肝纤维化指标检测在非酒精性脂肪性肝病中应用价值

目的探讨非酒精性脂肪性肝病各期与血清肝纤维化标志物的关系。方法 126例非酒精性脂肪性肝病患者依据病情分为单纯性脂肪肝组51例,非酒精性脂肪性肝炎组42例,与非酒精性脂肪性肝炎相关肝硬化组33例,不嗜酒的体检健康者64名为对照组,检测4组血清透明质酸、Ⅲ型前胶原氨端肽、Ⅳ型胶原、层黏蛋白水平。结果非酒精性脂肪性肝炎组与非酒精性脂肪性肝炎相关肝硬化组各指标水平较对照组增高（P〈0.01）;单纯性脂肪肝组透明质酸与对照组比较差异有统计学意义（P〈0.05）;非酒精性脂肪性肝炎相关肝硬化组各指标水平高于非酒精性脂肪性肝炎组和单纯性脂肪肝组（P〈0.05）。结论肝纤维化血清学指标有助于了解非酒精性脂肪肝病患者肝纤维化程度。     

非酒精性脂肪肝患者血清肝纤维化检测的分析

本研究通过非酒精性脂肪肝患者的血清肝纤维化四项指标Ⅲ型前胶原肽（PCⅢ）、Ⅳ型胶原（CⅣ）、透明质酸（HA）、层黏蛋白（LN）检测，了解非酒精性脂肪肝患者肝纤维化的情况。     

非酒精性脂肪性肝病患者甲状腺激素水平变化及其与肝纤维化的关系

目的:探讨非酒精性脂肪性肝病(NAFLD)患者血清甲状腺激素水平变化与肝纤维化的关系及其意义。方法:采用放射免疫法检测123例NAFLD患者及56例对照组的血清甲状腺激素(T3、T4、TSH)及透明质酸(HA)、层粘连蛋白(LN)、Ⅲ型前胶原氨基末端肽(PⅢNP)、Ⅳ型胶原(CⅣ)等反应肝纤维化的血清学指标。结果:对照组与非酒精性单纯性脂肪肝(NASFL)组、非酒精性脂肪性肝炎(NASH)组血清T3浓度随病情进展逐渐降低,差异有统计学意义(P<0.01);3组间血清T4、TSH浓度比较差异无显著性(P>0.05);NASFL患者血清HA、PⅢNP浓度与较对照组升高,差异有统计学意义(P<0.01),而CⅣ、LN浓度差异无统计学意义(P>0.05);NASH组血清HA、PⅢNP、CⅣ、LN浓度均高于健康对照组及NAFL组,差异有统计学意义(P<0.01);NASFL患者血清T3水平与HA呈负相关关系(P<0.05);NASH组患者血清T3水平与HA、PⅢNP、CⅣ、LN均呈负相关关系(P<0.05)。结论:NAFLD患者血清T3水平降低,其下降程度与病情及肝纤维化严重程度一致;检测NAFLD患者血清T3变化对判断病情及预后有一定的临床价值。     

肝纤维化四项血清学指标及肝图象动态分析研究

慢性乙型病毒性肝炎是常见病和多发病,由于该病不易彻底治愈,后期常常引起肝纤维化,发展为肝硬化。Ⅲ型前胶原(PC-Ⅲ)、Ⅳ型胶原(Ⅳ-C)、层粘连蛋白(LN)和透明质酸(HA)与肝脏功能密切相关。为了观察血清PC-Ⅲ、Ⅳ-C、LN和HA在肝纤维化过程中的变化,我们应用放射免疫分析(RIA)方法,对151例慢性病毒性肝炎患者血清PC-Ⅲ、Ⅳ-C、LN和HA含量进行了检测,并与肝组织定量纤维图象分析进行了对比分析,现将结果报告如下。     

210例肝病患者血清肝纤维化指标检测结果分析

目的 探讨血清透明质酸(HA)、Ⅲ型前胶原(PC-Ⅲ)、Ⅳ型胶原(Ⅳ-C)和层黏连蛋白(LN)检测在肝纤维化诊断中的价值及其临床意义.方法 采用放射免疫法检测210例肝病患者及55例健康者血清HA、PC-Ⅲ、Ⅳ-C和LN水平.结果 慢性乙型病毒性肝炎(简称慢性乙肝)、肝硬化、肝癌患者血清LN、HA、PC-Ⅲ和Ⅳ-C水平高于健康者(P＜0.05),肝硬化、肝癌患者血清LN、HA和Ⅳ-C水平高于慢性乙肝患者(P＜0.05),肝硬化、肝癌患者血清PC-Ⅲ水平与慢性乙肝患者比较无统计学差异(P＞0.05),急性肝炎、丙型病毒性肝炎患者血清LN、HA、PC-Ⅲ和Ⅳ-C水平与健康者比较没有统计学差异(P＞0.05).结论 LN、HA、PC-Ⅲ和Ⅳ-C是反映肝脏状况和肝纤维化程度的良好指标,动态观察其变化可用于判断患者病情进展,也可用于判断患者治疗效果.     

银杏叶提取物对非酒精性脂肪性肝炎肝损伤的保护作用

目的:研究银杏叶提取物对非酒精性脂肪性肝炎大鼠肝损伤的保护作用.方法:Wistar大鼠随机分成3组,正常组予正常饮食喂养,模型组予高脂饮食喂养,治疗组予高脂饮食同时给予6 mg/kg的银杏叶提取物喂养,每天1次.于12周末处死大鼠,测血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶、透明质酸(HA)、层粘连蛋白(LN)、Ⅲ型前胶原肽(PCⅢ)和Ⅳ型胶原(C-Ⅳ);取肝组织作HE染色,病理分级,同时检测超氧化物歧化酶(SOD)和丙二醛(MDA)含量.结果:与模型组比较,治疗组肝细胞损害较轻,肝功明显改善,肝组织中MDA含量下降,SOD含量上升,且反映肝纤维化的指标HA、LN、PCⅢ和C-Ⅳ均显著降低(P＜0.01).结论:银杏叶提取物具有抑制非酒精性脂肪性肝炎肝损伤的作用.     

自身免疫性肝病患者肝纤维化血清标志物检测的意义

目的 探讨血清透明质酸(HA)、Ⅲ型前胶原(PCⅢ)、Ⅳ型胶原(CⅣ)和层粘连蛋白(LN)对自身免疫性肝病(ALD)患者肝纤维化诊断及鉴别的意义.方法 采用增强化学发光免疫分析法对37例原发性胆汁性肝硬化(PBC)患者、25例自身免疫性肝炎(AIH)患者、33例肝硬化患者、37例病毒性肝炎患者及20例健康体检者血清HA、PCⅢ、CⅣ、LN进行检测,并对部分患者在治疗6个月后再次检测上述指标,同时和部分肝功能指标进行相关性分析.结果 ALD患者4项肝纤维化指标均高于健康对照组(均P<0.05);AIH组4项指标均高于病毒性肝炎组(均P<0.01),ROC曲线下面积分别为0.823、0.849、0.824和0.830; PBC组CⅣ和LN低于肝硬化组(P<0.05);两组ALD患者在经治疗6个月后,上述指标均明显下降(均P<0.05).结论 肝纤维化血清标志物HA、PCⅢ、CⅣ和LN对于ALD患者肝纤维化的诊断及和病毒性肝炎的鉴别具有一定价值,并能间接反映肝脏炎症的情况.     

血清“肝纤四项”检查在诊断肝纤维化程度中的作用

目的分析Ⅲ型前胶原（PCⅢ）、Ⅳ型胶原（Ⅳ-C）、层粘连蛋白（LN）和透明质酸酶（HA）在诊断肝纤维化程度的作用。方法采用化学发光法测定120例病毒性肝炎患者及80例健康献血者血清PCⅢ、Ⅳ-C、LN和HA水平,结合病理结果分析其与肝纤维化程度的关系。结果上述四项血清学指标在肝炎患者中均明显升高,以肝硬化者为最高,其升高程度与肝纤维化及肝病严重程度呈正相关。结论血清PCⅢ、Ⅳ-C、LN和HA水平与肝纤维化程度相关,可作为反映慢性肝病肝纤维化严重程度和预后的指标。     

瘦素和转化生长因子β1对非酒精性脂肪性肝炎患者肝纤维化的影响

目的Ⅲ型前胶原对非酒精性脂肪性肝炎（NASH）患者血清中转化生长因子13,（TGF—β1）和瘦素水平进行检测,并分析两者之间的相关性,从而探讨两者对肝纤维化的影响。方法检测32例NASH患者血清瘦素水平以及TGF—β1水平,同时选取31例单纯性脂肪肝,24例健康人作为对照组进行比较,同时检测NASH患者的血清肝纤维化指标透明脂酸（HA）、层黏蛋白（LN）、Ⅲ型前胶原（PC Ⅲ）,并对血清瘦素水平以及TGF—β1水平、肝纤维化指标进行相关性分析。结果NASH患者血清瘦素水平以及TGF-β1水平明显高于对照组,差异有显著性,并且NASH患者血清瘦素水平、TGF—β1水平以及肝纤维化指标之间呈正相关。结论瘦素在NASH发病中具有独立的致病作用,并可能是通过TGF—β1系统而导致肝纤维化形成。     

瘦素和转化生长因子β_1对非酒精性脂肪性肝炎患者肝纤维化的促进作用研究

目的针对非酒精性脂肪性肝炎（NASH）患者体内转化生长因子β1（TGF-β1）和瘦素与肝纤维化之间的相关性进行研究,从而阐述两者对肝纤维化的促进作用。方法检测NASH患者血清瘦素水平以及TGF-β1水平,同时检测NASH患者的血清肝纤维化指标透明质酸（HA）、板层素（LN）、Ⅲ型前胶原肽（PCⅢ）等,其结果与单纯性脂肪肝患者及健康对照者进行组间比较,最后对血清瘦素、TGF-β1与肝纤维化指标进行相关性分析。结果 NASH患者血清瘦素水平以及TGF-β1水平明显高于对照组,差异有显著性,并且NASH患者血清瘦素水平、TGF-β1水平以及肝纤维化指标之间呈正相关。结论瘦素和TGF-β1是NASH进展为肝纤维化过程中的重要因子,但其分子机制需进一步深入研究。     

肝移植后肝功能的异常★

背景：肝移植后导致肝功能异常原因复杂，早期弄清引起肝功能异常的原因对治疗至关重要。目的：较全面的了解肝移植后可以导致肝功能异常的原因，以便应用于临床诊治。方法：应用计算机检索CNKI和FMJS数据库，采用医学主题词检索，检索词为“肝移植；肝功能异常；转氨酶异常；胆红素升高；原因”或“liver transplantation；abnormal liver function；transaminase abnormalities；bilirubin increased, and causes”，时间范围为1991年1月至2012年7月，共检索到98篇文章，选择文章主要内容与肝移植后肝功能异常直接相关的、发表在权威杂志上的文章共35篇进行综述。结果与结论：肝移植后导致肝功能异常的原因众多，临床表现复杂。最常见的原因依次是急性排斥反应、胆道并发症及病毒感染。肝移植后早期，尤其是1个月内出现肝功能异常，需警惕小体积综合征和原发性移植物无功的发生。各种原因引起的肝功能异常，转氨酶及胆红素升高的程度不尽相同。急性排斥反应、自身免疫性肝炎、病毒感染、门静脉及肝静脉狭窄、缺血-再灌注损伤等转氨酶升高较胆红素升高显著；慢性排斥反应、胆道并发症、肝动脉狭窄、原发性胆汁性肝硬化、原发性硬化性胆管炎等早期以梗阻酶碱性磷酸酶、谷氨酰转移酶、总胆红素、直接胆红素升高为主；肿瘤导致的肝功能异常视肿瘤大小、压迫部位不同，可表现出以转氨酶升高为主或以胆红素升高为主。此外，各种原因多有其特殊病史，仔细询问病史有助于早期诊断。临床工作中，应重视尽量详尽的采集病史，根据转氨酶和胆红素升高的具体情况，首先考虑引起肝功能异常的常见原因，经临床证实排除后再考虑其他相对不常见原因，并结合实验室检查、影像学检查及肝脏穿刺病理活检，尽早明确病因及治疗。     

Acute liver failure: liver support therapies

PURPOSE OF REVIEW: We summarize the therapeutic approach to patients with acute liver failure with the main focus on bioartificial and artificial liver support. We also describe specific and general therapeutic approaches based upon recent advances in the understanding of the pathophysiology of acute liver failure. RECENT FINDINGS: Bioartificial liver support systems use hepatocytes in an extracorporeal device connected to the patient's circulation. Artificial liver support is intended to remove protein-bound toxins and water-soluble toxins without providing synthetic function. Both systems improve clinical and biochemical parameters and can be applied safely to patients. Although bioartificial liver-assist devices have not been shown to improve the survival of patients with acute liver failure, further development is underway. Artificial liver support systems have been shown to alter several pathophysiological mechanisms involved in the development of acute liver failure but survival data are still limited. SUMMARY: Mortality in patients with acute liver failure is still unacceptably high. The most effective treatment, liver transplantation, is a limited resource and so other therapeutic options to bridge patients to recovery or stabilization have to be considered. Better understanding of the pathophysiology of acute liver failure and device development is necessary to achieve the elusive goal of effective extracorporeal liver assist.     

晚期肝癌合并肝包膜下出血或肝破裂出血的护理

目的总结晚期肝癌并肝包膜下出血或肝破裂出血的护理要点。方法2001年1月~2004年12月对本院收治的56例晚期肝癌并肝包膜下出血或肝破裂出血病人进行抢救治疗,并配合护理。结果治疗总有效率为80.4%,死亡率为12.5%。结论晚期肝癌并肝包膜下出血或肝破裂出血,病情变化快,死亡率高,护理的重点在于止痛、止血、并发症的急救、病情观察,心理及支持性的护理,并开展健康教育,尽量消除各种诱发因素,有效地控制出血和防止再出血,从而提高病人的生活质量。     

Lipid peroxidation of the liver in liver disease

Material of puncture biopsy of the human liver left after morphological study was used to explore enzymatic and non-enzymatic lipid peroxidation, NADH-ferricyanide reductase activity, the content of triglycerides, cholesterol and protein. It was shown that the degree of lipid peroxidation varies considerably in different liver diseases. The highest degree of lipid peroxidation was discovered in patients with fibrosis accompanied by the symptoms of fatty dystrophy. It was established that the rate of peroxidation does not directly correlate with the level of liver lipid infiltration. It is concluded that NADH-ferricyanide reductase activity mirrors adequately the nature of a liver disease and can be used as a highly sensitive and very specific enzymatic test.     

Antipyrine kinetics in liver disease and liver transplantation

Antipyrine kinetics were studied in seven normal subjects, 10 patients with liver disease, and 13 clinically stable patients who received a liver transplant. Five patients were studied both before and after liver transplantation. Antipyrine concentrations in saliva after oral dosing were measured by HPLC. The antipyrine t1/2 was significantly longer (P less than 0.05) in patients with liver disease than in patients undergoing liver transplantation and normal subjects. Antipyrine clearance was not significantly different between patients undergoing liver transplantation and normal subjects, but it was significantly reduced (P less than 0.05) in patients with liver disease. In five patients who were studied before and after liver transplantation, there was a significant (P less than 0.05) increase in the antipyrine clearance and a marked reduction in its t1/2 after liver transplantation. These results indicate that liver transplantation improves the drug metabolizing ability of patients with liver disease and that the oxidative metabolizing capacity of the liver in clinically stable patients after liver transplantation is similar to that of normal subjects.     

Management of chronic liver failure until liver transplantation

Chronic liver failure is an important cause of morbidity and mortality and is the long-term consequence of many chronic liver diseases. In addition to determining the specific cause of the chronic liver disease, which may be amenable to targeted therapy, it is important to treat the sequelae of chronic liver failure effectively to improve quality of life, to prolong survival, and to provide a bridge to liver transplantation. Once a patient who has chronic liver failure develops hepatic decompensation, liver transplantation is the definitive treatment for those who qualify. Management of chronic liver failure is the focus of this article.