Hepatocyte and nuclear areas and fatty infiltration of the liver in chronic alcoholic liver disease

In 117 patients affected by chronic alcoholic liver disease, we have histomorphometrically determined hepatocyte and nuclear areas, total amount of fat and total amount of fibrosis, comparing them with the following clinical and biochemical parameters: ascites, encephalopathy, jaundice, spiders, collateral circulation, splenomegaly, prothrombin activity, serum albumin, gammaglobulin, bilirubin, ASAT, ALAT, GGT, leukocyte and platelet count, and daily consumption of ethanol. Both hepatocyte and nuclear areas closely correlated with most of the parameters indicative of hepatic function derangement, whereas fat amount correlated with them inversely, but positively with the daily consumption of ethanol. The degree of fibrosis was greater in patients with a worse hepatic function, and there was a direct relationship between the degree of fibrosis and hepatocyte and nuclear areas, and an inverse one between the degree of fibrosis and the total amount of fat.     

肝硬化CT表现与肝纤维化因子的关系

目的 探讨肝纤维化因子的检测数据及其与CT扫描图像表现之间的关系。方法对89例住院患者的CT图像进行肝硬化CT分级：0级（无肝硬化）,Ⅰ级,Ⅱ级,Ⅲ级,Ⅳ级。然后与其血清联合检测肝纤维化因子[Ⅲ型前胶原肽（PCⅢ）、Ⅳ型胶原（Ⅳ-C）、层粘连蛋白（LN）、透明质酸（HA）]的检测数据进行对比分析。结果0级无肝硬化患者中,四项指标均无升高;CT表现为Ⅰ级的肝硬化患者中,Ⅳ-C略有升高;CT表现为Ⅱ级的肝硬化患者中,Ⅳ-C、HA略有升高;CT表现为Ⅲ级的肝硬化患者中,Ⅳ-C、HA、LN三项升高,以HA为显著;CT表现为Ⅳ级的肝硬化患者中,四项指标均有显著升高。结论随着肝硬化CT表现的明显,各项肝纤维化因子的升高也显著,两者呈正相关。     

血清瘦素与慢性乙型肝炎合并酒精性肝病肝纤维化的关系

目的 研究血清瘦素与慢性乙型肝炎合并酒精性肝病(CHB+ALD)肝纤维化的关系.方法 选择CHB+ALD患者17例、肝硬化(LC)15例、慢性乙型肝炎(CHB)19例,以12例男性健康受试者(NC)为对照组.采用ELISA法测定各组血清瘦素水平,同步检测血清肝纤维化指标透明质酸(HA)、层粘连蛋白(IN)、前胶原蛋白(PCⅢ)和Ⅳ型胶原(Ⅳ-C),对结果进行分析.结果 CHB+ALD组血清瘦素水平(6.79±24.12)μg/L高于对照组(4.27±7.18) μg/L(P＜0.05),单纯CHB组差异无统计学意义,CHB+ALD组患者肝纤维化四项指标高于单纯CHB组及NC组;CHB+ALD组血清瘦素水平与血清肝纤维化四项指标呈正相关(P＜0.05或P＜0.01).结论 血清瘦素是CHB+ALD患者肝纤维化形成的促进因子之一.     

思美泰治疗酒精性肝硬化临床疗效观察

目的:观察思美泰治疗酒精性肝硬化的临床疗效和安全性.方法:将临床明确诊断酒精性肝硬化的120例住院病人随机分为两组,治疗组在常规护肝基础上给予思美泰1.0,每日一次静脉滴注,对照组仅给予常规护肝治疗,疗程4周.结果:治疗组显效率66.7％,总有效率为74％；对照组显效率为50％,总有效率为71.6％.两组比较,治疗组显...     

Blood antioxidant levels in patients with alcoholic liver disease correlate with the degree of liver impairment and are not specific to alcoholic liver injury itself

BACKGROUND: Enhanced production of reactive oxygen species may play a pathogenic role in alcoholic liver injury. AIMS: To investigate whether various antioxidant parameters in blood are affected in different stages of alcoholic liver disease and how specific the changes are relative to non-alcoholic cirrhosis. METHODS: Patients with alcohol abuse without cirrhosis (n=14), with alcoholic cirrhosis [Child-Pugh scores A (n=9), B (n=5) and C (n=18)] and with non-alcoholic cirrhosis [Child-Pugh score C (n=6)] and healthy controls (n=13) were studied. Levels of reduced glutathione and glutathione peroxidase activity in blood, erythrocytic superoxide dismutase activity and carotenoids, alpha-tocopherol and malondialdehyde in plasma were measured. RESULTS: Levels of reduced glutathione were significantly decreased in Child-Pugh score C cirrhotics, alcoholic or not in origin, whereas oxidized glutathione and glutathione peroxidase activity were not affected. Superoxide dismutase activity and alpha-tocopherol levels were not significantly different in the various groups. Carotenoid levels were significantly lower in alcoholic cirrhotics (Child-Pugh score C) vs. controls. Malondialdehyde levels were elevated only in cirrhotics Child-Pugh score C, alcoholic or non-alcoholic. CONCLUSIONS: Levels of reduced glutathione and malondialdehyde reflect the degree of liver impairment, more than the relation with alcohol intake. Decreases in several antioxidant levels are not specific to alcoholic liver injury.     

Polymorphism in glutathione-S-transferases: A risk factor in alcoholic liver cirrhosis

In a case-control study, association of polymorphism in glutathione-S-transferases (GSTM1, GSTT1, GSTP1), involved in detoxification of reactive oxygen species (ROS), was studied with alcoholic liver cirrhosis. The study included 175 alcoholic cirrhotic patients (ACPs), 140 non-alcoholic cirrhotic patients (NACPs), visiting Sanjay Gandhi Post Graduate Institute of Medical Sciences (SGPGI), Lucknow, India, 255 non-alcoholic controls and 140 alcoholic controls. The data showed an increase in risk to alcoholic cirrhosis in ACPs with GSTM1 (null) genotype when compared with non-alcoholic controls (OR: 1.7; 95% CI: 1.15–2.56) or alcoholic controls (OR: 1.7; 95% CI: 1.07–2.73). Significant increase in risk was also observed in ACPs with variant genotype of GSTP1 when compared with non-alcoholic controls (OR: 1.65; 95% CI: 1.12–2.43). A much higher risk to alcoholic liver cirrhosis was observed in patients carrying combination of null genotypes of GSTM1 and GSTT1 (OR: 2.8; 95% CI: 1.3–6.06) or variant genotype of GSTP1 and null genotype of GSTM1 (OR: 2.8; 95% CI: 1.58–4.90) or GSTT1 (OR: 2.16; 95% CI: 1.08–4.28). Likewise, greater risk for alcoholic cirrhosis was observed in patients carrying combination of GSTM1, GSTT1 (null) and variant genotype of GSTP1 (OR: 5.8; 95% CI: 2.17–15.80). Our data further showed that interaction of GSTs with variant genotype of manganese superoxide dismutase (MnSOD), which detoxifies free radicals, or cytochrome P450 2E1, which generates free radicals, resulted in several fold increase in risk to alcoholic liver cirrhosis in ACPs when compared with non-alcoholic controls thus demonstrating the role of gene–gene interactions in modulating the risk to alcoholic liver cirrhosis.     

Correlation of percutaneous liver biopsy fragmentation with the degree of fibrosis

BACKGROUND: Although fragmentation of a liver biopsy specimen has been considered to be suggestive of cirrhosis, the evidence for this is difficult to find in the published literature. AIM: To determine whether fragmentation of percutaneous liver biopsy specimens correlates with the degree of fibrosis. METHODS: One hundred and eighty-six patients underwent percutaneous liver biopsy prospectively. The specimens were measured for the length and number of fragments. The extent of fibrosis was scored by a pathologist blind to the clinical data. Length and fragmentation data were compared between the different stages. RESULTS: The overall median fragment length was 1.85 cm and the median fragment number was four. Specimens with advanced fibrosis (stages III-IV) had more fragments than those with no or mild fibrosis (stages 0-II) (P < 0.0001). The aggregate fragment length decreased with increasing stage of fibrosis (P < 0.0001). Specimens with greater than 12 fragments were seen only with advanced fibrosis. CONCLUSIONS: Fragmentation of percutaneous liver biopsy specimens is common and increases with progression from early to advanced fibrosis. Fibrotic specimens fragment more often and more extensively.     

还原型谷胱甘肽对慢性肝病患者肝细胞损害及肝纤维化程度的影响

目的探讨还原型谷胱甘肽治疗慢性肝病患者的疗效及作用机制。方法对40例慢性肝炎（cH）、30例活动性肝硬化（Hc）、25例慢性重症肝炎（CHH）患者．使用还原型谷胱甘肽12g静脉滴注．每日1次．疗程为45d．治疗前后检测患者血清中白细胞介素6（IL-6）、lL-8、肿瘤坏死因子口（TNF-α）、Ⅲ型前胶原（PCⅢ）、透明质酸（HA）、ALT、AST、TBil，同时25例患者进行了肝组织活检。结果慢性肝炎组、活动性肝硬化组、慢性重症肝炎组治疗后IL-6、IL-8、TNF-α、PCⅢ、HA、ALT、AST、TBiI各项检测值均比治疗前明显下降．P值均〈0．01．差异有统计学意义。25例肝组织活检治疗前肝纤维化1、2、3、4期病例数分别为8、7、5、5例：炎症活动度1、2、3、4级病例数分别为6、4、7、8例：治疗后肝纤维化1、2、3、4期病例数分别为12、10、2、1例；炎症活动度1、2、3、4级病例数分别为他、8、2、2例，治疗后肝纤维化程度和炎症活动度得到明显改善。结论还原型谷胱甘肽可以降低慢性肝病患者血清中IL-6、IL-8、TNF-α浓度，控制肝脏炎症．保护肝细胞．对阻止肝纤维化有明显作用。     

Gender difference of clinical features in Japanese patients with alcoholic liver cirrhosis]

Gender difference of alcohol intake and laboratory data was investigated in 165 Japanese patients with alcoholic liver cirrhosis. Mean age of first drinking and habitual drinking were higher in female. Duration of drinking was shorter in female. Although cumulative alcohol intake was larger in male, mean daily alcohol intake did not differ in both gender. Moreover, daily alcohol intake adjusted to body weight was significantly larger in female. Body mass index, serum levels of total protein, albumin and cholinesterase were significantly decreased in female. Platelet counts on admission did not differ in both gender. However, it was significantly increased in female after one month abstinence. C reactive protein, ammonia and serum levels of total bilirubin were significantly higher in female as compared to male. In conclusion, female alcoholics seems to progress to liver cirrhosis earlier because of high daily alcohol intake adjusted to body weight, poor nutritional condition and inflammation caused by endotoxin.     

丹参素和泮托拉唑对肝硬化大鼠肝部分切除术后肝再生的影响研究

目的以肝硬化大鼠为动物模型,研究药物对肝硬化大鼠肝部分切除术后肝再生的影响。方法取健康的Wistar雄性大鼠64只,以60%CCl4油溶液0.3ml/100g皮下注射,同时饮用5%酒精溶液,45d后制成肝硬化动物模型。模型大鼠随机分为4组,16只/组。全麻下均行左、中叶肝切除术。术后各组按以下方案处理:对照组皮下注射生理盐水1mg·kg-1·d-1,丹参素组腹腔注射18mg·kg-1·d-1,泮托拉唑组皮下注射0.2mg·kg-1·d-1,两药合用组同时给予丹参素(tanshinol)腹腔注射18mg·kg-1·d-1,泮托拉唑(pantoprazole)皮下注射0.2mg·kg-1·d-1,连续给药2周,抽取静脉血样,取肝脏组织,检测肝功能、有丝分裂指数(MI)、增生细胞核抗原(PCNA)、细胞核DNA含量。结果丹参素组、泮托拉唑组及两药合用组MI、PCNA阳性染色细胞量、细胞核DNA含量均高于对照组(P<0.05),两药合用组MI、PCNA阳性染色细胞量、细胞核DNA含量均高于丹参素组、泮托拉唑组(P<0.05),但各组间肝功能变化无明显差异。结论丹参素、泮托拉唑及两药合用均对肝硬化大鼠肝部分切除术后肝细胞再生有促进作用。     

超声造影在肝硬化基础上低度和高度不典型增生结节的显像观察

目的探讨超声造影在肝硬化基础上低度和高度不典型增生结节的表现。方法对本院2009年6月～2011年6月经病理确诊的17个低度和20个高度不典型增生结节患者的二维超声和超声造影检查资料进行回顾性分析,观测指标为病灶的大小、回声、边界、声晕及血供。结果超声造影显示低度不典型增生结节（LGDN）和高度不典型增生结节（HGDN）在动脉期、门脉期、延迟期表现无明显差异,差异无统计学意义（P〉0.05）。结论超声造影在肝硬化基础上低度和高度不典型增生结节的表现相似;对LGDN与HGDN只有通过穿刺病理检查确诊,但通过超声造影的三期表现及各期增强水平表现,可以反映出肝脏不同的血供变化,对肝细胞癌的早期诊断提供帮助。     

血清肝纤维化标志物在肝硬化诊断中的价值

目的 研究血清肝纤维化标志物(LN、PⅢP、CⅣ)对肝硬化的诊断价值。方法 检测184例病毒性肝炎患血清肝纤维化标志物(LN、PⅢP、CⅣ)，检测结果经F检验(方差分析)及q检验确定统计学意义。结果 血清肝纤维化标志物(LN、PⅢP、CⅣ)，在肝炎肝硬化患中检测水平最高，与急性肝炎、慢性肝炎差异均具有显性(P＜o．01)。结论 血清肝纤维化标志物(LN、PⅢP、CⅣ)对肝炎肝硬化诊断具有明显的指导价值。     

环氧化酶-2与肝纤维化的关系研究

环氧化酶-2抑制剂抗肝纤维化形成的具体分子机制存在广泛争议。目前研究认为抑制环氧化酶-2对化学损伤性肝纤维化模型有治疗作用,却对免疫性肝纤维化模型起加重作用。该文综述了环氧化酶-2对肝纤维化的影响,旨在为不同病因导致肝纤维化的有效治疗提供新的途径或靶点。     

肝硬化门脉高压与内皮素的关系探讨

目的探讨肝硬化门脉高压（Ｐｏｒｔａｌ ｈｙｐｅｒｔｅｎｓｉｏｎ，ＰＴＨ）的血流动力学变化及其与血中内皮素（ＥＴ）的关系。方法４８例肝硬化ＰＴＨ病人（代偿期１８例，失代偿期３０例）及３２例正常人作为研究对象，应用双功多普勒测定门、脾静脉血流量（ＰＶＢＦ＆ＳＶＢＦ），同步测定血中ＥＴ的水平，并分析ＰＶＢＦ＆ＳＶＢＦ的相关性。结果门脉系统高血流动力学改变存在于肝硬化ＰＴＨ发病的始终，ＥＴ的生成与门脉高血流动力学变化无相关性。     

Total serum testosterone estimation and ultrasonographic volumetric evaluation of testes in patients with alcoholic liver cirrhosis

In the course of cirrhosis, a variety of disturbances of endocrine glands occur. Degenerative changes in the testes with atrophia and fibrosis of the glandular tissue are often found in men. Twenty-one males with compensated alcoholic liver cirrhosis were studied. The age ranged from 29 to 61 years (mean 47,1). Efficiency of the liver was evaluated according to Child classification. HBC (this needs to be spelled out in parenthesis) or HBV (Hepatitis B Virus) infections were excluded. Levels of serum testosterone were determined and the volume size of the testes was measured using 7,5 MHz sector probe, B&K Medical ultrasonograph, 3535 model. Volume size of the testes was measured in 22 healthy control volunteers, as well; age ranged from 25 to 66 years (mean-46,6). All patients were interviewed about sexual function, particularly possible erectile dysfunction using IIEF-5 questionnaire. The mean testosterone level was 8,89 umol/l (ranged: 7,4–10,9 umol/l) in the study patients [the normal range interval: 8,2–34,6 umol/l]. The level was below the normal range in 4 patients, and low but within the normal range in the remaining patients. Statistically significant lower values of both testes volumes were estimated in patients with compensated alcoholic liver cirrhosis in comparison to healthy controls (p<0,001), however only 5 (23,81 %) study group subjects admitted impaired libido and erectile dysfunction. Decreased levels of testosterone in the peripheral blood and diminished volume size of testes are found in patients suffering from alcoholic liver cirrhosis. Erectile dysfunction in patients with liver cirrhosis needs further evaluation.     

Methylcellulose prevents the regression of carbon tetrachloride-induced liver fibrosis and cirrhosis in rats

Male F344 rats were treated with carbon tetrachloride (CCl4; 0.3 ml/kg per os, 3 times a week) for 2 mo. At the end of the CCl4 administration out of the 65 animals 30 received methylcellulose (MCL; 3.85 ml/kg, 5% solution, per os, 3 times a week) for 6 wk. Thirty-five rats did not receive any further treatment. The fibrotic change caused by CCl4 reached its maximum 2 wk after the end of the treatment. After this, the severity of the fibrotic change regressed spontaneously. This regression was not observable in the liver of rats that received MCL. The fact that MCL is used as a solvent for drugs and as a food additive underlines the importance of the effect of this compound on chronic liver injury.