八项生化新指标与不同肝脏疾病的关系研究

目的:探讨亮氨酸氨基肽酶(LAP)、天冬氨酸氨基转移酶同工酶(ASTm)、N-乙酰-β-D氨基葡萄糖苷酶(NAG)、α-岩藻糖苷酶(AFU)、甲胎蛋白(AFP)、前白蛋白(PAB)、谷氨酸脱氢酶(GLDH)、腺苷脱氨酶(ADA)八项指标在肝病诊断中的意义.方法:使用全自动生化分析仪对300例各种肝病和150例正常人血清中八项新指标进行检测,对检测结果进行统计学分析.结果:在急性肝炎时LAP、ASTm、GLDH、ADA和AFU均显著增高;肝硬化时ADA、AFU和NAG均显著升高,PAB降低;重型肝炎时ADA和NAG显著升高,PAB和AFU降低;肝癌时LAP、AFU、AFP、NAG和ADA均显著升高,PAB下降.结论:在急性肝炎时AFU、LAP和ASTm具有较高应用价值;肝硬化时ADA具有较高应用价值;重型肝炎时PAB和AFU具有较高应用价值;肝癌时LAP和AFP应用价值较高.     

ALT、AST、GGT、CHE在肝病中的诊断价值

目的探讨肝脏疾病时肝脏酶的变化关系.方法采用速率法,测定113例肝病患者空腹血清丙氨酸氨基转移酶(ALT)、天冬氨酸转氨酶(AST)、γ-谷氨酰基转移酶(GGT)、胆碱酯酶(CHE),并与32例正常体检者作对照组比较.结果各型肝病患者的血清ALT、急性黄疸肝炎组的血清GGT及慢性肝炎重度组血清AST活性均显著升高(p＜0.01),慢性肝炎重度、肝硬化患者CHE活性均明显降低(p＜0.01).结论血清ALT、AST、GGT、CHE是肝病较为敏感指标,作为肝功能检测组合.有助于肝病的鉴别诊断和判断预后.     

血清MAO、5'-NT及SAA联合检测在肝脏疾病诊断中的应用价值

目的 探讨血清单胺氧化酶(MAO)、5'-核苷酸酶(5'-NT)、淀粉样蛋白A(SAA)联合诊断肝脏疾病的价值.方法 选择2017年3月至2019年12月我院门诊及住院治疗的110例肝病及100例健康成年人作为研究对象,所有受试者测定血清MAO、5'-NT、SAA水平.收集天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)等肝生化指标,比较两组受试者指标差异并分析诊断价值.结果 肝脏疾病组患者血清MAO、5'-NT、SAA水平及肝生化指标AST、ALT水平均显著高于对照组,差异具统计学意义(P<0.05);Pearson相关性分析示,血清MAO、5'-NT水平与肝生化指标AST、ALT指标呈正相关关系(P<0.05);ROC曲线分析示,血清MAO、5'-NT、SAA水平单独诊断肝脏疾病的曲线下面积(AUC)分别为0.754、0.773、0.722,当截点值为9.26 U/L、23.77 U/L、7.26 mg/L时,约登指数最大;MAO+5'-NT、MAO+SAA、5'-NT+SAA、三者联合诊断的AUC分别为0.796、0.784、0.789、0.805,三者联合诊断价值最高.结论 肝脏疾病患者伴有血清MAO、5'-NT、SAA水平的明显升高,临床可将其单独或联合检测用于诊断、评估肝脏病变.     

ALT、AST、GGT、CHE在肝病中的诊断价值

目的 探讨肝脏疾病时肝脏酶的变化关系，方法 采用速率法，测定113例肝病患者空腹血清丙氨酸氨基转移酶（ALT）、天冬氨酸转氨酶（AST）、γ-谷氨酰基转移酶（GGT）、胆碱酯酶（CHE），并与32例正常体检者作对照组比较。结果 各型肝病患者的血清ALT、急性黄疸肝炎组的血清GGT及慢性肝炎重度组血清AST活性均显著升高（p〈0．01），慢性肝炎重度、肝硬化患者CHE活性均明显降低（P〈0．01）。结论 血清ALT、AST、GGT、CHE是肝病较为敏感指标，作为肝功能检测组合。有助于肝病的鉴别诊断和判断预后。     

肝功能检验与脂肪肝的相关性分析

目的：探讨肝功能检验与脂肪肝相关性。方法对两组临床资料进行回顾性分析,整个操作严格按操作规程进行,分析内容包括肝功能检验项目、检验结果等,将所得资料给予统计学分析后得出结论。结果研究组脂肪肝患者与对照组健康人群临床资料分析可知,研究组TBA、LDH、ALT、AST、ADA、GGT、AKP、GLB、AFU、5'-NT水平均显著高于对照组,TP、ALB、CHE水平则显著低于对照组,对比结果具有统计学意义(<0.05)。结论临床医生应准确掌握脂肪肝临床特征,对疑似患者积极给予实验室肝功能检验,根据检验结果准确判断病情并提供针对性的治疗措施,提高脂肪肝诊断正确率及降低临床误诊、漏诊几率,保障患者生活质量及生命安全。     

血清GP73在肝病患者中的表达水平

目的：探讨GP73的检测在肝脏疾病临床诊断中的应用价值。方法：收集295例各类肝脏疾病患者（213例病毒性肝炎、26例酒精性肝炎、23例自身免疫性肝炎和33例非酒精性脂肪肝）及33例健康对照组血清,采用酶联免疫分析和化学发光分析分别对血清GP73进行定量检测,并对治疗前后进行分析比较;应用生化分析仪检测ALT、ALP、AST、GGT、CHE、ALB、TBIL、AFP的含量,运用荧光定量PCR方法检测HBVDNA拷贝,分析不同肝病患者血清GP73含量与其他指标的关系。结果：治疗前病毒性肝炎组、酒精性肝炎组、自身免疫性肝炎组其GP73含量的中位数均〉健康对照组（U分别为240．4、24．0和27．0）,非酒精性脂肪肝组与健康对照组无统计学意义（U=157．5,P〉0．05）;病毒性肝炎组与酒精性肝炎组、自身免疫性肝炎组比较有统计学意义（U分别为760．5和1299．0,P〈0．05）;病毒性肝炎组、自身免疫性肝炎组治疗前后均有统计学意义（u分别为67．2、99．4,P〈0．01）,酒精性肝炎组治疗前后无统计学意义（U为1322,P〉0．05）。血清GP73与CHE、ALB呈负相关（r分别为-0．454,-0．469）,与GGT、TBIL呈正相关（r分别为0．34和0．39）。结论：血清GP73在病毒性肝炎、酒精性肝炎和自身免疫性肝炎中表达上调,可作为病毒性肝炎和自身免疫性肝炎患者治疗疗效的观察指标之一。     

肝脏疾病患者血清酶活性与凝血四项的变化规律及辅助诊断价值研究

通过对ALT、AST、ALP、GGT、CHE和凝血四项的检测,探讨其在肝病鉴别诊断中的临床价值.用罗氏Modular全自动生化分析仪检测患者ALT 、AST 、ALP、GGT,应用强生干化学分析仪检测CHE,应用Stago检测凝血四项,经病理学和影像学确诊的35例肝炎患者、32例肝硬化患者、80例肝癌患者及50例健康体...     

血清TBA、ADA、CHE及PA检测诊断肝病的价值

本文通过对血清总胆汁酸(TBA)、腺苷脱氨酶(ADA)、胆碱酯酶(CHE)及前白蛋白(PA)这四项指标进行联检,以探讨其在肝病诊断中的价值,现将结果报告如下。1资料和方法1.1一般资料选择2010年1月～2011年5月就诊于我院的门诊及住院肝病患者共235例(男125,女110),各型肝病经临床确诊,且符合全国病毒性肝炎及肝病学术会议制定     

血清GGT、ALP及ADA在肝癌诊断中的临床价值

目的探讨血清R-谷氨酰转移酶(GGT)、碱性磷酸酶(ALP)和腺苷脱氨酶(ADA)检测对肝癌诊疗的临床意义。方法随机选取肝癌患者、良性肝病患者及健康体检者(正常对照组)各45例,分别检测其血清GGT、ALP及ADA含量,统计分析各组间结果差异,并比较三种指标单独或联合检测对肝癌诊断的敏感性和特异性。结果血清GGT、ALP及ADA含量在肝癌患者组明显高于良性肝病患者组及正常对照组,差异有统计学意义(P0.05);对肝癌的诊断:单项检测GGT、ALP及ADA的敏感性分别为84%、69%、78%,特异性分别为76%、89%、91%;三项联合检测的敏感性为91%,特异性为69%。结论三项联合检测提高了对肝癌诊断的敏感性,有利于肝癌的早期诊断,降低了对肝癌的漏诊率。     

丙型肝炎患者HCV-RNA载量与抗-HCV检测的临床意义探讨

目的探讨丙型病毒性肝炎患者血清HCV-RNA载量与抗-HCV浓度检测的临床意义。方法采用荧光定量PCR对本院2016年1月-2017年7月就诊的113例丙型病毒性肝炎患者和30例健康对照进行HCV-RNA载量检测并对基因组测序分型,同时使用ELISA检测抗-HCV浓度,全自动生化分析仪检测血清AST、ALT、TBIL浓度。结果陕西榆林地区丙肝患者主要基因型为HCV1型82例(72.57%);2型10例(8.85%);3型5例(4.42%);6型7例(6.19%)。随着HCV-RNA的增加,抗-HCV阳性率有所增高,两者一致性增高。丙肝患者抗-HCV的S/CO值均高于健康对照组,差异有统计学意义。HCV-RNA四个载量水平不同组间除中、低载量组AST无统计学意义外,ALT、AST、TBIL水平比较差异均有统计学意义。结论 HCV-RNA联合抗-HCV检测与肝功能相关指标(AST、ALT、TBIL)检测三者相互结合,对于丙型病毒性肝炎患者的早期诊断和疗效监测具有重要的意义。     

肝移植供肝切取与修整技术

目的：总结临床肝移植供肝切取与修整技术。方法：采用原位腹主动脉、门静脉双路灌注及肝。肾联合快速切取法切取供肝及。肾40例次，并施行同种异体肝移植40例，其中3例行肝。肾联合移植。结果：全组供肝平均热缺血时间为4min，切取时间为25min，保存时间为6h。全组移植肝均于恢复血流10min内有金黄色胆汁泌出，1周左右肝功能恢复正常。结论：我院开展的供肝、肾的切取与修整技术在临床实际应用中取得满意的效果，为移植手术的成功提供了可靠的保证。     

Haemophilus parainfluenzae Liver Abscess after Successful Liver Transplantation

Haemophilus parainfluenzae was isolated from a bile specimen and from an aspirate of a liver abscess in a 58-year-old liver-transplanted woman that was indicative of an invasion of the graft by an ascending route. Drug therapy, immunosuppression, rejection therapy, and Roux-en-Y choledochojejunostomy may have contributed to the septic course. Interdisciplinary cooperation was instrumental in diagnosis and successful management in this case.     

Inflammatory Pathways in Liver Homeostasis and Liver Injury

The liver is a unique organ with respect to its anatomical location, allowing continuous blood flow from the gastrointestinal tract through the sinusoids, and its cellular composition, comprising metabolically active hepatocytes, nonhepatocytic parenchymal cells, and various immune cell populations. Cytokines are key mediators within the complex interplay of intrahepatic immune cells and hepatocytes, as they can activate effector functions of immune cells, as well as hepatocytic intracellular signaling pathways controlling cellular homeostasis. Kupffer cells and liver-infiltrating monocyte-derived macrophages are primary sources of cytokines such as tumor-necrosis factor-alpha (TNF-alpha) and interleukin-6. The liver is also enriched in natural killer (NK) and NK T cells, which fulfill functions in pathogen defense, T cell recruitment, and modulation of liver injury. TNF-alpha can activate specific intracellular pathways in hepatocytes that influence cell fate in different manners, e.g., proapoptotic signals via the caspase cascade, but also survival pathways, namely the nuclear factor (NF)-kappaB pathway. NF-kappaB regulates important functions in liver physiology and pathology. Recent experiments with genetically modified mice demonstrated important and partly controversial functions of this pathway, e.g., in cytokine-mediated hepatocyte apoptosis or ischemia–reperfusion injury. The exact dissection of the contribution of recruited and resident immune cells, their soluble cytokine and chemokine mediators, and the intracellular hepatocytic response in liver homeostasis and injury could potentially identify novel targets for the treatment of acute and chronic liver disease, liver fibrosis, or cirrhosis.     

Liver immunobiology

Tle liver has a number of important functions in innate and adaptive immunity. Contributions to the innate (nonspecific) immune system include production of acute phase proteins, nonspecific phagocytosis of particles, nonspecific pinocytosis of molecules, and nonspecific cell killing. Hepatic involvement in innate immunity contributes to the systemic response to local inflammation, clearance of particles and soluble molecules from the circulation, and killing of invading cells such as neoplastic cells. Liver involvement in the adaptive (specific) immune system includes deletion of activated T cells, induction of tolerance to ingested and self-antigens, extrathymic proliferation of T cells, and deletion of many of the signaling and effector molecules. Hepatic involvement in adaptive immunity allows clearance of activated T cells and signaling molecules following inflammatory reactions, and promotes immunologic tolerance toward potentially antigenic proteins that are absorbed from the intestinal tract. The liver is a major site of extrathymic T cell development, which assumes increasing significance with aging in mammals. Perturbations in hepatic structure or function can result in significant ramifications in both the innate and adaptive immune systems.     

Liver fibrosis

Knowledge on the development and progression of liver fibrosis has grown exponentially in the past decade. At present, liver fibrogenesis is referred to as a dynamic process involving complex cellular and molecular mechanisms, resulting from the chronic activation of the tissue repair mechanisms that follows reiterated liver tissue injury. The identification and characterization of the cell types and of the different mediators involved in this process has allowed a “re-visitation” of several issues related to liver cirrhosis and its immediate consequences. Among these, evaluation of the relationships occurring between fibrogenesis and portal hypertension, cholestasis and the development of hepatocellular carcinoma, represent some of the hottest areas of research in this field of hepatology. The elucidation of many of the cellular and molecular mechanisms responsible for the progression of liver fibrosis has provided a sound basis for the development of pharmacological strategies able to modulate this important pathophysiological process.