防治酒精性肝病最有效的措施:戒酒

长期大量饮酒可引起酒精性肝病(alcoholic liverdisease,ALD)。ALD包括轻度酒精性肝损伤(mild al—coholic injury,MAI)、酒精性脂肪肝(alcoholic fattyliver,AFL)、酒精性肝炎(alcoholic hepatitis,AH)和酒精性肝硬化(alcoholic liver cirrhosis,AC)。目前普遍对男性饮酒折合乙醇量>40 g/d,女性>20 g/d,连续5年以上者定为嗜酒者。ALD的严重程度与饮酒量呈正     

青少年脂肪肝：狂饮与肥胖

青少年肝脏损害的原因中增长最快的就是肥胖和饮酒,狂饮与肥胖具有相似的肝脏病理组织学特点,相互作用加重肝脏损伤、加速疾病的进展。有效控制酒精消耗和肥胖比纠正单独因素可以获得更大的收益。     

脂肪肝与非脂肪肝患者血常规的差异分析

目的探讨成人脂肪肝患者与非脂肪肝患者血常规的差异。方法选用沈阳地区2008年3月～2008年12月参加体检的18岁以上人群为研究对象,对肝脏彩色多普勒检查诊断的脂肪肝与非脂肪肝患者,采用问卷咨询、体格检查和生化检查外,重点探讨脂肪肝与血常规之间的关系,数据用SPSS16.0软件分析。结果入选人群共8842名,B超共检出脂肪肝3306例,占37.39%,其中酒精性、非酒精性脂肪肝分别占15%（1326名）和22.39%（1980名）,与非脂肪肝组（NAFL）相比,脂肪肝组（AFL）WBC（白细胞计数）、EO%（嗜酸性细胞比率）、RBC（红细胞计数）、HGB（血红蛋白浓度）、HCT（红细胞比积测定）、MCH（平均红细胞Hb含量）、MCHC（平均红细胞Hb浓度）、RDW（红细胞分布宽度）、PDW（血小板分布宽度）显著增加（P〈0.01）;LYM%（淋巴细胞比率）、MONO%（单核细胞比率）、MCV（平均细胞容积）、P-LCR（大型血小板比率）、MPV（平均血小板体积）等明显增加（P〈0.05）;PLT（血小板计数）明显减少（P〈0.05）;与非酒精性脂肪肝组（NAFL）比,酒精性脂肪肝（AFL）组RBC、HGB、HCT、MCV、MCHC等显著增加（P〈0.01）,LYM%明显减少（P〈0.05）,MCH、MONO%（单核细胞比率）明显增加（P〈0.05）。结论脂肪肝患者中白细胞总数及分类（除中性粒细胞百分比外）明显高于非脂肪肝组,红细胞系统（除MCHC外）也有类似的趋势,而血小板计数明显低于非脂肪肝组;而酒精性和非酒精性脂肪肝相比,红细胞系统显著增加,尤其MCV更加明显,而白细胞系统（除LYM%明显减少外）和血小板系统大部分无显著变化。说明简单的血常规及分类检查对脂肪肝的临床诊断和病因诊断具有重要的意义。     

非酒精性脂肪肝病

第十二届世界消化病学会议于 2 0 0 2年 2月在泰国曼谷召开 ,这是继 1998年第十一届世界消化病学术会议(奥地利维也纳 )之后的又一次“奥林匹克式”的国际盛会 ,百余个国家的万余名医师出席了这次大会。会议内容广泛 ,涉及到多方面的新进展。《临床消化病杂志》曾相继及时报道了 1994年第十届及 1998年第十一届世界消化病学术大会的部分专题内容 ,受到广大读者欢迎。本期我们又组织华中科技大学同济医学院协和医院消化科医师整理了第十二届世界消化病学会大会上所涉及的近 4年来国际上在消化疾病某些领域中的最新进展 ,供同道们参考。     

酒精性脂肪肝研究现状与进展

酒精性脂肪肝（AFLD）是指长期饮酒导致的脂肪肝，是目前临床上最为常见的肝脏疾病之一。本文主要目的是对AFLD的临床病理特点、发病机制以及可能的分子学机制进行综述，同时介绍目前治疗AFLD的策略。     

非酒精性脂肪肝的药物治疗进展

非酒精性脂肪肝作为肝硬化和终末期肝病的病因之一，在临床上日益受到重视。它是一种以肝细胞脂肪变性和脂肪储积为病理特征，病变主体在肝小叶，无过量饮酒史的一种临床综合征。在病理上分为三种类型;单纯性脂肪肝；脂肪性肝炎；脂肪性肝硬化。本病发生的危险因素分别是;年龄45岁以上、体重指数≥26、2型糖尿病及AST／ALT比值〈1。虽然非酒精性脂肪肝的发病机制尚未完全明了，但肝脏脂质代谢障碍、胰岛素抵抗、细胞因子作用、肝细胞色素P4502E1（cYP2E1）和CYP4A表达增加、氧应激和脂质过氧化、免疫反应、遗传因素等多种相关因素均参与了发病。近来有提出以氧应激和脂质过氧化为中心的“二次打击”学说，即一次打击诱发脂肪变性，在应激产生的细胞因子、原有致病因素持续存在、肝星状细胞活化等作用下发生“二次打击”，导致肝脏发生炎症、坏死、纤维化、细胞凋亡等。非酒精性脂肪肝至今尚无完全有效的药物治疗，基础治疗主要是控制饮食和减轻体重。Eriksson等报告3例超重50％～60％的非酒精性脂肪肝炎患者，     

酒精性脂肪肝的治疗进展

酒精性脂肪肝（AFLD）是指长期饮酒导致的脂肪肝，是现在临床上最为常见的肝病之一。目前认为，酒精性脂肪肝治疗上主要有戒酒、营养及药物治疗等方法。近年来，有关这方面的研究很多，本文对此作以下阐述。     

糖尿病性脂肪肝与酒精性脂肪肝临床特点分析

目的观察糖尿病性脂肪肝与酒精性脂肪肝的临床特点。方法收集我院2010年1月到2015年1月收治的酒精性脂肪肝患者40例,糖尿病性脂肪肝患者(非酒精)62例,通过问卷调查和全自动生化分析检查患者基本临床资料和生化指标。结果酒精性脂肪肝中男性比例为67.50%,高于糖尿病性脂肪肝为56.45%,但差异无统计学意义(P0.05)。年龄、病程、BMI等在两组间差异无统计学意义(P均0.05),糖尿病性脂肪肝同时发生高血压、高血糖、高尿酸血症、肥胖症等比例高于酒精性脂肪肝,冠心病、胆石症低于酒精性脂肪肝,差异均具有统计学意义(P均0.05)。糖尿病性脂肪肝中GGT、TG、TC、LDL-C、UA、ApoA、AST、ALT等肝功能指标高于相应酒精性脂肪肝,Alb、TBil等低于相应酒精性脂肪肝,差异具有统计学意义(P均0.05),HDL-C在两组间差异无统计学意义(P0.05)。结论糖尿病性脂肪肝同时伴有高血压、高血脂、高血糖患者较多,并且肝功能损害较酒精性脂肪肝大。     

内毒素与脂肪肝的关系研究进展

脂肪肝时常伴有肠源性内毒素血症,内毒素不仅对肝细胞有直接的损伤作用,而且可通过激活库普弗细胞(KC)释放一系列生物活性物质,以及可能促进肝脏自然杀伤T细胞减少,导致促炎和抗炎免疫反应失衡,引起肝脏损害,从而加重内毒素的作用.     

肝炎后脂肪肝与酒精性脂肪肝超声声像图对比分析

本文对肝炎后脂肪肝与酒精性脂肪肝的超声声像图表现进行了探讨,发现二者有较明显的差异,现总结分析如下。 1 资料与分析 1.1 收集1998～2000年门诊及住院患者205例,全部行超声检查,其中肝炎后脂肪肝102例,男     

Nonalcoholic fatty liver hepatitis and fatty cirrhosis mimicking alcoholic liver diseases

Non-alcoholic steatosis hepatitis and fatty cirrhosis represents an unfamiliar liver disease of yet unknown etiology, which is usually indistinguishable from alcoholic lesions by histological criteria. For the affected patients this means automatically the inappropriate assumption of hidden alcohol abuse. Out of 1467 liver biopsies during 1979 to 1982 we selected 25 patients (group I), who either denied alcohol intake or reported negligible consumption. None of them had taken steatogenous drugs or had been treated by jejuno-ileal bypass operation for morbid obesity. Nevertheless, in all cases liver biopsy demonstrated changes that were thought to be characteristic of alcoholic liver disease. This group was compared with an additional series of 25 patients (group II, selected out of 342 alcoholics), who admitted to a mean daily alcohol ingestion of 145 +/- 37 g. According to body weight, sex ratio, estimated degree of hepatocellular fat deposition and relation of steatosis hepatitis (n = 15) to fatty cirrhosis (n = 12) there were no differences between both groups. In contrast to the alcoholics (group II) significantly lower (p less than 0.001) values of serum gamma-glutamyltransferase (127 +/- 138 vs 669 +/- 588 U/l) and mean corpuscular erythrocyte volume (89 +/- 4,7 vs 102 +/- 7,8 fl) occurred among the abstinent patients (group I). However, the considerable overlap of measured values argued against a sufficiently discriminative function of both parameters. On the other hand, the serum SGOT/SGPT ratio (I: 1,0 +/- 0,4 vs II: 3,5 +/- 1,4) as well as the serum immunoglobulin-index IgG/IgA (I: 5,6 +/- 2,1 vs II: 2,7 +/- 0,7) allowed a more than 90% separation between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypoxia and fatty liver

The liver is a central organ that metabolizes excessive nutrients for storage in the form of glycogen and lipids and supplies energy-producing substrates to the peripheral tissues to maintain their function, even under starved conditions. These processes require a considerable amount of oxygen, which causes a steep oxygen gradient throughout the hepatic lobules. Alcohol consumption and/or excessive food intake can alter the hepatic metabolic balance drastically, which can precipitate fatty liver disease, a major cause of chronic liver diseases worldwide, ranging from simple steatosis, through steatohepatitis and hepatic fibrosis, to liver cirrhosis. Altered hepatic metabolism and tissue remodeling in fatty liver disease further disrupt hepatic oxygen homeostasis, resulting in severe liver hypoxia. As master regulators of adaptive responses to hypoxic stress, hypoxia-inducible factors (HIFs) modulate various cellular and organ functions, including erythropoiesis, angiogenesis, metabolic demand, and cell survival, by activating their target genes during fetal development and also in many disease conditions such as cancer, heart failure, and diabetes. In the past decade, it has become clear that HIFs serve as key factors in the regulation of lipid metabolism and fatty liver formation. This review discusses the molecular mechanisms by which hypoxia and HIFs regulate lipid metabolism in the development and progression of fatty liver disease.     

非酒精性脂肪性肝病与肝移植

随着生活水平的提高,非酒精性脂肪性肝病(nonalcoholic fatty liver disease,NAFLD)在人群中的发病率越来越高.非酒精性脂肪性肝炎(nonalcoholic steatohepatitis,NASH)是NAFLD的最严重类型,在发达国家已成为临床上最常见的慢性肝病类型.     

非酒精性脂肪性肝病与肝硬化

非酒精性脂肪性肝病（Nonalcoholic fatty liver disease, NAFLD）发病与胰岛素抵抗（Insulin resistance, IR） 和遗传易感性密切相关,病理学改变与酒精性肝病（Alcoholic liver disease, ALD）相似,但无过量饮酒史^[1]。在此要强调NAFL与NASH的不同,NAFL是指病理活检显示肝脏脂肪变性,但是不具有肝纤维化或气球样变性的肝细胞损伤。NASH指在肝脏脂肪变基础上出现气球样肝细胞损伤伴或不伴肝纤维化^[2],NASH发生肝纤维化、肝硬化、肝细胞癌风险明显增高,而NAFL则很低^[2],NASH是NAFL发生肝硬化的必经阶段^[3]。     

Abstinence in patients with alcoholic liver cirrhosis: A follow-up study

Aim:  To investigate the proportion of patients with alcoholic cirrhosis who abstained from alcohol after contact with a hepatology unit, the predictors for abstinence, and the role of clinical and psychosocial factors in short-term mortality in these patients.
Methods:  Eighty-seven consecutive patients with alcoholic cirrhosis from a transplant center were included. Data on cirrhosis severity and complications, as well as on abstinence and psychosocial factors were collected. Patients were followed up for 19 (12–25) months. Data on abstinence during follow up, alcohol abuse treatment, psychiatric contact, severity of cirrhosis, mortality, and liver transplantation were analyzed.
Results:  Prior to inclusion, 53/87 (61%) patients had abstained from alcohol for 24 months (interquartile range: 18–33). Twenty percent had a history of other substance abuse, 47% had undergone alcohol abuse treatment, and 21% had a previous psychiatric diagnosis. Forty-eight percent lived with a partner, 23% worked/studied, and 53% were pensioners. During follow up, 26% died, 20% received a liver transplant, 55% abstained from alcohol, 47% received alcohol abuse treatment, and 33% had psychiatric contact. In a multivariate analysis, abstinence during follow up was found to be related to abstinence upon inclusion in the study, to the model for end-stage liver disease (MELD) score at follow up, and to no abuse treatment in a detoxification unit, whereas mortality was related to index MELD and alcohol abuse treatment during follow up. Neither abstinence nor mortality was related to psychosocial factors.
Conclusion:  More than half of patients with alcoholic cirrhosis were found to abstain from alcohol during follow up, which was related to prior documentation of abstinence and cirrhosis severity. Cirrhosis severity (expressed as the MELD) and alcohol abuse treatment during follow up were related to short-term mortality.