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.
目的 比较进展性慢性肝病及重症肝炎患者原位肝移植(OLT)围手术期凝血功能的变化。方法 回顾性分析我中心2004年1月至2005年12月期间行OLT治疗进展性慢性肝病及重症肝炎患者各37例的围手术期血小板(PLT)、凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)及纤维蛋白原(FIB)的变化。结果 2组患者除术前PT、APTT,术后第5 d PLT、FIB和术后第7 d FIB的差异有统计学意义外（plt;0.05），其余时段2组患者的PLT、PT、APTT及FIB 间差异均无统计学意义（Pgt;0.05）, 提示重症肝炎患者凝血功能损害更为严重； OLT术后，2组患者的凝血功能均逐渐恢复正常, 但并非完全同步。结论 进展性慢性肝病与重症肝炎患者OLT围手术期凝血功能变化显著，应注意监测及处理，但术后2组间各指标间比较差异并不明显。
Objective To summarize the current progress in diagnosis and treatment of polycystic liver disease, and provide ideas for further research direction and clinical practice of polycystic liver disease. Method The domestic and foreign literature about polycystic liver disease was reviewed, screened, and summarized. Results The diagnosis, evaluation, and classification of polycystic liver disease were mainly performed clinically by abdominal ultrasound and CT. Surgical treatment was the main treatment, including aspiration sclerotherapy, fenestration, segmental hepatectomy, and liver transplantation. Conclusions The classification and evaluation scheme of polycystic liver disease needs to be improved, and its medical treatment still needs further research. Estrogen receptor and gonadotropin-releasing hormone receptor are promising therapeutic targets.
目的:评价电脑肝病治疗仪治疗病毒性肝炎的疗效及不良反应。方法:将116例病毒性肝炎患者随机分为治疗组及对照组,治疗组60例,对照组56例。两组均以抗炎、保肝、降酶、退黄、对症为治则。治疗组加用电脑肝病仪治疗，每日一次。结果:治疗组在消化道症状改善方面有效率950%,黄疸消退方面有效率902%。谷丙转氨酶恢复方面有效率85%。而对照组分别为8214%、6786%和7143%。结论:电脑肝病治疗仪治疗肝病能迅速改善消化道症状,有效降低黄疸、转氨酶,未见明显不良反应。
ObjectiveTo analyze the incidence of bacterial lung infection after orthotopic liver transplantation and its risk factors. MethodsNinety-six patients with end-stage liver disease who underwent liver transplantation from Jan. 2010 to Jun. 2012 in our hospital were retrospectively analyzed. The relationship of preoperative, intraoperative, and postoperative variables with early postoperative bacterial lung infection was explored by multivariate non-conditional logistic regression. ResultsTwenty-nine cases of 96 cases after liver transplantation occurred early bacterial lung infection, and the infection rate was 30.21%(29/96), in which G-aerobic bacteria infection accounted for 65.52%(19/29), and G+ aerobic bacteria accounted for 34.48%(10/29). Preoperative model for end-stage liver disease score(OR=2.165, P=0.001), intraoperative blood transfusion(OR=1.952, P=0.003), average of plasma creatinine during 3 days after operation(OR=1.913, P=0.001), liquid negative balance time during 3 days after operation(OR=0.916, P=0.023), and postoperative hospital stay(OR=1.923, P=0.003) were all associated with early postoperative bacterial lung infection. ConclusionsRetrograde reperfusion in orthotopic liver transplantation patients are susceptible to bacterial lung infections. Improving basic status before operation, controlling volume of intraoperative blood transfusion, the volume of transfusion, and postoperative hospital stay, and improving renal function can reduce incidence of early postoperative bacterial lung infection.
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.
目的:探讨激素及免疫抑制剂导致乙肝病毒再激活所致的肝损害的危害性及治疗效果，指导临床治疗。方法：总结本院近2年收治的7例慢性乙肝病毒感染者在使用激素及免疫抑制剂致肝炎再激活并加重患者的临床资料进行分析。结果：慢性乙肝病毒感染者因各种原因使用激素及免疫抑制剂所导致的慢性乙肝的复发加重，病情发展迅速，病死率高。结论：抗乙肝病毒治疗是预防肝病复发并恶化的关键，在激素或免疫抑制剂治疗前和治疗中都应使乙肝病毒降至尽可能低的水平。
摘要:目的: 研究蜕皮甾酮对非酒精性脂肪性肝病大鼠模型肿瘤坏死因子α(TNFα)与核因子κB(NFκB)表达的影响，并探索其可能的作用机制。 方法 :健康成年SD大鼠36只,随机分为正常对照组12只与实验组24只;正常对照组喂以普通基础饲料,实验组应用高脂饲料喂养。实验12周末时将造模成功的实验组大鼠随机分为模型组与蜕皮甾酮治疗组2个亚组,每组12只;正常对照组喂以普通基础饲料至16周,模型组继续应用改良高脂饲料喂养至16周,蜕皮甾酮治疗组大鼠在高脂饮食同时加用蜕皮甾酮灌胃。实验16周末时处死3组所有大鼠;检测肝脏指数,血清与肝组织生化指标及肝组织病理改变;ELISA法检测肝脏TNFα水平;免疫组化检测各组大鼠肝组织中核因子κB蛋白表达情况。 结果 :蜕皮甾酮治疗组血清胆固醇(TC)、丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)明显低于模型组(212±058比263±024,Plt;005;5336±1848比8460±3627,P＜005;14020±3595比24359±3638,P＜001);蜕皮甾酮治疗组与模型组相比肝组织丙二醛(MDA)水平降低明显(18454±1645比23928±2376,P＜001),超氧化物歧化酶(SOD)活力增加显著(942±052比518±043,P＜001),肝脏指数显著降低(435±037比504±046,P＜001)，肝组织脂肪变性程度和炎症活动度明显减轻(546±037比630±049,P＜001)。蜕皮甾酮治疗组与模型组相比TNFα与核因子κB水平明显减轻(4304±748比6156±727,2465±539比4504±746,P值均＜001)。 结论 :蜕皮甾酮具有改善高脂饮食诱发的非酒精性脂肪性肝病大鼠肝脏酶学功能,通过增加肝组织SOD的含量和减少MDA的含量来减轻肝组织氧化应激水平,减轻肝组织TNFα和核因子κB来减轻肝脏炎症,发挥防治非酒精性脂肪性肝病的作用。Abstract: Objective: To investigate the effect and possible mechanism of ecdysterone on the expression of tumor necrosis factoralpha (TNFα) and nuclear factor κ B (NFκB) in rats with nonalcoholic fatty liver disease of rats. Methods : A total of 36 male Sprague Dawley rats were randomly divided into two groups, who were fed with highfat diet (experimental group, n=24) and normal basic food (normal control, n=12) respectively. At the end of the 12th week, the experimental group was randomly divided into two subgroups: model group and ecdysterone group, each group contained 12 rats. From the 13th week, the rats in the normal control group and model group were lavaged with normal sodium, and the rats in the ecdysterone group were lavaged with ecdysterone at 10 mg·kg-1·d-1. At the end of the 16th week, all rats were weighed, narcotized, sacrificed, and the liver index, biochemical indicators in serum and liver tissues and the hepatic pathological changes were observed. The expression of TNFα was detected by ELISA and the expression of NFκB was measured by immunohistochemical staining. Results : At the end 16th week in ecdysterone group, the serum levels of cholesterol (TC), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were reduced markedly (212±058 vs 263±024 and 5336±1848 vs 8460±3627, both P＜005; 14020±3595 vs 24359±3638, P＜001); the tissue content of malondialdehyde (MDA) was decreased evidently (18454±1645 vs 23928±2376, P＜001), while the activity of superoxide dismutase (SOD) was enhanced notably (942±052 vs 518±043, P＜001); the liver index was decreased significantly in comparison with that inmodel group (435±037 vs 504±046, P＜001); the degree of fatty degeneration and inflammation were relieved dramatically (546±037 vs 630±049, P＜001). The expression of TNFα and the levels of NFκB were significantly lower (4304±748 vs 6156±727 and 2465±539 vs 4504±746, both P＜001) in ecdysterone group compared with model group. Conclusion : The effects of ecdysterone in preventing NAFLD in rats could be related to the increase of SOD content in hepatic tissue and the decrease of MDA content, tumor necrosis factorα and NFκB.
ObjectiveObjective To summarize the latest research progress on the copper death mechanism in metabolic associated fatty liver disease (MAFLD) and to provide new avenues for the treatment of MAFLD. MethodsWe reviewed recent domestic and international research on copper and copper death in MAFLD, and summarized the role of copper death mechanisms in the pathogenesis of MAFLD and related treatments. ResultsCopper death is primarily caused by abnormal intracellular copper accumulation binding to acylated proteins in the tricarboxylic acid cycle, leading to protein oligomerization, downregulation of iron-sulfur cluster protein expression, triggering a toxic stress response, and ultimately cell death. The occurrence and progression of MAFLD are closely associated with genes associated with the copper death pathway. Imbalanced copper metabolism can lead to insulin resistance, causing abnormalities in blood glucose and lipid metabolism, promoting fat accumulation in the liver, and ultimately contributing to the development of MAFLD. Targeting genes involved in the copper death pathway can delay the progression of MAFLD. ConclusionThe occurrence and progression of MAFLD are closely linked to the copper death signaling pathway, with copper metabolism imbalance as a core component. This pathway not only directly leads to hepatocyte death but also triggers insulin resistance and abnormal lipid metabolism, jointly driving the progression of MAFLD. Therefore, targeted regulation of the copper death pathway is a novel therapeutic strategy to slow the progression of MAFLD.