 1-4 of treatment and after drug withdrawal for 8 weeks （P<0.05）. At week 4 of treatment， the experimental group had a significantly greater reduction in alanine aminotransferase than the control group （P<0.05）， and at week 8 after drug withdrawal， the experimental group had a significantly greater reduction in alanine aminotransferase and aspartate aminotransferase than the control group （all P<0.05）. One patient in the experimental group （1.12%） experienced an adverse event， which was determined to be associated with the progression of viral hepatitis. Conclusion Shuganning injection can effectively improve liver injury， with good long-term efficacy and a low incidence rate of adverse reactions.
2026, 42(6): 1358-1366.
DOI: 10.12449/JCH260618
Abstract:
Objective To investigate the risk factors for postpancreatectomy acute pancreatitis （PPAP） after minimally invasive pancreaticoduodenectomy （MIPD） and their association with major complications， to improve the understanding of PPAP and postoperative pancreatic fistula （POPF）， and to reduce the incidence rates of PPAP and POPF. Methods A retrospective analysis was performed for the clinical data of 114 patients who underwent MIPD in Department of Hepatobiliary and Pancreatic Surgery， The First Affiliated Hospital of University of South China， from March 2015 to December 2023， and the definition of PPAP and its diagnostic criteria provided by the International Study Group of Pancreatic Surgery were used to determine the presence or absence of PPAP. The independent samples t-test or the Mann-Whitney U rank sum test was used for comparison of continuous data between groups， and the Kruskal-Wallis H test was used for comparison between multiple groups， and the Dunn-test was used for further comparison between two groups.； the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups.， and the Bonferroni-test was used for further comparison between two groups. The multivariate logistic regression analysis was used to identify the risk factors for PPAP after MIPD. Results Of all 114 patients undergoing MIPD， 27 （23.7%） experienced PPAP. The multivariate analysis showed that main pancreatic duct diameter ≤3 mm （odds ratio ［OR］=5.083， 95% confidence interval ［CI］： 1.703 — 15.172， P=0.004）， soft pancreatic texture （OR=5.925， 95%CI： 1.986 — 17.677， P=0.001）， and C-reactive protein ≥180 mg/L on day 1 after surgery （OR=5.419， 95%CI： 1.586 — 18.513， P=0.007） were independent risk factors for the onset of PPAP after MIPD. Clinical analyses showed that the patients with PPAP tended to have significantly higher incidence rates of POPF， peritoneal infection， Clavien-Dindo grade 3/4 complications， discharge with tube， and 90-day postoperative death （χ2 =5.676， 5.460， 9.863， 5.439， and 4.207， all P<0.05）. Conclusion Main pancreatic duct diameter， pancreatic texture， and C-reactive protein on day 1 after surgery are closely associated with the onset of PPAP after MIPD， and PPAP can lead to other postoperative complications and even death.
2026, 42(6): 1367-1374.
DOI: 10.12449/JCH260619
Abstract:
Objective To investigate the value of triglyceride-glucose index （TyG） and triglyceride-glucose-body mass index （TyG-BMI） in predicting new-onset diabetes mellitus （NODM） after distal pancreatectomy （DP）. Methods A retrospective analysis was performed for the clinical data of 161 patients without diabetes before surgery who underwent DP in The First Affiliated Hospital of Xinjiang Medical University from January 2020 to December 2024， and according to the presence or absence of NODM after surgery， they were divided into NODM group and non-NODM group. Baseline clinical data were compared between groups. A multivariate logistic regression analysis was used to investigate the association of TyG and TyG-BMI with NODM， and the restricted cubic spline model was used to analyze the dose-response relationship between TyG/TyG-BMI and the risk of NODM. The receiver operating characteristic （ROC） curve was used to assess the performance of TyG and TyG-BMI in predicting NODM. Results Among the 161 patients included in the analysis， 43 （26.7%） developed NODM after DP. Compared with the non-NODM group， the NODM group had significantly higher TyG （8.89±0.57 vs 8.54±0.56， P<0.001） and TyG-BMI ［232.18 （195.31 — 249.68） vs 195.39 （178.92 — 221.38）， P<0.001］. The multivariate logistic regression analysis showed that after adjustment for age， sex， and hemoglobin A1c， both TyG （odds ratio ［OR］=2.78， 95% confidence interval ［CI］： 1.43 — 5.39， P=0.003） and TyG-BMI （OR=1.02， 95%CI： 1.01 — 1.04， P<0.001） remained independent risk factors for NODM after DP. The restricted cubic spline analysis showed an approximately linear positive correlation between TyG/TyG-BMI and the risk of NODM. The ROC curve analysis showed that TyG and TyG-BMI had a moderate predictive value for NODM after DP， with an area under the ROC curve of 0.725 （95%CI： 0.683 — 0.867） and 0.719 （95%CI： 0.610 — 0.810）， respectively. Conclusion TyG and TyG-BMI are independent predictive factors for the onset of NODM after DP， with a certain predictive value in the diagnosis of NODM. These two simple metabolic indicators may become helpful tools for the early identification of patients at a high risk of NODM after DP.
2026, 42(6): 1375-1382.
DOI: 10.12449/JCH260620
Abstract:
Objective To investigate the application value of a predictive model constructed based on quantitative imaging parameters and serum tumor markers in predicting the postoperative prognosis of patients with pancreatic ductal adenocarcinoma （PDAC）. Methods A retrospective study was conducted among 146 patients with PDAC who underwent radical resection in Hebei Medical University Fourth Hospital from April 2020 to March 2023， and the patients were divided into a training set with 102 patients and a validation set of 44 patients at a ratio of 7∶3 using the completely randomized method. All patients underwent enhanced computed tomography （CT） and multi-parametric magnetic resonance imaging scans， and CT values in the arterial phase， the venous phase， and the delayed phase were recorded， as well as apparent diffusion coefficient （ADC） at b = 800 s/mm2 and signal intensity （SI） of T2 weighted imaging. The serum levels of carbohydrate antigen 19-9 （CA19-9） and carcinoembryonic antigen （CEA） were also measured. The independent-samples t test was used for comparison of continuous data between groups， and the chi-square test was used for comparison of categorical data between groups. Kaplan-Meier survival curves were plotted for survival analysis； the univariate and multivariate Logistic regression analysis was used to investigate the association of clinical and imaging indicators with prognosis； the least absolute shrinkage and selection operator （LASSO）-Cox regression model was used to identify the important influencing factors for prognosis， and a prognostic prediction model was constructed. The receiver operating characteristic （ROC） curve was used to analyze the predictive value of the model in predicting prognosis in both the training set and the validation set. Results The Kaplan-Meier survival curve analysis showed a median survival time of 33.00 months in the training set and 32.00 months in the validation set， with no significant difference between the training set and the validation set （P>0.05）. The univariate analysis showed that patient age， degree of tumor differentiation， lymph node metastasis， tumor stage， vascular invasion， CA19-9， CEA， ADC value， and SI value were significantly associated with the survival prognosis of patients （χ²=5.906， 13.116， 12.807， 17.277， 14.611， 7.275， 14.339， 9.506， and 13.137， all P<0.05）. The LASSO-Cox multivariate regression analysis showed that six factors were incorporated into the regression model， i.e.， tumor stage （HR=8.934， 95%CI： 3.215 — 21.562， P<0.001）， lymph node metastasis （HR=2.971， 95%CI： 1.298 — 5.647， P=0.002）， CA19-9 （HR=3.948， 95%CI： 1.758 — 8.994， P<0.001）， CEA （HR=1.965， 95%CI： 1.083 — 3.664， P=0.039）， ADC value （HR=2.873， 95%CI： 1.307 — 6.037， P=0.003）， and SI value （HR=3.107， 95%CI： 1.264 — 7.339， P=0.001）. The nomogram model constructed based on these factors had an area under the ROC curve of 0.845 （95%CI： 0.774 — 0.915） in the training set and 0.919 （95%CI： 0.870 — 0.967） in the validation set. Conclusion The combined model of quantitative imaging parameters and serum tumor markers constructed based on LASSO-Cox regression can effectively predict the postoperative prognosis of PDAC patients， thereby helping to identify high-risk patients and guide decision-making for adjuvant therapy.
2026, 42(6): 1383-1387.
DOI: 10.12449/JCH260621
Abstract:
Fecal microbiota transplantation （FMT） has been widely used in the treatment of gastrointestinal disorders， particularly Clostridium difficile infection， while there are few reports of its application in the diagnosis and treatment of cirrhotic ascites. This article reports a case of a patient with cirrhotic ascites and chronic diarrhea who received FMT with oral capsules， demonstrating significant short-term efficacy without any adverse reactions， in order to provide a reference for the application of FMT in the treatment of liver diseases.
Fecal microbiota transplantation （FMT） has been widely used in the treatment of gastrointestinal disorders， particularly Clostridium difficile infection， while there are few reports of its application in the diagnosis and treatment of cirrhotic ascites. This article reports a case of a patient with cirrhotic ascites and chronic diarrhea who received FMT with oral capsules， demonstrating significant short-term efficacy without any adverse reactions， in order to provide a reference for the application of FMT in the treatment of liver diseases.
2026, 42(6): 1388-1390.
DOI: 10.12449/JCH260622
Abstract:
Subacute cholecystitis complicated by gallbladder perforation often manifests as inflammatory lesions around the gallbladder， and it is extremely rare for this condition to cause massive hemorrhage into the omental bursa with secondary infection and result in massive hemorrhagic abscess. This article reports a case of a female patient， aged 68 years， who experienced massive hemorrhagic abscess in the omental bursa due to localized perforation and bleeding caused by a stone impacted in the gallbladder neck. The patient had a history of gallstones for 30 years and was admitted to Tianjin Nankai Hospital， Tianjin Medical University， after tertiary referral due to aggravated abdominal pain， chills， and fever. After comprehensive assessment by a multidisciplinary team， the patient underwent emergency laparoscopic cholecystectomy and clearance of the hemorrhagic abscess in the omental bursa. The patient recovered well and was discharged on day 10 after surgery， with good conditions during follow-up.
Subacute cholecystitis complicated by gallbladder perforation often manifests as inflammatory lesions around the gallbladder， and it is extremely rare for this condition to cause massive hemorrhage into the omental bursa with secondary infection and result in massive hemorrhagic abscess. This article reports a case of a female patient， aged 68 years， who experienced massive hemorrhagic abscess in the omental bursa due to localized perforation and bleeding caused by a stone impacted in the gallbladder neck. The patient had a history of gallstones for 30 years and was admitted to Tianjin Nankai Hospital， Tianjin Medical University， after tertiary referral due to aggravated abdominal pain， chills， and fever. After comprehensive assessment by a multidisciplinary team， the patient underwent emergency laparoscopic cholecystectomy and clearance of the hemorrhagic abscess in the omental bursa. The patient recovered well and was discharged on day 10 after surgery， with good conditions during follow-up.
2026, 42(6): 1391-1397.
DOI: 10.12449/JCH260623
Abstract:
Metabolic associated fatty liver disease （MAFLD） is a chronic liver disease with a rapidly increasing incidence rate worldwide， and its complex pathogenesis is closely associated with O-linked β-N-acetylglucosamine （O-GlcNAc） modification. As a dynamic and reversible post-translational modification of proteins， O-GlcNAc modification is mainly regulated by O-GlcNAc transferase and O-GlcNAcase. O-GlcNAc modification can drive hepatic steatosis， exacerbate insulin resistance， and impair mitochondrial function， thereby leading to the aggravation of metabolic disorders， promoting inflammation response， and driving the progression of MAFLD to metabolic associated steatohepatitis and hepatic fibrosis. This article systematically reviews the latest research advances in the role of O-GlcNAc modification in the development and progression of MAFLD， in order to provide theoretical support and research direction for a deeper understanding of the pathological mechanism of MAFLD and the development of effective therapeutic strategies.
Metabolic associated fatty liver disease （MAFLD） is a chronic liver disease with a rapidly increasing incidence rate worldwide， and its complex pathogenesis is closely associated with O-linked β-N-acetylglucosamine （O-GlcNAc） modification. As a dynamic and reversible post-translational modification of proteins， O-GlcNAc modification is mainly regulated by O-GlcNAc transferase and O-GlcNAcase. O-GlcNAc modification can drive hepatic steatosis， exacerbate insulin resistance， and impair mitochondrial function， thereby leading to the aggravation of metabolic disorders， promoting inflammation response， and driving the progression of MAFLD to metabolic associated steatohepatitis and hepatic fibrosis. This article systematically reviews the latest research advances in the role of O-GlcNAc modification in the development and progression of MAFLD， in order to provide theoretical support and research direction for a deeper understanding of the pathological mechanism of MAFLD and the development of effective therapeutic strategies.
2026, 42(6): 1398-1403.
DOI: 10.12449/JCH260624
Abstract:
Metabolic associated fatty liver disease （MAFLD） is a highly prevalent chronic liver disease worldwide， and the mechanism underlying its progression to metabolic associated steatohepatitis and liver fibrosis remain unclear. Endoplasmic reticulum stress （ERS） and ferroptosis （Fer） are deeply involved in the pathological evolution of MAFLD. This article systematically reviews the core regulatory mechanisms of ERS and its role in regulating lipid metabolism， inflammation response， and cell apoptosis in MAFLD. It also analyzes the core mechanism of Fer and discusses the predisposing factors for Fer in the pathological microenvironment of MAFLD， as well as the role of Fer in exacerbating hepatocyte death and activating the progression of liver fibrosis. This article proposes that the crosstalk between ERS and Fer is a key driver for the progression of MAFLD， which provides new references and ideas for the clinical intervention of MAFLD.
Metabolic associated fatty liver disease （MAFLD） is a highly prevalent chronic liver disease worldwide， and the mechanism underlying its progression to metabolic associated steatohepatitis and liver fibrosis remain unclear. Endoplasmic reticulum stress （ERS） and ferroptosis （Fer） are deeply involved in the pathological evolution of MAFLD. This article systematically reviews the core regulatory mechanisms of ERS and its role in regulating lipid metabolism， inflammation response， and cell apoptosis in MAFLD. It also analyzes the core mechanism of Fer and discusses the predisposing factors for Fer in the pathological microenvironment of MAFLD， as well as the role of Fer in exacerbating hepatocyte death and activating the progression of liver fibrosis. This article proposes that the crosstalk between ERS and Fer is a key driver for the progression of MAFLD， which provides new references and ideas for the clinical intervention of MAFLD.
2026, 42(6): 1404-1410.
DOI: 10.12449/JCH260625
Abstract:
The pathogenesis of metabolic associated fatty liver disease （MAFLD） is closely associated with gut microbiota dysbiosis. Dysbiosis can lead to translocation of bacterial derivatives （such as lipopolysaccharide）， which drives hepatic inflammatory response and metabolic imbalance by activating Toll-like receptors （TLR） and their downstream signaling pathways. This article systematically reviews the mechanism of action of the gut microbiota-TLR axis in MAFLD， and elaborates on the function of the key receptors such as TLR2 and TLR4 and the lesser-studied members （TLR5， TLR7， and TLR9）. This article also summarizes the downstream signaling events after TLR activation， including the canonical NF-κB and MAPK pathways， as well as the role of the JAK-STAT and PI3K-Akt pathways in the pathological mechanism of MAFLD. Finally， this article reviews the potential intervention strategies for MAFLD by targeting gut microbiota and regulating the gut microbiota-TLR signaling axis， in order to provide new ideas for clinical prevention and treatment.
The pathogenesis of metabolic associated fatty liver disease （MAFLD） is closely associated with gut microbiota dysbiosis. Dysbiosis can lead to translocation of bacterial derivatives （such as lipopolysaccharide）， which drives hepatic inflammatory response and metabolic imbalance by activating Toll-like receptors （TLR） and their downstream signaling pathways. This article systematically reviews the mechanism of action of the gut microbiota-TLR axis in MAFLD， and elaborates on the function of the key receptors such as TLR2 and TLR4 and the lesser-studied members （TLR5， TLR7， and TLR9）. This article also summarizes the downstream signaling events after TLR activation， including the canonical NF-κB and MAPK pathways， as well as the role of the JAK-STAT and PI3K-Akt pathways in the pathological mechanism of MAFLD. Finally， this article reviews the potential intervention strategies for MAFLD by targeting gut microbiota and regulating the gut microbiota-TLR signaling axis， in order to provide new ideas for clinical prevention and treatment.
2026, 42(6): 1411-1418.
DOI: 10.12449/JCH260626
Abstract:
Metabolic associated fatty liver disease （MAFLD） is the most prevalent chronic liver disease worldwide， and its progression is closely associated with the development of liver fibrosis， liver cirrhosis， and even hepatocellular carcinoma. However， there is still a lack of effective therapies for MAFLD in clinical practice. Telomere is the protective structure at the end of chromosomes， and telomere shortening and functional impairment have been identified as one of the key factors regulating the pathological progression of MAFLD. This article systematically reviews the core mechanism of action of telomere regulation in MAFLD， including its molecular functions in nucleotide metabolism， oxidative stress， and epigenetic regulation， as well as its pathological effect in hepatocytes and hepatic stellate cells. In addition， this article explores the clinical prospects of telomeres as biomarkers and therapeutic targets for MAFLD， in order to provide a theoretical reference for improving the precise diagnosis and treatment system of MAFLD.
Metabolic associated fatty liver disease （MAFLD） is the most prevalent chronic liver disease worldwide， and its progression is closely associated with the development of liver fibrosis， liver cirrhosis， and even hepatocellular carcinoma. However， there is still a lack of effective therapies for MAFLD in clinical practice. Telomere is the protective structure at the end of chromosomes， and telomere shortening and functional impairment have been identified as one of the key factors regulating the pathological progression of MAFLD. This article systematically reviews the core mechanism of action of telomere regulation in MAFLD， including its molecular functions in nucleotide metabolism， oxidative stress， and epigenetic regulation， as well as its pathological effect in hepatocytes and hepatic stellate cells. In addition， this article explores the clinical prospects of telomeres as biomarkers and therapeutic targets for MAFLD， in order to provide a theoretical reference for improving the precise diagnosis and treatment system of MAFLD.
2026, 42(6): 1419-1425.
DOI: 10.12449/JCH260627
Abstract:
Autoimmune hepatitis （AIH） is a chronic inflammatory liver disease mediated by T lymphocytes， and it can progress to liver cirrhosis or even liver failure without timely intervention. As a natural flavonoid compound， naringenin （NAR） shows a potential value in the prevention and treatment of AIH through multiple mechanisms such as remodeling immune homeostasis， targeted inhibition of inflammatory pathways， antioxidation， regulating hepatocyte metabolism and apoptosis， improving mitochondrial function， and regulating intestinal flora. However， the clinical translation and application of NAR is limited by issues such as low bioavailability and insufficient efficiency of liver-targeted delivery. This article systematically reviews the mechanism of action of NAR in the prevention and treatment of AIH， explores the potential signaling pathways involved in this process， and analyzes existing challenges in its translation and application and future research directions， so as to provide a reference for further research on NAR and its application in the prevention and treatment of AIH.
Autoimmune hepatitis （AIH） is a chronic inflammatory liver disease mediated by T lymphocytes， and it can progress to liver cirrhosis or even liver failure without timely intervention. As a natural flavonoid compound， naringenin （NAR） shows a potential value in the prevention and treatment of AIH through multiple mechanisms such as remodeling immune homeostasis， targeted inhibition of inflammatory pathways， antioxidation， regulating hepatocyte metabolism and apoptosis， improving mitochondrial function， and regulating intestinal flora. However， the clinical translation and application of NAR is limited by issues such as low bioavailability and insufficient efficiency of liver-targeted delivery. This article systematically reviews the mechanism of action of NAR in the prevention and treatment of AIH， explores the potential signaling pathways involved in this process， and analyzes existing challenges in its translation and application and future research directions， so as to provide a reference for further research on NAR and its application in the prevention and treatment of AIH.
2026, 42(6): 1426-1432.
DOI: 10.12449/JCH260628
Abstract:
Liver fibrosis is a critical pathological process in the progression of chronic liver diseases and is mainly driven by the activation of hepatic stellate cells， and it is characterized by excessive deposition of extracellular matrix. Programmed cell death is widely observed in liver fibrosis and plays diverse roles in different types of cells. It is not only a mechanism for maintaining cellular homeostasis through metabolism， but it can also regulate the development and progression of diseases. Ferroptosis has recently emerged as a research focus due to its close association with lipid metabolism. This article systematically reviews the related concepts of lipid metabolism， ferroptosis， and liver fibrosis， analyzes the bridging role and dual regulatory function of ferroptosis in lipid metabolism and liver fibrosis， and further highlights the clinical application value of targeting ferroptosis in hepatic stellate cells for the treatment of liver fibrosis， in order to provide new perspectives for the mechanistic studies on liver fibrosis and the optimization of related clinical intervention strategies.
Liver fibrosis is a critical pathological process in the progression of chronic liver diseases and is mainly driven by the activation of hepatic stellate cells， and it is characterized by excessive deposition of extracellular matrix. Programmed cell death is widely observed in liver fibrosis and plays diverse roles in different types of cells. It is not only a mechanism for maintaining cellular homeostasis through metabolism， but it can also regulate the development and progression of diseases. Ferroptosis has recently emerged as a research focus due to its close association with lipid metabolism. This article systematically reviews the related concepts of lipid metabolism， ferroptosis， and liver fibrosis， analyzes the bridging role and dual regulatory function of ferroptosis in lipid metabolism and liver fibrosis， and further highlights the clinical application value of targeting ferroptosis in hepatic stellate cells for the treatment of liver fibrosis， in order to provide new perspectives for the mechanistic studies on liver fibrosis and the optimization of related clinical intervention strategies.
2026, 42(6): 1433-1438.
DOI: 10.12449/JCH260629
Abstract:
Small intestinal bacterial overgrowth （SIBO） is significantly more prevalent in patients with liver cirrhosis. Recent studies indicate that SIBO is not merely a concomitant phenomenon but a key driver of cirrhosis progression via the “gut-liver axis” mechanism. This review innovatively proposes a “microbiota-immunity-fibrosis” pathological positive feedback loop model， systematically elucidating the sequential pathological process through which SIBO drives disease progression via multiple mechanisms—including disruption of intestinal barrier function， facilitation of bacterial and endotoxin translocation， induction of systemic inflammatory responses， and acceleration of hepatic fibrosis. Furthermore， it provides a systematic evaluation of the clinical application value and limitations of current SIBO-targeted therapeutic strategies， such as antibiotic therapy， microbial modulation， herbal medicine interventions， and dietary therapies. This work aims to establish a theoretical foundation and identify future research directions for the development of multi-targeted and personalized comprehensive treatment strategies.
Small intestinal bacterial overgrowth （SIBO） is significantly more prevalent in patients with liver cirrhosis. Recent studies indicate that SIBO is not merely a concomitant phenomenon but a key driver of cirrhosis progression via the “gut-liver axis” mechanism. This review innovatively proposes a “microbiota-immunity-fibrosis” pathological positive feedback loop model， systematically elucidating the sequential pathological process through which SIBO drives disease progression via multiple mechanisms—including disruption of intestinal barrier function， facilitation of bacterial and endotoxin translocation， induction of systemic inflammatory responses， and acceleration of hepatic fibrosis. Furthermore， it provides a systematic evaluation of the clinical application value and limitations of current SIBO-targeted therapeutic strategies， such as antibiotic therapy， microbial modulation， herbal medicine interventions， and dietary therapies. This work aims to establish a theoretical foundation and identify future research directions for the development of multi-targeted and personalized comprehensive treatment strategies.
2026, 42(6): 1439-1446.
DOI: 10.12449/JCH260630
Abstract:
Hepatocellular carcinoma （HCC） is highly prevalent worldwide with a high mortality rate. Despite the continuous advances in current treatment methods such as surgery， targeted drugs， and immunotherapy， there is still a lack of significant improvement in the 5-year survival rate of patients due to strong tumor heterogeneity， high metastatic potential， and a high drug resistance rate. Therefore， it is urgently needed to identify new therapeutic targets. The aberrant activation of Yes-associated protein （YAP） is a pivotal hub for cell proliferation， metastasis， and immune evasion of HCC. This article systematically reviews the multiple regulatory mechanisms underlying YAP activation in HCC， including the promotion of YAP nuclear translocation by Hippo pathway inactivation， G protein-coupled receptor signal activation， and changes in mechanical stress of extracellular matrix. Meanwhile， it summarizes the synergistic crosstalk between YAP and non-classical pathways such as the Wnt pathway， as well as its specific role in remodeling the immune microenvironment and facilitating tumor immune escape by upregulating programmed death ligand 1. In addition， it reviews the development of new technologies such as YAP-TEAD inhibitors and proteolysis-targeting chimera and points out that interactions between the multiple regulatory mechanisms of YAP is a key contributor to tumor heterogeneity and therapeutic resistance. Future research should focus on developing novel inhibitors targeting the YAP regulatory network， designing combined therapy strategies， and establishing molecular biomarker detection systems， which may become pivotal directions for promoting precise treatment of HCC.
Hepatocellular carcinoma （HCC） is highly prevalent worldwide with a high mortality rate. Despite the continuous advances in current treatment methods such as surgery， targeted drugs， and immunotherapy， there is still a lack of significant improvement in the 5-year survival rate of patients due to strong tumor heterogeneity， high metastatic potential， and a high drug resistance rate. Therefore， it is urgently needed to identify new therapeutic targets. The aberrant activation of Yes-associated protein （YAP） is a pivotal hub for cell proliferation， metastasis， and immune evasion of HCC. This article systematically reviews the multiple regulatory mechanisms underlying YAP activation in HCC， including the promotion of YAP nuclear translocation by Hippo pathway inactivation， G protein-coupled receptor signal activation， and changes in mechanical stress of extracellular matrix. Meanwhile， it summarizes the synergistic crosstalk between YAP and non-classical pathways such as the Wnt pathway， as well as its specific role in remodeling the immune microenvironment and facilitating tumor immune escape by upregulating programmed death ligand 1. In addition， it reviews the development of new technologies such as YAP-TEAD inhibitors and proteolysis-targeting chimera and points out that interactions between the multiple regulatory mechanisms of YAP is a key contributor to tumor heterogeneity and therapeutic resistance. Future research should focus on developing novel inhibitors targeting the YAP regulatory network， designing combined therapy strategies， and establishing molecular biomarker detection systems， which may become pivotal directions for promoting precise treatment of HCC.
2026, 42(6): 1447-1453.
DOI: 10.12449/JCH260631
Abstract:
Liver cancer is one of the most prevalent malignant tumors worldwide. Conventional radiotherapy and chemotherapy are often limited by poor targeting efficiency and significant adverse effects. Nanovesicle delivery systems have emerged as a research hotspot due to their superior biocompatibility and targeting potential. This article introduces the fundamental characteristics and main types of nanovesicles， elaborates on their mechanisms in targeting the liver， deeply analyzes their application potential in the treatment of liver cancer and related research advances， and discusses future challenges and development trends， in order to provide a reference for further research and clinical application of nanovesicles in targeted therapy for liver cancer.
Liver cancer is one of the most prevalent malignant tumors worldwide. Conventional radiotherapy and chemotherapy are often limited by poor targeting efficiency and significant adverse effects. Nanovesicle delivery systems have emerged as a research hotspot due to their superior biocompatibility and targeting potential. This article introduces the fundamental characteristics and main types of nanovesicles， elaborates on their mechanisms in targeting the liver， deeply analyzes their application potential in the treatment of liver cancer and related research advances， and discusses future challenges and development trends， in order to provide a reference for further research and clinical application of nanovesicles in targeted therapy for liver cancer.
2026, 42(6): 1454-1461.
DOI: 10.12449/JCH260632
Abstract:
The liver is a vital metabolic organ sustaining human life activities， and its dysfunction is closely associated with various liver diseases. In recent years， an increasing number of studies have shown that semaphorins （SEMA） play a significant role in pathological processes such as immune inflammatory response， tumor progression， and fibrosis in liver diseases by interacting with their receptors plexins and neuropilins. This article reviews the expression， functions， and molecular mechanisms of different SEMA in viral hepatitis， hepatocellular carcinoma， liver fibrosis， nonalcoholic fatty liver disease， and hepatic ischemia-reperfusion injury， and it also explores the potential application value of SEMA in the diagnosis and treatment of liver diseases， in order to provide new ideas for precise diagnosis and targeted treatment of liver diseases.
The liver is a vital metabolic organ sustaining human life activities， and its dysfunction is closely associated with various liver diseases. In recent years， an increasing number of studies have shown that semaphorins （SEMA） play a significant role in pathological processes such as immune inflammatory response， tumor progression， and fibrosis in liver diseases by interacting with their receptors plexins and neuropilins. This article reviews the expression， functions， and molecular mechanisms of different SEMA in viral hepatitis， hepatocellular carcinoma， liver fibrosis， nonalcoholic fatty liver disease， and hepatic ischemia-reperfusion injury， and it also explores the potential application value of SEMA in the diagnosis and treatment of liver diseases， in order to provide new ideas for precise diagnosis and targeted treatment of liver diseases.
2026, 42(6): 1462-1468.
DOI: 10.12449/JCH260633
Abstract:
Liver transplantation is the standard treatment for end-stage liver disease， but it has long been limited by the shortage of donor livers. In clinical practice， three types of donor liver （domino donor livers， small-for-size grafts， and steatotic donor livers） are limited due to issues such as metabolic defects， insufficient volume， and poor quality. This article systematically reviews the definition， clinical application， and bottlenecks of the above three types of donor livers and elaborates on the unique value and clinical practice advances of auxiliary liver transplantation （a special surgical procedure that retains part or all of the recipient’s own liver and superimposes donor liver function support） in avoiding small-for-size syndrome， compensating for metabolic defects， and expanding the application of marginal livers， in order to provide a targeted clinical practice reference for optimizing liver transplantation strategies for end-stage liver disease and improving donor liver utilization rate.
Liver transplantation is the standard treatment for end-stage liver disease， but it has long been limited by the shortage of donor livers. In clinical practice， three types of donor liver （domino donor livers， small-for-size grafts， and steatotic donor livers） are limited due to issues such as metabolic defects， insufficient volume， and poor quality. This article systematically reviews the definition， clinical application， and bottlenecks of the above three types of donor livers and elaborates on the unique value and clinical practice advances of auxiliary liver transplantation （a special surgical procedure that retains part or all of the recipient’s own liver and superimposes donor liver function support） in avoiding small-for-size syndrome， compensating for metabolic defects， and expanding the application of marginal livers， in order to provide a targeted clinical practice reference for optimizing liver transplantation strategies for end-stage liver disease and improving donor liver utilization rate.
2026, 42(6): 1469-1474.
DOI: 10.12449/JCH260634
Abstract:
Acute pancreatitis （AP） often has an acute onset， and although most cases are self-limiting， there is still a risk of rapid deterioration， posing a serious threat to the lives of patients. Currently， traditional assessment tools such as clinical scoring systems and serum biomarkers are widely used to determine disease severity and prognosis. To enhance the accuracy of assessment， combined detection strategies integrating different scores and biomarkers are often used in clinical practice； however， there are still certain limitations such as insufficient specificity， limited early sensitivity， and a lack of consistent cut-off values. Therefore， current studies are actively exploring novel biomarkers with superior specificity and sensitivity and continuously optimizing their combined application strategies. This article summarizes the current application status of traditional assessment tools and reviews the research advances in novel biomarkers.
Acute pancreatitis （AP） often has an acute onset， and although most cases are self-limiting， there is still a risk of rapid deterioration， posing a serious threat to the lives of patients. Currently， traditional assessment tools such as clinical scoring systems and serum biomarkers are widely used to determine disease severity and prognosis. To enhance the accuracy of assessment， combined detection strategies integrating different scores and biomarkers are often used in clinical practice； however， there are still certain limitations such as insufficient specificity， limited early sensitivity， and a lack of consistent cut-off values. Therefore， current studies are actively exploring novel biomarkers with superior specificity and sensitivity and continuously optimizing their combined application strategies. This article summarizes the current application status of traditional assessment tools and reviews the research advances in novel biomarkers.
2026, 42(6): 1475-1480.
DOI: 10.12449/JCH260635
Abstract:
Pancreatic diseases are characterized by difficulties in diagnosis and treatment， as well as complex pathogenic mechanisms. Combined drug therapy can enhance therapeutic efficacy， overcome drug resistance， and reduce adverse effects through synergistic interactions and has thus emerged as an important strategy for improving the treatment of pancreatic diseases. This article systematically reviews the commonly used methods for evaluating the synergistic effect of drug combinations， including isobologram analysis， the Chou-Talalay method， Jin’s formula， and the weighted sum method， as well as the theoretical basis， applicability， and limitations of each method， and this article also summarizes the recent advances in their application in pancreatic diseases including pancreatic cancer and acute pancreatitis. By comparing the characteristics of different methods in terms of measurement accuracy and experimental dependence， this article further proposes a framework for evaluating the effect of multi-drug combinations tailored to pancreatic diseases， thereby providing a basis for the screening and optimization of drug combination regimens， as well as new perspectives for the future development of synergistic evaluation models and combined therapeutic strategies.
Pancreatic diseases are characterized by difficulties in diagnosis and treatment， as well as complex pathogenic mechanisms. Combined drug therapy can enhance therapeutic efficacy， overcome drug resistance， and reduce adverse effects through synergistic interactions and has thus emerged as an important strategy for improving the treatment of pancreatic diseases. This article systematically reviews the commonly used methods for evaluating the synergistic effect of drug combinations， including isobologram analysis， the Chou-Talalay method， Jin’s formula， and the weighted sum method， as well as the theoretical basis， applicability， and limitations of each method， and this article also summarizes the recent advances in their application in pancreatic diseases including pancreatic cancer and acute pancreatitis. By comparing the characteristics of different methods in terms of measurement accuracy and experimental dependence， this article further proposes a framework for evaluating the effect of multi-drug combinations tailored to pancreatic diseases， thereby providing a basis for the screening and optimization of drug combination regimens， as well as new perspectives for the future development of synergistic evaluation models and combined therapeutic strategies.
2026, 42(6): 1481-1488.
DOI: 10.12449/JCH260636
Abstract:
Pancreatic cancer is characterized by occult clinical manifestations and high malignancy， and conventional imaging examinations and carbohydrate antigen 19-9 lack sufficient sensitivity and specificity for detecting early-stage pancreatic cancer lesions. Difficulty in early diagnosis severely restricts the long-term survival of pancreatic cancer patients. Liquid biopsy targets the biomarkers in body fluid samples， including circulating tumor cells， circulating tumor DNA， circulating tumor microRNA， and extracellular vesicles， showing the advantages of noninvasiveness and continuous monitoring. This review systematically summarizes the latest advances in liquid biopsy for the early screening and diagnosis， recurrence prediction， and prognostic assessment of pancreatic cancer， aiming to provide new insights and references for precision screening of high-risk populations and the clinical translation of liquid biopsy.
Pancreatic cancer is characterized by occult clinical manifestations and high malignancy， and conventional imaging examinations and carbohydrate antigen 19-9 lack sufficient sensitivity and specificity for detecting early-stage pancreatic cancer lesions. Difficulty in early diagnosis severely restricts the long-term survival of pancreatic cancer patients. Liquid biopsy targets the biomarkers in body fluid samples， including circulating tumor cells， circulating tumor DNA， circulating tumor microRNA， and extracellular vesicles， showing the advantages of noninvasiveness and continuous monitoring. This review systematically summarizes the latest advances in liquid biopsy for the early screening and diagnosis， recurrence prediction， and prognostic assessment of pancreatic cancer， aiming to provide new insights and references for precision screening of high-risk populations and the clinical translation of liquid biopsy.
2026, 42(6): 1252-1252.
DOI: 10.12449/JCH2606.gwqkjpwzjj1
Abstract:
2026, 42(6): 1259-1259.
DOI: 10.12449/JCH2606.gwqkjpwzjj2
Abstract:
2026, 42(6): 1341-1341.
DOI: 10.12449/JCH2606.gwqkjpwzjj3
Abstract:
2026, 42(6): 1387-1387.
DOI: 10.12449/JCH2606.gwqkjpwzjj4
Abstract:
2026, 42(6): 1384-1384.
DOI: 10.12449/JCH2606.zhixie
Abstract:
2015, 31(12): 1941-1960.
doi: 10.3969/j.issn.1001-5256.2015.12.002
Abstract:
2019, 35(12): 2706-2711.
doi: 10.3969/j.issn.1001-5256.2019.12.013
Abstract:
2011, 27(1): 113-128.
Abstract:
2011, 27(1): 110-112.
Abstract:
2018, 34(10): 2109-2120.
doi: 10.3969/j.issn.1001-5256.2018.10.011
Abstract:
2015, 31(12): 1980-1988.
doi: 10.3969/j.issn.1001-5256.2015.12.004
Abstract:
2017, 33(8): 1419-1431.
doi: 10.3969/j.issn.1001-5256.2017.08.003
Abstract:
2016, 32(1): 9-22.
doi: 10.3969/j.issn.1001-5256.2016.01.002
Abstract:
2019, 35(12): 2648-2669.
doi: 10.3969/j.issn.1001-5256.2019.12.007
Abstract:
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- 1Current situation in the research of Gilbert’s syndrome
- 2Review of acute pancreatitis scoring systems
- 3Clinical value of 13C-methacetin breath test for assessing liver function in patients with cirrhosis
- 4Studies on relevant gactors of Child-Pugh grading in hepatic cirrhosis
- 5Meta-analysis of 111 patients with nonalcoholic steatohepatitis-associated hepatocellular carcinoma
- 6Relationship between Epstein-Barr virus infection and hepatic lesions in children
- 7Research state and prospect of hyponatremia in cirrhosis
- 8Congenital bile acid synthesis defect and cholestatic liver disease
- 9Interventional treatment for Budd-Chiari syndrome:reports of 883 cases
- 10
- 1The guideline of prevention and treatment for chronic hepatitis B: a 2015 update
- 2Chinese guidelines for the management of acute pancreatitis ( Shenyang , 2019 )
- 3The guideline of prevention and treatment for chronic hepatitis B(2010 version)
- 4Current situation in the research of Gilbert’s syndrome
- 5
- 6Comprehensive guidelines for the diagnosis and treatment of pancreatic cancer (2018 version)
- 7Consensus on the diagnosis and management of primary biliary cirrhosis (cholangitis)(2015)
- 8Diagnosis, management, and treatment of hepatocellular carcinoma (V2017)
- 9Consensus on the diagnosis and management of autoimmune hepatitis(2015)
- 10Guidelines for the prevention and treatment of chronic hepatitis B (version 2019)
International Database
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荷兰《医学文摘（网络版）》（Embase）（2023—） -
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美国《生命科学引文索引》（BIOSIS Citation Index）（2025—）
美国《生命科学信息预览》（BIOSIS Previews）（2025—）
美国《生命科学文摘》（Biological Abstracts）（2025—） -
美国《ProQuest健康与医学资源全文数据库》 -
美国《化学文摘（网络版）》（CA）来源期刊（2011—） -
瑞士《健康网络首创研究获取》（HINARI）来源期刊（1985—） -
美国《艾博思科数据库》（Eh，EBSCOhost）来源期刊（2013—） -
英国《国际农业与生物科学研究中心》（CABI）来源期刊（2011—） -
ISSN国际中心《开放学术资源库》（ROAD）（2023—） -
世界卫生组织《西太平洋地区医学索引（WPRIM）》来源期刊（2016—） -
印度《J-Gate全球电子期刊获取门户》（J-Gate）（2026—） -
《日本科学技术振兴机构数据库（中国）》（JSTChina）来源期刊（2018—） -
俄罗斯《文摘杂志》（AJ，VINITI）来源期刊（2013—） -
美国《乌利希期刊指南（网络版）》（Ulrichsweb）注册期刊（2018—） -
英国《欧洲学术出版中心数据库》（EuroPub）来源期刊（2024—） -
波兰《哥白尼索引》（ICI）来源期刊（2011—）
