ObjectiveTo explore the relationship between liver transplantation procedure with or without preservation of retrohepatic vena cava and postoperative reinfection of hepatitis B virus.MethodsHepatitis B virus makers of 15 retrohepatic vena cava samples from hepatitis B virus active replicating recipients was detected using immunohistochemistry stain LSAB and HBV DNA hybridization in situ. Hepatitis B virus reinfection rate and survival rate after transplantation in classic group (20 cases) and piggyback group (7 cases) was analyzed retrospectively. ResultsHepatitis B virus makers including HBsAg and HBcAg and HBV DNA of all 15 retrohepatic vena cava samples, 10 from classic group and 5 from piggyback group, was negative. In classic group, 20 recipients were followedup 6-30 months, mean 18 months, only one case of hepatitis B recurrence was confirmed 22 months after operation; In piggyback group,7 recipients were followedup 5-12 months, mean 8 months, none of hepatitis B virus reinfection was encountered. Recurrence rate in classic group and piggyback group was 5.0%(1/20) and 0(0/7), respectively.ConclusionThis preliminary study indicated that the retrohepatic vena cava of hepatitis B virus active replicating recipients don’t have the residence and replication of hepatitis B virus particle. Orthotopic liver transplantation procedure with preservation of retrohepatic vena cava appears not to increase the hepatitis B virus reinfection rate in hepatitis B virus active replicating recipients after transplantation.
Objective To investigate and analyze the relationships among glucagon-like peptide-1 (GLP-1) level, chronic inflammation, and atherosclerosis in patients with non-alcoholic fatty liver disease (NAFLD). Methods From October 2016 to February 2017, using cross-sectional investigation, the GLP-1 level, chronic inflammation, and atherosclerosis were investigated in 80 subjects (40 NAFLD patients in NAFLD group, and 40 non-fatty liver disease participants in control group) who underwent physical examination at Xi’an Road Community Hospital. Results Compared with those in the control group, GLP-1 fasting level in patients with NAFLD [(9.09±1.03) vs. (9.15±1.06) pmol/L, P=0.807] and postprandial plasma GLP-1 [(15.96±3.37) vs. (17.46±4.76) pmol/L, P=0.108] had no changes. The correlations of GLP-1 level with chronic inflammation and insulin resistance (IR) were not significant either. The increased risk of carotid intima-media thickness related cardiovascular disease (CVD) in the NAFLD group was greater than that in the control group, and the difference was statistically significant [22 (55.0%)vs.13 (32.5%), P=0.043]. When the plasma lipoprotein-associated phospholipase A2 level increased, the risk of NAFLD increased [odd ratio (OR)=1.16, 95% confidence interval (CI) (1.02, 1.32), P=0.023]. Plasma ceramide kinase (CERK) in the NAFLD group was lower than that in the control group, and the difference was statistically significant [(12.36±2.45) vs. (18.33±3.71) ng/mL, P<0.001]. When the plasma CERK level of the fasting plasma was elevated, the risk of NAFLD decreased [OR=0.30, 95%CI (0.12, 0.78), P=0.014]. The homeostasis model assessment of insulin resistance (HOMA-IR) in the NAFLD group was higher than that in the control group, and the difference was statistically significant (2.46±2.53 vs. 1.11±0.66, P=0.002). The Matsuda index in the NAFLD group was less than that in the control group, and the difference was statistically significant (5.88±4.09 vs. 10.46±7.90, P=0.002). When HOMA-IR increased, the risk of NAFLD increased [OR=2.75, 95%CI (2.49, 3.12), P=0.036]. Conclusions Plasma GLP-1 level is not a sensitive indicator of chronic inflammation and IR in patients with NAFLD. Patients with NAFLD are in an increased risk of atherosclerosis and CVD. It suggests that NAFLD might be involved in chronic inflammation and IR. Chronic inflammation can cause IR, and then chronic inflammation and IR can cause NAFLD and subclinical atherosclerosis. In return for this, NAFLD increases chronic inflammation and IR.
【Abstract】ObjectiveTo investigate the changes and significances of the activity of blood coagulation and fibrinolysis in hepatectomy patients accompanied with chronic hepatic disease. MethodsThirtyfive patients who were accompanied with cirrhosis undertook surgery in the second affiliated hospital of Chongqing Medicall University from year 2003 to 2004 were divided into two groups: the first group of 18 cases received hepatectomy and the second group received nonhepatectomy surgical treatment. The (prothrombin time PT), (activated partial thromboplatin time APTT), (thrombin time TT), and the content of (Fibrinogen Fbg) and (Ddimer DD) in the blood drawn from peripheral veins were quantitatively measured by a fullyautomatic chromogenic and immunological assay machine (ACLFutura 9000,USA) at the phases of before operation, right after operation and 24hour after operation, respectively. ResultsAPTT in hepatectomy group increased significantly (P＜0.01) and were much higher than the nonhepatectomy group at corresponding phases (P＜0.01). PT in hepatectomy group increased even more significantly compared with that of preoperation and right after the operation (P＜0.01). The differences of TT at varying phases in hepatectomy group were of no significance (Pgt;0.05). There was also no significant difference of PT, APTT, and TT in nonhepatectomy group at varying phases. ConclusionThe function of blood coagulation is relatively poor and the secondary activity of fibrinolysis is overactivated in hepatectomy patients accompanied with chronic hepatic disease, which indicates a high risk of hemorrhage.
摘要:目的:分析慢性乙肝病毒攜帶者肝組織病理與年齡、病程、血清學及肝臟免疫組化指標的相關性,以確定孰是對病理進程影響最主要的指標。方法:對134例臨床診斷的慢性乙肝病毒攜帶者進行乙肝血清學標志物、肝功能、肝活組織病理及免疫組化的檢查。結果:①病理表現為不典型增生者HBeAg陰性組少于HBeAg陽性組,而表現為慢性肝炎者前者多于后者,差異均有顯著性;HBVDNAlt;105亞組分析兩組病理表現無統計學差異;兩種病理表現類型在年齡18~40歲組及gt;40歲組明顯多于lt;18歲,差異均有顯著性;兩種病理類型在免疫組化雙陽性組均多于單陽性組及全陰
【Abstract】Objective To introduce the birth and development of model of endstage liver disease (MELD) and evaluate its effect on liver transplantation(LT) as a new scoring system. Methods Literatures of MELD applied in LT were analyzed retrospectively. Results MELD scoring system was used for predicting the prognosis of patients with endstage liver disease and the death risk of candidates on waiting LT extensively and the order of organ sharing was determined by its predicable results. Conclusion MELD has been had a successful initial implementation for predicting the shortterm survival probability and mortality in patients with endstage liver disease, and meeting the goal of providing a system of allocation that emphasizes the urgency of the candidate while diminishing the reliance on waiting time, which has been proven to be a powerful tool for auditing the liver allocation system.
This study sought to investigate the in vivo antiviral effect of amantadine (AM) and biphenyl dimethyl dicarboxylate (DDB) on hepatitis B virus (HBV) in HBV replication mice. HBV replication-competent plasmid was transferred into male BALB/c mice by using hydrodynamics-based in vivo transfection procedure to develop HBV replication mouse model. The model mice were matched by body weigh, age and serum levels of hepatitis B e antigen (HBeAg) and were divided into four groups:AM group, DDB group, AM+DDB group and NS group, with the last one as control, and the mice of each group were administered corresponding agent orally twice a day, in a medication course lasting 3 d. On the third day, the mice were sacrificed 4-6 h after the last oral intake. HBV DNA replication intermediates in liver were analyzed by Southern blot hybridization. The serum hepatitis B surface antigen (HBsAg) and HBeAg were detected by enzyme linked immunosorbent assay (ELISA). Compared to the animals in the control group, HBV DNA replication intermediates in liver and HBsAg and HBeAg in serum from the AM and AM plus DDB group of mice decreased, and there was no difference between these two groups of mice. The levels of HBV DNA intermediate from liver and the serum HBsAg and HBeAg between the control and DDB group, however, were not obviously different. In conclusion, the inhibition effect of AM on HBV was detected, but treatment with DDB for 3 days did not influence the viral replication and expression of HBV in the HBV replication mice.
Objective To investigate the incidence and risk factors of non-alcoholic fatty liver disease (NAFLD) in patients with myocardial infarction. Methods A total of 634 patients with myocardial infarction from Beijing Anzhen Hospital were asked to take liver and gallbladder ultrasonography during hospitalization, and then divided into the NAFLD and non-NAFLD groups. The incidence and risk factors of the two groups were then analyzed. Results The incidence of NAFLD was 52.2% (331/634). Both body mass index (BMI) and serum alanine aminotransferase of the NAFLD group were higher than those of non-NAFLD group, with significant difference (Plt;0.05). The incidence of NAFLD was positively increased following the severity of coronary diseases (χ2=7.275, P=0.03). The result of multivariable logistic regression analysis showed BMI, multi-vessel lesions of coronary disease, and left main coronary artery lesion were the independent risk factors of NAFLD. Conclusion The myocardial infarction patients who are particularly complicated by overweight, multi-vessel lesions and left main coronary artery lesion have a higher incidence of NAFLD.
Liver fibrosis in chronic liver disease refers to the body’s repair response to sustained repeated necrosis or inflammation of liver cells, which results in fibrosis accompanied by relative or absolute lack of fiber degradation and deposition of extracellular matrix in the liver. Early and timely diagnosis and treatment of hepatic fibrosis are of great importance to patients with liver disease. A rational and complete diagnostic model of liver fibrosis should involve clinical pathology and histology, imaging, and serum biochemical markers. Liver biopsy has been regarded as the "gold standard" for the diagnosis of liver fibrosis and as a reference standard for other non-invasive diagnostic tests of liver fibrosis. Since it is invasive, liver biopsy is difficult to implement in clinical practice and a second liver biopsy is even more difficult. As for the non-invasive diagnosis of liver fibrosis, clinical symptoms and signs are not specific. The sensitivity and specificity of individual serum biochemical markers are still very weak, and imaging studies also lack specificity. The mathematical model “FibroTest” of serum biochemical markers has better diagnostic accuracy, but the calculation is complicated, making it difficult to achieve widespread use. There is insufficient evidence to suggest that the "gold standard" of liver biopsy can be replaced. Therefore, further research is needed to investigate how best to balance the benefits and harms of different tests, to identify the best combination, to simplify any calculation steps, to reduce costs, to avoid liver biopsy, and to find new, more specific and sensitive markers.
With the publication of a vast amount of clinical research on hepatocellular carcinoma (HCC), the American Association for the Study of Liver Diseases (AASLD), the National Comprehensive Cancer Network (NCCN), the American Society of Clinical Oncology (ASCO), and the National Health Commission of China have all updated their diagnostic and treatment guidelines for HCC. There are no differences in the definition of HCC risk populations among the AASLD 2023, NCCN 2024, and China Liver Cancer Staging and Treatment Guideline (CNLC) 2024. Notably, CNLC 2024 has updated its guidance on high-risk factors and prospective surveillance for HCC based on the characteristics of HCC patients in China. The four guidelines have seen significant updates in the areas of neoadjuvant and adjuvant therapies, local treatments, and systemic treatments for HCC. CNLC 2024 refines the indications for local treatment, improves systemic treatment, and introduces new first-line therapy, including camrelizumab combined with rivoceranib or tislelizumab. The second-line therapy nivolumab plus ipilimumab for advanced HCC are recommended by AASLD 2023, NCCN 2024, and ASCO 2024, which may become a new first-line therapeutic option for patients with advanced HCC. We compare and interpret these four guidelines in this paper.