肝硬化腹水和肝性胸水的治疗

腹水和肝性胸水是肝硬化失代偿期的并发症,其产生主要是由于门脉压升高、激活交感神经系统、肾素-血管紧张素-醛固酮系统、血浆胶体渗透压降低等因素有关,肝性胸水还有膈肌破裂形成裂孔等有关。治疗上多采用利尿剂、排放腹腔积液、输注白蛋白、腹水浓缩静脉回输、外科手术,甚至肝移植等综合治疗措施。     

瘦素与肝纤维化

瘦素是肥胖基因(ob基因)的编码产物,通过与其受体结合在体内发挥多种生物学作用,调节摄食、能量代谢、生殖、造血、免疫等生理功能.参与炎性反应、损伤修复等病理生理过程.肝纤维化是多种原因所致慢性肝损伤的修复反应,是各种慢性肝病共同的病理基础.研究发现瘦素与肝纤维化的发生发展有一定的关系,本文就此作一综述.     

肝星状细胞与肝纤维化研究进展

肝星状细胞(HSC)是肝脏的一种非实质细胞,HSC活化导致细胞外基质(ECM)的增加是肝纤维化形成并最终导致肝硬化、肝功能衰竭的主要原因.因此,加强对HSC激活与凋亡调控机制的研究,有助于我们对肝纤维化发生的本质的认识,从而能更有效地防治肝纤维化.     

肝星状细胞及相关细胞因子在肝纤维化形成中的作用

肝纤维化(hepatic fibrosis)是指肝脏内弥漫性细胞外基质(extracellular matrix,ECM)过度沉积的病理过程.肝星状细胞(hepatic stellate cells,HSC)被认为是ECM的主要来源细胞,在肝纤维化发生发展中起着关键作用.另外,各种病因引起肝细胞损伤时,Kupffers细胞(KF),肝窦内皮细胞等分泌一系列细胞因子,通过旁分泌和自分泌方式作用于邻近的HSC,影响其增殖,趋化和ECM代谢.因此,HSC及细胞因子与肝纤维化的发生发展关系极为密切,阐明其关系,有助于以HSC为靶点的肝纤维化方面的研究,现就其关系分别综述如下.     

肝星状细胞的活化与肝纤维化

肝纤维化是机体对损伤的一种修复作用，即使可以应用基因或其他疗法彻底消除纤维化，但机体对抑制或消除纤维化后将产生何种反应及后果尚难预测。肝星状细胞（hepatic stellate cells，HSC）是引起肝纤维化的主要细胞，对HSC与其活化型一肌成纤维细胞（myofibroblast，MF）在肝损伤中作用的研究已颇为深入，而HSC激活在肝纤维化发生、发展中的作用甚为重要。     

肝星状细胞在血吸虫病肝纤维化形成及调控中的作用

肝星状细胞(hepatic stellate cell,HSC)是肝脏组织的一种间质细胞,具有多种生理功能,对肝纤维化的形成与转归起到关键作用.HSC同样在血吸虫病肝纤维化形成及其调节中起到重要作用.该文就HSC的生物学特性、活化及其在血吸虫病肝纤维化中的作用作一综述.     

过氧化物酶体增殖物激活受体γ与肝星状细胞在肝纤维化中的关系

肝纤维化是慢性肝损伤后常见的形态学表现，大多数是由慢性肝脏疾病发展而来。而肝损伤（肝实质炎症、坏死）激活肝星状细胞（HSC）引起大量细胞外基质沉积，是肝纤维化发生机制的中心环节。在正常肝脏中，HSC处于静息状态，细胞质中脂滴丰富，具有合成和分泌少量细胞外基质和胶原酶的能力。在肝损伤及各种慢性肝病时，HSC被激活转化为肌成纤维母样细胞，发生明显的形态和结构变化：细胞质中脂滴减少或消失，增殖迁移活性明显增强，分泌多种细胞因子和黏附分子，合成各种细胞外基质（ECM）的能力明显增强，抑制基质金属蛋白酶（MMPs）的合成和分泌，而上调基质金属蛋白酶抑制剂（TIMPs）的表达，同时发生多种基因表达的改变。     

肝包虫病与肝囊肿CT表现比较*

目的 探讨使用256排CT检查在鉴别肝包虫病与肝囊肿方面的临床价值。方法 2017年4月～2020年11月我院诊治的肝囊肿患者77例和肝包虫病患者34例接受256排CT增强扫描检查,采用ELISA法检测血清抗囊液抗原抗体(EgCF)、抗头节抗原抗体(EgP)、抗囊液半纯化抗原抗体(EgB)和抗泡球蚴抗体(Em2)。结果 本组肝包虫病患者术前血液嗜酸性粒细胞计数为(0.3±0.1)×10⁹/L,显著高于肝囊肿患者【(0.1±0.1)×10⁹/L,P＜0.05】;肝包虫病患者血清抗EgCF抗体和抗EgB抗体阳性率分别为85.3%和61.8%,均显著高于肝囊肿患者【分别为31.2%和0.0%,P＜0.05】;增强CT扫描,肝包虫病患者肝内存在类圆形、圆形或分叶状囊性灶,囊壁钙化;在入组的111例患者中,CT检查将3例(2.7%)肝包虫病误诊为肝囊肿,1例(1.0%)肝包虫病被误诊为肝转移癌,2例(1.8%)肝囊肿被误诊为肝包虫病。结论 CT检查能很好地显示肝包虫病囊性病灶的影像学特征,对鉴别肝包虫病与肝囊肿有帮助,为临床治疗提供可靠的影像学依据。     

Doppler study of hepatic vein in cirrhotic patients： Correlation with liver dysfunction and hepatic hemodynamics

INTRODUCTIONThere are many studies on inflow to the liver in liver cirrhosis (LC) in relation to hepatic dysfunction and portal hypertension. In LC, there are changes in liver parenchyma as well as alteration of hepatic vasculature, including morphologica…     

肝血管瘤、肝细胞癌和肝血管平滑肌脂肪瘤超声造影特点观察*

目的 探讨肝血管瘤(HCH)、肝细胞癌(HCC)和肝血管平滑肌脂肪瘤(HAML)患者肝内病灶超声造影特点。方法 2017年11月～2020年11月我院诊治的肝占位病变患者112例,所有患者入院后均在治疗前接受常规超声和超声造影检查,观察肝内病灶数目、大小、边界、回声、形态、血供等信息,同时观察超声造影检查过程中动脉期、门静脉期和延迟期病灶的增强模式。结果 经组织病理学检查诊断为HCH患者39例,HCC患者64例和HMAL患者9例;HCH患者女性占比为66.7%,显著高于HCC或HAML患者(分别为18.8%和33.3%,P＜0.05),HCC患者年龄为(57.5±5.8)岁,HMAL患者年龄为(55.3±5.1)岁,均显著大于HCH患者【(46.2±5.2)岁,P<0.05】,HCC患者存在HBV感染发生率为76.6%,显著高于HMAL患者的28.6%或HCH患者的12.8%(P<0.05);在普通超声检查,HCC病灶边界不清、实质呈低回声和混合回声占比分别为65.6%、43.8%和42.2%,显著高于HCH病灶的2.6%、10.3%和7.7%或HAML病灶的0.0%、11.1%和11.1%(P＜0.05),HCH、HCC和HAML患者肝内病灶数目、病灶大小、形态和血供比较,差异无统计学意义(P＞0.05);在超声造影检查方面,HCH病灶在动脉期呈高增强占比为92.3%,显著高于HCC病灶的87.5%或HMAL病灶的88.9%(P＜0.05),HCC病灶门静脉期和延迟期呈低增强占比分别为65.6%和90.6%,显著高于HCH病灶的5.1%和43.6%或HMAL病灶的11.1%和22.2%(P＜0.05)。结论 HAML、HCH和HCC病灶在超声检查方面各具特点,而超声造影检查更具诊断和鉴别诊断价值,值得进一步研究。     

亚临床型肝性脑病

亚临床肝性脑病 (ＳｕｂｃｌｉｎｉｃａｌＨｅｐａｔｉｃＥｎ ｃｅｐｈａｌｏｐａｔｈｙ ,ＳＨＥ)是指慢性肝病病人无明显肝性脑病临床表现和血生化检测异常 ,仅能用精细的智力试验和 (或 )电生理检测才能诊断的肝性脑病。慢性肝病及肝硬化为常见病。ＳＨＥ为肝硬化的常见并发症 ,潜隐性大 ,不易被发现 ,患者虽形似正常 ,但操作能力和应激能力减低 ,使从事高空、机械、驾驶等工种的患者易发生意外。随着我国人民生活水平提高 ,驾车者逐渐增加 ,忽视对ＳＨＥ早期诊断和治疗 ,对患者和社会均会带来不利影响。　　亚临床型肝性脑病的流行病学Ｓ…     

肝纤维化的诊断和评估

肝纤维化是一种病理状态，又是一组临床和病理学综合征，其诊断有赖于临床评估、血清生化指标检测、影像学检查和组织病理学检查等。除了组织病理学诊断外，目前尚无准确和敏感的肝纤维化非创伤性的诊断方法，准确诊断和评估肝纤维化程度对肝纤维化的防治及其预后评估有非常重要的意义。     

Regulation of hepatic blood flow: the hepatic arterial buffer response revisited

The interest in the liver dates back to ancient times when it was considered to be the seat of life processes. The liver is indeed essential to life,not only due to its complex functions in biosynthesis,metabolism and clearance,but also its dramatic role as the blood volume reservoir. Among parenchymal organs,blood flow to the liver is unique due to the dual supply from the portal vein and the hepatic artery. Knowledge of the mutual communication of both the hepatic artery and the portal vein is essential to understand hepatic physiology and pathophysiology. To distinguish the individual importance of each of these inflows in normal and abnormal states is still a challenging task and the subject of on-going research. A central mechanism that controls and allows constancy of hepatic blood flow is the hepatic arterial buffer response. The current paper reviews the relevance of this intimate hepatic blood flow regulatory system in health and disease. We exclusively focus on the endogenous interrelationship between the hepatic arterial and portal venous inflow circuits in liver resection and transplantation,as well as inflammatory and chronic liver diseases. We do not consider the hepatic microvascular anatomy,as this has been the subject of another recent review.     

姜黄素预防肝纤维化作用与肝星状细胞的关系

目的观察姜黄素预防大鼠肝纤维化作用及活化肝星状细胞(HSC)的数目、分布、凋亡等变化,并探讨两者间的关系。方法以四氯化碳制作大鼠肝纤维化模型,同时按每100 g体重分别给予20、10、5 mg姜黄素灌胃处理,设立正常对照组、肝纤维化组和阳性对照组;8周后处死大鼠,留取肝左叶行HE、Masson染色,参照肝纤维化半定量计分系统进行肝纤维化程度评分,免疫组织化学方法检测α-平滑肌肌动蛋白以了解活化HSC的数量变化, TUNEL与肌源性特异性标志物结合蛋白(Desmin)免疫组织化学双染法检测HSC凋亡。结果姜黄素可明显改善四氯化碳所致大鼠肝纤维化的病理学改变;α-平滑肌肌动蛋白在肝纤维化时表达明显增多,姜黄素使活化HSC数量减少, }[SC凋亡增加,与对照组比较差异具有统计学意义(P<0．05),且具有量效关系。结论姜黄素可抑制HSC活化、增殖,诱导HSC凋亡,可能为预防肝纤维化的作用机制之一。     

Hemodynamic changes in hepatic sinusoids of hepatic steatosis mice

BACKGROUND Fatty liver(FL) is now a worldwide disease. For decades, researchers have been kept trying to elucidate the mechanism of FL at the molecular level, but rarely involve the study of morphology and medical physics. Traditionally, it was believed that hemodynamic changes occur only when fibrosis occurs, but it has been proved that these changes already show in steatosis stage, which may help to reveal the pathogenesis and its progress. Because the pseudolobules are not formed during the steatosis stage, this phenomenon may be caused by the compression of the liver microcirculation and changes in the hemodynamics.AIM To understand the pathogenesis of hepatic steatosis and to study the hemodynamic changes associated with hepatic steatosis.METHODS Eight-week-old male C57 BL/6 mice were divided into three groups randomly(control group, 2-wk group, and 4-wk group), with 16 mice per group. A hepatic steatosis model was established by subcutaneous injection of carbon tetrachloride in mice. After establishing the model, liver tissue from mice was stained with hematoxylin and eosin(HE), and oil red O stains. Blood was collected from the angular vein, and hemorheological parameters were estimated. A two-photon fluorescence microscope was used to examine the flow properties of red blood cells in the hepatic sinusoids.RESULTS Oil red O staining indicated lipid accumulation in the liver after CCl_4 treatment.HE staining indicated narrowing of the hepatic sinusoidal vessels. No significant difference was observed between the 2-wk and 4-wk groups of mice onmorphological examination. Hemorheological tests included whole blood viscosity(mPas, γ = 10 s-1/γ = 100 s-1)(8.83 ± 2.22/4.69 ± 1.16, 7.73 ± 2.46/4.22 ±1.32, and 8.06 ± 2.88/4.22 ± 1.50), red blood cell volume(%)(51.00 ± 4.00, 42.00 ±5.00, and 40.00 ± 3.00), the content of plasma fibrinase(g/L)(3.80 ± 0.50, 2.90 ±0.80, and 2.30 ± 0.70), erythrocyte deformation index(%)(44.49 ± 5.81, 48.00 ±15.29, and 44.36 ± 15.01), erythrocyte electrophoresis rate(mm/s per V/m)(0.55 ±0.11, 0.50 ± 0.11, and 0.60 ± 0.20), revealing pathological changes in plasma components and red blood cells of hepatic steatosis. Assessment of blood flow velocity in the hepatic sinusoids with a laser Doppler flowmeter(mL/min per100 g)(94.43 ± 14.64, 80.00 ± 12.12, and 67.26 ± 5.92) and two-photon laser scanning microscope(μm/s)(325.68 ± 112.66, 213.53 ± 65.33, and 173.26 ± 44.02)revealed that as the modeling time increased, the blood flow velocity in the hepatic sinusoids decreased gradually, and the diameter of the hepatic sinusoids became smaller(μm)(10.28 ± 1.40, 6.84 ± 0.93, and 5.82 ± 0.79).CONCLUSION The inner diameter of the hepatic sinusoids decreases along with the decrease in the blood flow velocity within the sinusoids and the changes in the systemic hemorheology.     

Treatment of colorectal cancer hepatic metastases by hepatic artery chemotherapy

Our clinical experience with 69 patients with metastatic colorectal cancer to the liver treated with hepatic artery chemotherapy is reviewed. All patients have had a minimum of six months follow-up. The Infusaid^® implantable drug delivery system was used by direct laparotomy in one third, and via the transaxillary approach in the remaining two thirds. Two thirds of the patients had at least 25 percent of the liver replaced with tumor. Chemotherapeutic agents included FUdR, mitomycin C, and BCNU. The overall response rate was 51 percent and 69 percent for the three-drug combination. Efficacy was not different in patients who had received prior systemic fluorouracil. Median survival from start of hepatic artery chemotherapy was one year.     

亚临床肝性脑病的流行病学调查

目的 了解亚临床肝性脑病(SHE)患病率及相关因素。 方法 对409例肝硬化患者进行数字连接试验(NCT)和数字符号试验(DST)检查。 结果 肝硬化患者SHE患病率为51.3％,肝硬化与正常对照组各年龄段及总的NCT、DST差异均有显著性,t=4.108～25.231,P<0.01。Child—pugh A、B、C级患者的患病率分别为39.9％(75/188)、55.2％(79/143)、71.8％(56/78),三组间差异有显著性,x2=23.910,P<0.01。小于35、35～44、45～54、55～64和大于64岁五个年龄段的患病率、性别、吸烟与否、酒精性和非酒精性肝硬化患者、不同文化程度,患者之间的患病率比较差异均无显著性。Logistic回归分析显示SHE患病率仅与Child—pugh分级相关,而与年龄、性别、吸烟、病因和文化程度无关。 结论 肝硬化患者SHE患病率为51.3％。Child-pugh分级是重要的危险因子。     

肝星状细胞凋亡及其影响因素的研究进展

肝星状细胞是位于肝血窦内皮细胞与肝细胞之间的一种肝非实质细胞,它的凋亡被认为是肝纤维化自发性恢复的中心环节.有关肝星状细胞凋亡的机制复杂,目前认为主要有死亡受体途径、线粒体途径、内质网途径、神经生长因子途径、外周型苯二氮卓受体途径和过氧化物酶增殖物活化受体途径等.     

肝星状细胞的可塑性及其对肝纤维化的意义

在肝纤维化形成过程中,肝星状细胞(hepatic stellate cells,HSC)发挥着重要的作用.基础和临床研究结果显示,在特殊的内环境因素的影响下HSC具有朝多方向分化的潜能.对HSC命运的干预能够在一定程度上预防肝纤维化的发生,甚至逆转肝纤维化,因此HSC的可塑性研究可能为慢性肝病治疗开辟一条新途径.本文就HSC的起源、结构、可塑性及其对肝纤维化的潜在治疗意义作一综述.     

结缔组织生长因子与肝纤维化的研究进展

肝纤维化是大多数慢性肝病共有的组织学改变,因此,能否终止肝纤维化的进展甚或逆转至正常,是治疗慢性肝病的关键.在肝纤维化的发病机制及治疗研究中,细胞因子网络始终是人们研究的热点.结缔组织生长因子(connective tissuegrowth factor CTGF)是一种新发现的细胞因子,1991年由Bradham等从人脐静脉内皮细胞(HUVEC)培养液中分离所得,为富含半胱氨酸的多肽.目前,CTGF在肝纤维化的研究中已成为新的热点.本文就CTGF的结构,生物学特性,主要调节因素及其与肝纤维化的关系作一综述.