超声弹性成像对肝脏病变的诊断价值

超声弹性成像是一种新兴的超声诊断技术,近年来在慢性肝脏疾病的诊断、监测中发挥了重要作用。介绍了超声弹性成像的原理及分类、不同类型超声弹性成像技术在肝脏疾病中的应用价值和研究进展。指出超声弹性成像具有定性及定量分析肝组织硬度的能力,弥补了传统超声成像的不足,丰富了诊断信息,具有重要的临床应用价值及广阔的应用前景。     

瞬时弹性成像技术在慢性乙型肝炎中的应用进展

肝活检是诊断肝脏疾病的金标准,胃镜是诊断食管胃静脉曲张的金标准;但二者均为有创检查,因此应用受限。近年来瞬时弹性成像技术作为无创检测,临床已经广泛采用。介绍了瞬时弹性成像技术在慢性乙型肝炎患者肝纤维化、肝脂肪变、肝硬化及肝癌等方面的最新进展。未来可在乙型肝炎肝硬化和肝癌早期联合诊疗方面进行更多研究。     

肝纤维化及早期肝硬化的超声研究进展

随着超声医学检测技术的不断提高,他已成为肝纤维化及早期肝硬化的重要诊断和评价手段.二维超声用于显示肝脏形态及回声,是超声诊断的基础手段.彩色多普勒和频谱多普勒可以显示门静脉系统血流情况,不仅可以作为评价肝实质病变程度的指标,也是判断门脉高压及相关并发症的有效指标.超声造影提供了良好的血池示踪剂,能够反映肝脏的血流灌注,从而能够评估肝脏疾病的严重程度.近年来出现的弹性成像通过测量肝组织弹性模量的差异评估肝脏病变程度.Fibroscan在分期诊断慢性丙型肝炎肝纤维化、监测肝硬化门静脉高压发展中表现出了优异的诊断价值,为无创性诊断肝硬化提供了新的发展方向.以上技术综合应用于临床,大大提高了肝脏疾病的诊断成功率.本文就超声医学在肝纤维化及早期肝硬化诊断中的作用,从以上几个方面作一综述.     

非侵入性诊断肝纤维化模型研究进展

正肝纤维化是慢性肝损伤后的一种损伤修复反应,是所有慢性肝脏疾病的长期临床过程,是正常肝组织纤维化转换并组建异常结构结节的过程。传统的肝活检术仍是肝纤维化诊断的金指标,新型分子标志物及瞬时弹性成像技术出现为临床诊断提供了有效的诊断依据,可减少甚至替代肝活检术在临床上的运用。肝脏纤维化是慢性肝损伤后的修复反应,是肝脏内的细胞外基质累积的结果。肝纤维化的精确诊断是慢性肝病至关重     

肝脏CT灌注检测技术在肝脏疾病中的临床应用

肝脏具有双重血供.在各种病理情况下,肝动、静脉和门静脉之间的血流动力学发生复杂的变化.此文综述了CT灌注成像在肝脏疾病的诊断、治疗及评估中的重要价值.     

瞬时弹性成像联合声触诊组织量化技术诊断慢性HBV携带者肝纤维化与病理的对照性研究

目的:探讨瞬时弹性成像联合声触诊组织量化技术对慢性HBV携带者肝纤维化的诊断及与病理结果的相关性。方法:选择120例慢性HBV携带者,分别采用瞬时弹性成像和声触诊组织量化技术对受试者进行检测,并与病理检测结果进行对比分析。结果:采用声触诊组织量化技术检测结果显示,慢性HBV携带者肝剪切波速随病理纤维化分期的增加而逐步增高;采用瞬时弹性成像技术检测结果示随着肝纤维化程度的加重,肝脏组织硬度值逐渐升高。由此推断,肝剪切波速度和肝脏组织硬度值越大,肝纤维化程度往往越重。两者联合应用,其敏感度、特异度、准确度均较单一检测技术高,表明两者联合应用对于肝纤维化具有更高的诊断价值。结论:瞬时弹性成像和声触诊组织量化技术可无创性地反映肝组织的弹性硬度,两者联合应用能够提高诊断的特异性、敏感性、准确性,为临床诊断和治疗肝纤维化提供更有价值的信息。     

Fibroscan对肝纤维化诊断价值的研究进展

近年来,国内外学者关注于肝纤维化的无创性诊断.其中,多种血清纤维化指标检验及影像学检查是目前临床较为常用的无创性评估肝纤维化的方法,但敏感性和特异性不高.Fibroscan是一种对肝纤维化进行定量诊断的新技术,以瞬时弹性成像为原理,通过对肝脏硬度指标的测量进行肝纤维化程度评估.本文就其工作原理、临界值确定、诊断价值及应用现状进行综述.     

非酒精性脂肪性肝病患者肝纤维化筛查、评估路径及管理

非酒精性脂肪性肝病(NAFLD)并非良性疾病, 尤其是非酒精性脂肪性肝炎(NASH)合并肝纤维化F2～4患者发生肝脏相关事件和死亡的风险较高, 因此, 被认为是"有风险"的NASH。我国NAFLD患者群体庞大, 如何筛查出存在肝纤维化人群是一个重要社会经济学问题。目前, 肝纤维化的无创诊断方法(NITs)有血清学模型、基于振动控制瞬时弹性成像及磁共振弹性成像的肝硬度检测, 现结合近年来NITs的研究进展及NAFLD国内外防治指南, 梳理了NAFLD患者肝纤维化筛查、评估路径及管理建议。     

超声弹性成像对肝纤维化分级的评估

肝纤维化为多数肝病发展的重要阶段,早期准确诊断肝纤维化分级对制订个性化治疗方案、降低病死率尤为重要,超声弹性成像以独到的优点越来越受到临床医师的青睐。比较了瞬时弹性成像、声脉冲辐射弹性成像、实时剪切波弹性成像、实时组织弹性成像在肝纤维化不同分级中诊断的准确度、敏感度及特异度的差异,以期提高临床医生对不同超声弹性成像方法在肝纤维化分级诊断中优势及不足的认识。     

瞬时弹性成像与实时组织弹性成像评估肝纤维化的比较

目的 对比分析瞬时弹性成像和实时组织弹性成像评估慢性肝病肝纤维化的价值.方法 对92例行肝组织学检查的慢性肝病患者同时行瞬时弹性成像和实时组织弹性成像检查,以肝组织病理学检查结果为金标准,比较瞬时弹性成像和实时组织弹性成像与肝纤维化病理分期的相关系数、诊断肝纤维化的受试者工作特征曲线下面积. 结果 瞬时弹性成像与肝纤维化病理分期的相关系数(r=0.755,95％ CI0.651 ～ 0.831,P=0.000)高于实时组织弹性成像(r=0.481,95％CI0.306 ～ 0.624,P=0.000),Z=3.07,P=0.002.瞬时弹性成像和实时组织弹性成像诊断肝纤维化(S≥2)、肝硬化(S=4)的受试者工作特征曲线下面积分别为0.903和0.740、0.915和0.786,瞬时弹性成像高于实时组织弹性成像(P值分别为0.003和0.020). 结论 瞬时弹性成像诊断慢性肝病肝纤维化效能优于实时组织弹性成像,但后者与二维超声图像融合,具有广泛的应用前景.     

Reconstruction of hepatic organoid by hepatic stem cells

Recent advances in culture methods, stem cell research, and tissue engineering provide clues for making tissues in vitro that are functionally and structurally similar to hepatic tissues. To reconstruct hepatic organoids, two approaches to establish the methods have been proposed: the use of cells and the combination of cells and a scaffold (called tissue engineering). Recently, the coculture of hepatic cells (mature hepatocytes, small hepatocytes, hepatoblasts) and hepatic nonparenchymal cells has been reported to form hepatic organoids that possess differentiated hepatic functions. On the other hand, hepatocytes in a roller bottle were shown to form specific structures, consisting of biliary epithelial cells, connective tissue, mature hepatocytes, and endothelial cells. In this review, the studies of hepatic tissue formation in vitro will be summarized.     

成年小鼠肝组织中长期体外培养的探讨

目的探讨成年肝组织(AHT)体外中长期培养的各项活性指标,寻求以AHT替代成年肝细胞(AHC)培养的方法。方法以0.5mm3大小的肝组织贴壁于盖破片上,静置培养48h后改为旋转培养,每2天作半量换液1次,并取盖玻片作HE染色观察肝组织内细胞存活状况,第26天时结束培养观察;取培养第6天的肝组织设对照组、大黄素实验组、胆红素代谢组,分别行大黄素抗内毒素实验和胆红素代谢实验。结果在对照组,AHT染色鲜明、细胞存活良好;大黄素实验组呈现大黄素的抗内毒素作用而明显提高AHT的细胞活性;胆红素代谢实验组的总胆红素、直接胆红素、间接胆红素分别下降13.69%、19.85%、10.38%。结论AHT保持了体内三维立体结构,体外培养存活期可达26天,生物代谢活性良好,并有省时、操作简便、低成本的优点。     

Increased expression of connective tissue growth factor in fibrotic human liver and in activated hepatic stellate cells

BACKGROUND/AIMS: Connective tissue growth factor is a recently described mitogenic protein implicated in a variety of fibrotic disorders. Connective tissue growth factor may be a downstream mediator of the pro-fibrotic and mitogenic actions of transforming growth factor-beta, promoting extracellular matrix deposition and fibrogenesis. As transforming growth factor-beta is considered important to the pathogenesis of hepatic fibrosis, we examined the possible contribution of connective tissue growth factor to this process. METHODS: Connective tissue growth factor expression was examined in normal and fibrotic human and rat livers using RT-PCR and ribonuclease protection assays, and in primary cultures of rat hepatic stellate cells by Northern and Western blotting. RESULTS: Ribonuclease protection assays demonstrated connective tissue growth factor mRNA was increased 3-5-fold in human fibrotic liver compared with normal. RT-PCR showed this mRNA was increased in carbon-tetrachloride-treated rat liver. Northern analysis showed connective tissue growth factor mRNA was increasingly expressed during progressive activation of cultured rat hepatic stellate cells. Western analysis confirmed that freshly isolated hepatic stellate cells secreted relatively little connective tissue growth factor compared with hepatic stellate cells activated in culture. Hepatic stellate cells stimulated with transforming growth factor-beta showed increased expression of connective tissue growth factor mRNA and protein. CONCLUSIONS: Connective tissue growth factor mRNA is consistently upregulated in human liver cirrhosis of various aetiologies, supporting a role for this growth factor in hepatic fibrogenesis. Our studies suggest that hepatic stellate cells may be an important source of hepatic connective tissue growth factor in vivo, particularly following stimulation with transforming growth factor-beta.     

Oxygen metabolism of the liver during an HA clamp: HV saturation and free radicals

BACKGROUND/AIMS: To clarify changes in the hepatic oxygen metabolism and tissue damage resulting from oxygen-derived free radical generation from polymorphonuclear cells during a hepatic arterial clamp. METHODOLOGY: Subjects were 32 male Wistar rats. Hepatic tissue blood flow, and hepatic venous chemiluminescence, indicating oxygen-derived free radicals from polymorphonuclear cells, and liver lipid peroxide were measured, and hepatic and portal venous blood gas analysis were performed before and after 130 minutes of hepatic arterial clamping. RESULTS: Hepatic tissue blood flow decreased by hepatic arterial clamp. The values of hepatic arterial oxygen pressure (HTBF), hepatic venous oxygen saturation (ShvO2), and O2 contents after hepatic arterial clamp were lower than those before hepatic arterial clamp (P = 0.035, 0.024, and 0.028, respectively). Hepatic venous chemiluminescence decreased and the lipid peroxide level of the liver increased by hepatic arterial clamp (P = 0.001). CONCLUSIONS: ShvO2 is useful for the evaluation of hepatic oxygen metabolism and hepatic tissue blood flow during acute hepatic arterial clamp. This condition should prepare the following tissue damage due to oxygen-derived free radicals from polymorphonuclear cells.     

肝脏肿瘤缺血再灌注损伤后超氧化物歧化酶和丙二醛的改变及意义

目的　探讨缺血再灌注对肿瘤组织的影响及其意义。方法　通过超声引导将VX2肿瘤组织混悬液穿刺注射到新西兰兔肝脏左中叶 ,建立肝脏肿瘤模型 ,用无损伤血管钳阻断肿瘤所在肝叶的肝动脉分支 60min后去除血管阻断恢复血流 ,随机将模型动物分为缺血再灌注前 (对照 )、缺血再灌注后 0min、1h、1d、3d、1周 6个时间组 ,取肝脏组织和肿瘤组织 ,分别测定超氧化物歧化酶 (SOD)和丙二醛 (MDA)的含量。结果　肝脏组织中的SOD含量于缺血再灌注后迅速下降 ,至 0min达最低点 ,随后有所升高 ,至 7d时仍明显低于缺血再灌注前水平 ,各组与对照组对比差异显著 (P <0 .0 0 1) ,而肿瘤组织的SOD含量变化趋势除了 1h达最低点外 ,其余皆与肝脏组织相似 ,各组与对照组对比差异显著 (P<0 .0 0 1) ;肝脏组织的MDA含量于 0min时升至最高 ,随后开始下降 ,至 7d时仍高于缺血再灌注前水平 ,各组与对照组对比差异显著 (P <0 .0 0 1) ,而肿瘤组织的MDA含量于 1h降至最低 ,随后有所升高 ,但至 7d时仍明显低于缺血再灌注前水平 ,各组与对照组比较差异显著 (P <0 .0 0 1)。结论　肿瘤组织缺血再灌注后氧自由基的生成和损伤较正常肝脏组织明显。     

Malnutrition and hypermetabolism are not risk factors for the presence of hepatic encephalopathy: a cross-sectional study

Background and Aim: Hepatic encephalopathy is a frequent complication of cirrhosis. The present retrospective investigation was conducted to characterize metabolic alterations in cirrhotic patients with and without hepatic encephalopathy. We tested the hypothesis that reduced nutritional status or the degree of tissue catabolism are associated with the presence of hepatic encephalopathy. Methods: We investigated 223 patients with histologically confirmed nonalcoholic cirrhosis without hepatic encephalopathy and with hepatic encephalopathy (grades 1–3). To assess liver function, nutritional status, and energy metabolism, a variety of biochemical and clinical tests were performed including anthropometric measurements, bioelectrical impedance analysis, and indirect calorimetry. Results: Nutritional status and tissue catabolism were not significantly different between patients with and without hepatic encephalopathy. Conclusions: Our data do not support the hypothesis that malnutrition or tissue catabolism are independent risk factors for the presence of hepatic encephalopathy in patients with nonalcoholic cirrhosis.     

Increased serum and hepatic tissue levels of interleukin-18 in patients with fulminant hepatic failure

BACKGROUND: Fulminant hepatic failure is a serious clinical condition associated with a high mortality rate. Interleukin (IL)-18 is a pro-inflammatory cytokine that is associated with several inflammatory diseases. The purpose of the present paper was therefore to investigate whether IL-18 is elevated in patients with fulminant hepatic failure. METHODS: Serum levels of IL-18 were measured in patients with fulminant hepatic failure before and after liver transplantation. Native liver tissue samples were collected and the tissue levels of IL-18 were determined. Liver tissues were stained immunohistochemically with antihuman IL-18 antibody. The serum levels of IL-1beta, IL-6, IL-8, IL-12, interferon-gamma, and tumor necrosis factor-alpha were also determined in patients with fulminant hepatic failure before and after liver transplantation. RESULTS: Elevated levels of IL-18 in serum and hepatic tissue were observed in patients with fulminant hepatic failure. Native liver tissue samples were immunohistochemically positive for IL-18. Interleukin-18 levels were markedly reduced after liver replacement. No other inflammatory cytokines were substantially elevated in patients with fulminant hepatic failure. CONCLUSION: The serum levels of IL-18 levels are elevated much more than those of other cytokines in patients with fulminant hepatic failure.     

肝性脑病的病因和防治探讨

肝性脑病至今仍以血液检查所见的生化代谢异常来解释，因不能圆满解释全面情况，需进一步探讨。不加选择收集70例肝硬化死亡者脑组织，分别作HE和免疫组化检查，观察病理改变和HBsAg、HBcAg表达。在70例脑组织标本中免疫组化染色HBsAg、HBcAg阳性者计30例，阳性率42.3%，临床上有肝性脑病表现者阳性率明显高于无表现者，脑组织病理改变较明显者，阳性率亦明显高于较轻者。肝硬化脑组织内出现HBsAg和HBcAg表达，而且阳性率与脑组织病理改变和是否出现临床表现密切有关。提示HBV侵及脑组织，导致病理形态改变可能是肝性脑病的病理基础，生化代谢异常可能仅是肝衰的表现。     

Enzyme Studies in Dogs with Extra-hepatic Biliary Obstruction

During biliary stasis the alkaline phosphatase in hepatic tissue increased earlier and decreased later after release of the obstruction than did that in the serum. Bile pigments persisted for a long time in hepatic tissue after release of biliary obstruction. The serum gamma-glutamyl transpeptidase first increased moderately and then decreased; in hepatic tissue the enzyme did not increase, but usually decreased slightly during the 3rd to 4th week of biliary stasis. Alkaline phosphatase and adenosine triphosphatase had similar patterns in hepatic tissue, displaying thickened, knotty canaliculi as well as increased sinusoidal pattern. Soon after ligation staining for acid phosphatase showed enhanced lysosomal picture, and later enzyme positive globules appeared around bile casts and lumps of bile pigment. No remarkable changes occurred in succinic dehydrogenase, monoamine oxidase, or non-specific esterase, except for loss of enzyme in fatty degenerated cells centrilobularly after prolonged biliary obstruction.     

Characterization of hepatic hemodynamics in cirrhotics and non-cirrhotics. Effect of glucagon infusion

The effect of glucagon on hepatic regional hemodynamics was investigated in patients with chronic liver disease during peritoneoscopy with reflectance spectrophotometry. When glucagon was infused intravenously in patients with a non-cirrhotic liver, the regional hepatic tissue oxygen consumption, as estimated spectrophotometrically, increased significantly, whereas the index of hepatic tissue blood volume did not change appreciably, and consequently, the oxygen saturation of hemoglobin in the hepatic tissue blood decreased. In contrast, the administration of glucagon in patients with liver cirrhosis resulted in a significant increase in the index of hepatic tissue blood volume and produced a minor increase in hepatic tissue oxygen consumption. The oxygen saturation of hepatic blood hemoglobin tended to increase in the cirrhotics. The result suggests the presence of functional vasoconstriction at the presinusoidal and/or sinusoidal vessels in the cirrhotic liver, possibly due to a decreased vasomotor activity and/or an abnormal regulatory function of vasoactive substances, which are released by glucagon.