124例酒精性肝病的临床分析

１２４例酒精性肝病的临床分析张道明，王远新，赵静波，王泰龄，张岚，张克伦，张晶分析了我院六年来经临床和肝活检病理检查诊断的酒精性肝病（ＡＬＤ）１２４例，分为纯ＡＬＤ６５例及合并肝炎病毒感染５９例两大类，每类中分五型，得出本组酒精性肝纤维化（ＡＦ）最多...     

慢性酒精性肝病分类的探讨（附124例肝穿分析）

观察１２４例酒精性肝病（ＡＬＤ）的病理变化，根据脂肪变（Ｆ），炎症（Ｈ）及纤维化（Ｆｂ）的程度，以优势原则进行分类，Ｆ，Ｈ，Ｆｂ均为一级者定为轻症酒精性肝病，各类中主要病变２，３，４级者分别定为该类的轻，中，重亚型，三项病变同级时，则以炎症为主要决定指标，共将ＡＬＤ分为５类，即轻症酒精性肝病（占３０．６％），酒精性脂肪肝（１０．５％）酒精性肝炎（１６．９％），酒精性肝纤维化（３４．７％）和酒精性肝     

酒精性肝病不同阶段大鼠胃乙醇脱氢酶活性变化研究

目的 探讨酒精性肝病（Ａｌｃｏｈｏｌｉｃ ｌｉｖｅｒ ｄｉｓｅａｓｅ，ＡＬＤ）不同病理阶段胃乙醇脱氢酶（Ａｌｃｏｈｏｌ ｄｅｈｙｄｒｏｇｅｎａｓｅ，ＡＤＨ）活性变化。方法 用酶组织细胞化学梁色技术，在光镜下观察酒精性肝病不同阶段胃ＡＤＨ活性变化，并用ＬＵＺＥＸ－Ｆ灰度图像分析仪半定量。结果 ＡＬＤ不同阶段胃ＡＤＨ活性进行性下降，差异有显著性（Ｐ〈０．０５）。结论 提示酒精性肝病不同阶段胃ＡＤＨ活性     

酒精性肝病实验室检查及预后观察

作者报道酒精性肝病（ＡＬＤ）４０例，病理诊断ＡＦ５例，ＡＨ１５例，ＡＣ１５例，ＭＣ５例。对ＡＬＤ实验室检查及预后作了探讨。结果提示ＧＧＴ试验，结合饮酒史与戒酒后变化，对ＡＦ、ＡＨ有诊断意义。甘氨胆酸于戒酒后无改变，对诊断ＡＬＤ的发展与预后有参考价值。     

酒精性肝病外周血单个核细胞转化生长因子β1mRNA表达的研究

转化生长因子 β1(ＴＧＦ β1)在慢性肝病的纤维化过程中起重要作用。但对酒精性肝病 (ＡＬＤ)中ＴＧＦ β1的作用研究甚少 ,外周血单个核细胞 (ＰＢＭＣ)的ＴＧＦ β1ｍＲＮＡ检测尚未见有报道。我们通过检测ＡＬＤ患者ＰＢＭＣ中的ＴＧＦ β1ｍＲＮＡ表达水平 ,以探讨其临床意义。一、材料与方法1 标本 :男性嗜酒者 10 7例 ,年龄 2 5～ 70岁 ,平均年龄4 3岁。按 1995年中华医学会肝病分会酒精性肝病及肝纤维化学术研讨会关于酒精性肝病诊断要点[1] 进行诊断分组 ,嗜酒无肝功能损害者 2 2例 ,酒精性脂肪肝 30例 ,酒精性肝炎31例 ,酒精性肝…     

肝病患者血浆纤维蛋白原亚组份及纤溶酶活性的变化

本文对９３例肝病患者进行了纤维蛋白原亚组分及纤溶酶活性（ＰＬ：Ａ）检测。结果表明纤维蛋白原总量（ＴＦ）在急肝和肝癌组中增高，肝硬化及重肝组显著低于正常人组；高分子量组份（ＨＦ）肝硬化和重肝组均显著减低；低分子量组份（ＬＦ）各组均高于正常人组，其中尤以肝硬化、重肝及肝癌组呈极显著升高；ＬＦ／ＨＦ比值除急肝和慢肝外，余均明显增高。故认为纤维蛋白原亚组分及其ＬＦ／ＨＦ比值的水平更能反映肝功的异常情况，对肝病的病情观察及判断预后均提供了良好指标。ＰＬ：Ａ水平在肝病各组中均呈不同程度的升高，表明肝病患者纤溶活性均增强，其增加的水平与其ＬＦ值呈正相关。     

非酒精性脂肪肝的诊断策略

非酒精性脂肪肝 (ｎｏｎａｌｃｏｈｏｌｉｃｆａｔｔｙｌｉｖｅｒ,ＮＡＦＬ) ,又称非酒精性脂肪性肝病 (ｎｏｎａｌｃｏｈｏｌｉｃｆａｔｔｙｌｉｖｅｒｄｉｓｅａｓｅ) ,是一种肝组织学改变与酒精性肝病(ａｌｃｏｈｏｌｉｃｌｉｖｅｒｄｉｓｅａｓｅ ,ＡＬＤ)相类似 ,但无过量饮酒史的临床病理综合征。根据病因 ,可将ＮＡＦＬ分为原发性和继发性两大类。前者主要与代谢综合征和遗传因素有关 ,而后者多与某些疾病或特殊原因有关。根据病理学改变及临床表现 ,可将ＮＡＦＬ分为单纯性ＮＡＦＬ和非酒精性脂肪性肝炎 (ｎｏｎ -ａｌｃｏｈｏｌｉ…     

代谢综合征与脂肪肝

脂肪肝是遗传 环境 代谢应激相关因素所致的以肝细胞脂肪变性为主的临床病理综合征 ,病理上主要包括单纯性脂肪肝、脂肪性肝炎和脂肪性肝硬化三种类型 ,临床上则有酒精性脂肪性肝病和非酒精性脂肪性肝病 (ＮＡＦＬＤ)之分 ,目前日益增多的脂肪肝主要为与胰岛素抵抗 (ＩＲ)密切相关的ＮＡＦＬＤ。多数情况下 ,ＮＡＦＬＤ为ＩＲ综合征 肥胖综合征 代谢综合征的组成成分之一 ,纠正代谢紊乱可能有助于ＮＡＦＬＤ的防治。1　代谢综合征与脂肪肝的关系1.1　脂肪肝与代谢综合征　流行病学研究显示 ,ＮＡＦＬＤ与肥胖、糖耐量异常 (ＩＧＴ)和糖…     

酒精性肝病与戒酒综合征的电解质及酸碱失衡

酒精性肝硬化（ＡＣ）、重症酒精肝炎（ＡＨ）、戒酒综合征（ＡＷＳ）和急性酒精中毒（ＡＩ）常并发电解质及酸碱失衡。治疗不当，易引起不良后果。本文报道，我院１９８６～１９９６年经病理诊断与资料较全的酒精性肝病３１例，着重对ＡＬＤ、ＡＷＳ及ＡＩ电解质及酸碱失...     

加强酒精性肝病的防治研究

加强酒精性肝病的防治研究江正辉（第三军医大学西南医院消化科重庆６３００３８）酒精性肝病（ＡＬＤ）在过去我国少见，因之对它的了解研究亦少。但近年来有迅速增加趋势，在有的地区，已成为仅次于病毒性肝炎的第二大肝病。长期大量饮酒，可引起脂肪肝（ＡＦ）、酒精性...     

酒精性肝病的随访(附28例11～17年随访)

目的观察ALD的远期预后。方法经统一发信及笔者前往一个专区用电话向患者单位及到生存者家中随访。结果仅获得有反馈信息者28例，占随访病例之20．6％，其中已死亡12人，占有信息病例之42．9％。仅2例再获14年后肝穿活检对比。按2006年2月中华医学会肝脏病学分会脂肪肝和酒精性肝病学组修订诊断标准。①轻症ALD41人获4人复信均健在。②酒精性脂肪肝（AFL）15例有1人复信，继续饮酒（精）100g／d，12年后两次脑出血，已偏瘫。③酒精性肝炎（AH）24例，获信息反馈7例，其中2例已死于肝硬化，另3例已肝硬化，此型最终多合并糖尿病。④45例酒精性肝纤维化（AF）有反馈信息者11例。其中7例已死亡。⑤酒精性肝硬化（AC）11例，有反馈信息者5例，其中3例已死亡。结论轻症ALD远期预后较好。AFL如不戒酒远期效果差，AH、AF预后不良凶险。ALD合并ABV／HCV感染者远期预后不佳，多发展为肝硬化，合并肝癌死亡。     

Cellular cytotoxicity against autologous hepatocytes in alcoholic liver disease

ABSTRACT— We tested lymphocyte cytotoxicity against autologous hepatocytes in patients with alcoholic liver disease (ALD). The following cytotoxicity values were found (mean ± SEM): alcohol-induced steatosis with or without fibrosis 16.5±2% (n = 29), alcoholic cirrhosis 28±4% (n = 13), controls with normal liver histology or minimal changes 6±2% (n = 11). The differences were statistically significant (both forms of ALD versus controls p<0.005). T-cell as well as non-T-cell-enriched lymphocyte fractions showed increased cytotoxicity in ALD. We did not observe a correlation between cellular cytotoxicity and the degree of biochemical or histological alterations within the groups tested. Thus, our study demonstrating enhanced cellular cytotoxicity against autologous hepatocytes in ALD further supports the hypothesis that cellular immune reactions are involved in the pathogenesis of ALD, especially of alcoholic cirrhosis.     

Alcohol-related liver disease: Clinical practice guidelines by the Latin American Association for the Study of the Liver (ALEH)

Alcohol-related liver disease (ALD) is a major cause of advanced chronic liver disease in Latin-America, although data on prevalence is limited. Public health policies aimed at reducing the alarming prevalence of alcohol use disorder in Latin-America should be implemented. ALD comprises a clinical-pathological spectrum that ranges from steatosis, steatohepatitis to advanced forms such as alcoholic hepatitis (AH), cirrhosis and hepatocellular carcinoma. Besides genetic factors, the amount of alcohol consumption is the most important risk factor for the development of ALD. Continuous consumption of more than 3 standard drinks per day in men and more than 2 drinks per day in women increases the risk of developing liver disease. The pathogenesis of ALD is only partially understood and recent translational studies have identified novel therapeutic targets. Early forms of ALD are often missed and most clinical attention is focused on AH, which is defined as an abrupt onset of jaundice and liver-related complications. In patients with potential confounding factors, a transjugular biopsy is recommended. The standard therapy for AH (i.e. prednisolone) has not evolved in the last decades yet promising new therapies (i.e. G-CSF, N-acetylcysteine) have been recently proposed. In both patients with early and severe ALD, prolonged abstinence is the most efficient therapeutic measure to decrease long-term morbidity and mortality. A multidisciplinary team including alcohol addiction specialists is recommended to manage patients with ALD. Liver transplantation should be considered in the management of patients with end-stage ALD that do not recover despite abstinence. In selected cases, increasing number of centers are proposing early transplantation for patients with severe AH not responding to medical therapy.     

住院的酒精性肝病患者临床疾病特点分析

目的：分析住院的酒精性肝病患者临床疾病的特点。方法对近10年收治的4379例各种酒精性肝病患者的疾病构成情况进行分析。结果2002年住院的酒精性肝病患者占住院的肝病患者的比例为1.74%,2006年为2.89%,2011年为4.18%,10年间上升了2.4倍;在酒精性肝病患者中,男性占97.69%（4278/4379）;酒精性肝硬化、酒精性肝病（未分类）、轻症酒精性肝炎为3种最常见的病种,分别占70.66%、10.44%和9.96%,而重症酒精性肝炎、酒精性肝衰竭和酒精性脂肪肝占比为4%左右;酒精性肝硬化患者平均年龄为49.6岁,而酒精性肝病重叠非酒精性脂肪性肝病患者平均年龄为36.9岁,两者差异有统计学意义（P＆lt;0.01）;轻症酒精性肝炎和酒精性脂肪肝治愈率分别为80.28%和91.58%,而重症酒精性肝炎为47.78%,差异有统计学意义（P＆lt;0.01）。结论住院的酒精性肝病患者占住院肝病患者的比例在不断上升,须重视对男性人群和疾病的早期干预。     

缺糖转铁蛋白对酒精性肝病的诊断意义

目的 评价缺糖转铁蛋白（CDT）对酒精性肝病的诊断价值。方法 选择76例酒精性肝病,55例嗜酒者,32例非酒精性肝病和27例健康者,分别检测谷氨酰转肽酶（GGT）等肝功能指标和CDT。结果 酒精性肝病组CDT阳性率为93.4%;CDT诊断酒精性肝病的灵敏度为93.4%,特异性为71.9%,诊断价值高于GGT、丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）。结论 CDT是诊断酒精性肝病较理想的指标。     

Perceptions of post-transplant recidivism in liver transplantation for alcoholic liver disease

Although alcoholic liver disease (ALD) is regarded as a common indication for liver transplantation (LT), debatable issues exist on the requirement for preceding alcoholic abstinence, appropriate indication criteria, predictive factors for alcoholic recidivism, and outcomes following living-donor LT. In most institutions, an abstinence period of six months before LT has been adopted as a mandatory selection criterion. Data indicating that pre-transplant abstinence is an associated predictive factor for alcoholic recidivism supports the reasoning behind this. However, conclusive evidence about the benefit of adopting an abstinence period is yet to be established. On the other hand, a limited number of reports available on living-donor LT experiences for ALD patients suggest that organ donations from relatives have no suppressive effect on alcoholic recidivism. Prevention of alcoholic recidivism has proved to be the most important treatment after LT based on the resultant inferior long-term outcome of patients. Further evaluations are still needed to establish strategies before and after LT for ALD.     

水飞蓟宾胶囊治疗酒精性脂肪肝45例疗效观察

目的观察水飞蓟宾胶囊治疗酒精性脂肪肝的疗效。方法选择酒精性脂肪肝90例,随机分为治疗组和对照组各45例,治疗组口服水飞蓟宾胶囊,对照组口服还原型谷胱甘肽片,疗程均为12周,并加强日常生活指导。结果治疗组总有效率为86.7%（39/45）,对照组为46.7%（21/45）,两组比较差异有显著统计学意义,且治疗组明显高于对照组（P〈0.01）。结论水飞蓟宾胶囊治疗酒精性脂肪肝疗效较好,可改善肝功能,降血脂,显著优于对照组,疗效确切,应用安全。     

Ethanol induced mitochondria injury and permeability transition pore opening： Role of mitochondria in alcoholic liver disease

AIM: To observe changes of mitochondria and investigate the effect of ethanol on mitochondrial perme- ability transition pore (PTP), mitochondrial membrane potential (MMP, ΔΨm) and intracellular calcium concentration in hepatocytes by establishing an animal model of alcoholic liver disease (ALD). METHODS: Fourty adult male Wistar rats were randomly divided into two groups, the model group (20) was administered alcohol intragastrically plus an Oliver oil diet to establish an ALD model, and the control group (20) was given an equal amount of normal saline. The ultramicrostructural changes of mitochondria were observed under electron microscopy. Mitochondria of liver was extracted, and patency of PTP, mitochondrial membrane potential (ΔΨm), mitochondrial mass and intracellular calcium concentration of isolated hepacytes were detected by flow cytometry using rhodamine123 (Rh123), Nonyl-Acridine Orange and calcium fluorescent probe Fluo-3/AM, respectively. RESULTS: Membrane and cristae were broken or disappeared in mitochondria in different shapes under electron microscopy. Some mitochondria showed U shape or megamitochondrion. In the model group, liver mitochondria PTP was broken, and mitochondria swelled, the absorbance at 450 nm, A540 decreased (0.0136 ± 0.0025 vs 0.0321 ± 0.0013, model vs control, P < 0.01); mitochondria transmembrane potential (239.4638 ± 12.7263 vs 377.5850 ± 16.8119, P < 0.01) was lowered; mitochondrial mass (17.4350 ± 1.9880 vs 31.6738 ± 3.4930, P < 0.01); and [Ca2 ]i was increased in liver cells (7.0020 ± 0.5008 vs 10.2050 ± 0.4701, P < 0.01).CONCLUSION: Chronic alcohol intake might lead to broken mitochondria PTP, decreased mitochondria membrane potential and injury, and elevated intracellular Ca2 production. Ethanol-induced chondriosome injury may be an important mechanism of alcoholic diseases.     

Fractionation of gamma-glutamyltransferase in patients with nonalcoholic fatty liver disease and alcoholic liver disease

AIM To assess how serum gamma-glutamyltransferase(GGT) fractions vary in patients with alcoholic liver disease(ALD) and non-alcoholic fatty liver disease(NAFLD). METHODS Serum samples were obtained from 14 patients with biopsy-proven alcoholic liver diseases and 9 patients with biopsy proven non-alcoholic fatty liver disease. In addition to these biopsy-proven cases, 16 obese(body mass index 25) patients without any history of alcohol consumption but with a fatty liver on ultrasound examination and with elevated GGT were included for an additional analysis. Serum GGT fractionation was conducted by high-performance gel filtration liquid chromatography and was separated into the four fractions, big-GGT, medium-GGT, small-GGT(s-GGT), and free-GGT(f-GGT).RESULTS The results were expressed as a ratio of each fraction including the total GGT(t-GGT). The s-GGT/t-GGT ratioswere lowest for the control group and highest for the ALD group. The differences between the control and NAFLD groups and also between the NAFLD and ALD groups were statistically significant. In contrast, the f-GGT/t-GGT ratios were highest in the control group and lowest in the ALD group, with the differences being statistically significant. As a result, the s-GGT/f-GGT ratios were markedly increased in the NAFLD group as compared with the control group. The increase of the s-GGT/t-GGT ratios, the decrease of the f-GGT/t-GGT ratios, and the increase of s-GGT/F-GGT ratios as compared with the control group subjects were also found in obese patients with clinically diagnosed fatty change of the liver.CONCLUSION Serum GGT fractionation by high-performance gel filtration liquid chromatography is potentially useful for the differential diagnosis of ALD and NAFLD.     

Hepatic non-parenchymal cells: Master regulators of alcoholic liver disease?

Chronic alcohol consumption is one of the most common causes of the progression of alcoholic liver disease(ALD). In the past, alcohol-mediated hepatocyte injury was assumed to be a significantly major cause of ALD. However, a huge number of recent and brilliant studies have demonstrated that hepatic non-parenchymal cells including Kupffer cells, hepatic stellate cells, liver sinusoidal endothelial cells and diverse types of lymphocytes play crucial roles in the pathogenesis of ALD by producing inflammatory mediators such as cytokines, oxidative stress, micro RNA, and lipid-originated metabolites(retinoic acid and endocannabinoids) or by directly interacting with parenchymal cells(hepatocytes). Therefore, understanding the comprehensive roles of hepatic nonparenchymal cells during the development of ALD will provide new integrative directions for the treatment of ALD. This review will address the roles of nonparenchymal cells in alcoholic steatosis, inflammation, and liver fibrosis and might help us to discover possible therapeutic targets and treatments involving modulating the non-parenchymal cells in ALD.