235例肝硬化病因分析

【目的】探讨肝硬化病因的特点。【方法】回顾性分析本院2000年1月至2008年12月235例肝硬化患者的病因。【结果】乙型病毒性肝炎引起者141例（60．0％）；丙型病毒性肝炎引起者8例（3．4％）；酒精性肝炎15例（6．4％）；乙肝合并酒精肝炎19例（8．1％）；乙肝合并丙肝4例（1．7％）；自身免疫病16例（6．8％）；其他因素5例（2．1％）；另有不明原因27例（11．5％）。9年间诊断肝硬化的住院患者较前无明显改变，但酒精因素（P〈0．05）、免疫因素（P〈0．05）所致的肝硬化患者人数构成比明显增加，而乙型病毒性肝炎后肝硬化的患者人数构成比相对下降（P〈0．01）。【结论】乙型病毒性肝炎仍然是肝硬化的主要病因，但是酒精性肝硬化和免疫性肝硬化呈上升趋势。     

肝硬化并上消化道出血52例临床分析

目的：探讨肝硬化合并上消化遭出血患者的出血原因，并指导治疗。方法：对52例肝硬化合并上消化遭出血患者均行急诊胃镜检查及Child-pugh分级。结果：（1）52例肝硬化合并上消化道出血的原因：静脉曲张破裂出血占51．92％，非静脉曲张破裂出血占48．08％，两者比较。无显著性差异（P〉0．05）。在Child—pughA级中。静脉曲张破裂出血占23．08％，非静脉曲张破裂出血占5．77％．两者比较，有显著性差异（P〈0．05），在Child-pughC级中，非静脉曲张破裂出血占25．00％，静脉曲张破裂出血占11．53％，两者比较。有显著性差异（P〈0．05）；（2）非静脉曲张破裂出血原因包括消化性溃疡和门脉高压性胃病，在Child-pughC级中，门脉高压性胃病出血占17．31％，消化性溃疡出血占7．69％，两者比较，有显著性差异（P〈0．05）。结论：肝硬化合并上消化道出血病因中．门脉高压性胃病及消化性溃疡也是消化道出血的重要原因，尤其在肝功能Child-pughC级的患者中更应引起重视。     

上消化道出血691例病因分析

目的 探讨上消化道出血（UGH）的病因及相关因素。方法 分析691例UGH住院患者的临床资料。结果 消化性溃疡、胃癌、急性胃黏膜病变（AGML）为UGH的常见病因，分别占35．0％、17．1％、18．2％；上消化道重度出血率以食管静脉曲张为高（48％）；冬春季高于夏秋季。结论 上消化道出血患者急诊胃镜，以明确病因。     

中西医结合防治肝硬化并发急性上消化道出血40例疗效观察

用活血化瘀、清热凉血中药及常规西医治疗方法，防治肝硬化急性上消化道出血患者的再出血４０例（中西医组），与常规西医治疗组４０例作对照。住院期间，中西医组发生再出血２例，占５．０％，均治愈；对照组发生再出血９例，占２２．５％，死亡３例，占７．５％。两组再出血的发生率比较，有极显著性差异（Ｐ＜０．０１）。随访１０个月，中西医组３５例中发生再出血６例，占１７．１％，死亡３例，占８．６％；对照组３０例中发生再出血１９例，占６３．３％，死亡８例，占２６．７％。出院后随访两组再出血的发生率亦有极显著性差异（Ｐ＜０．０１），说明中西医结合治疗肝硬化门脉高压、防治上消化道出血有显著效果。     

51例肝硬化合并上消化道出血的分析

目的：探讨肝硬化合并上消化道出血患者的临床特点。方法：回归分析了所收治的51例肝硬化合并上消化道出血患者的出血原因、出血诱因和治疗方法。结果：35例为食道胃底曲张静脉破裂出血（68．6％），9例为门脉高压性胃病出血（17．6％），7例为消化性溃疡出血（13．8％）。出血诱因包括饮酒10例（19．6％），药物（非甾体类为主）13例（25．5％），过度劳累10例（19．6％），精神刺激13例（25．5％），原因不明5例（9．8％）。出血与肝功分级、并发症有相关性（P〈0．01），与病因无相关性。经治疗，两周内无活动性出血45例，总有效率为88．2％。结论：对于肝硬化合并上消化道出血患者应及早查明出血原因并进行相应治疗。     

肝硬化合并上消化道出血50例的临床分析

目的观察肝硬化合并上消化道出血的病因及诱因，探讨肝硬化合并上消化道出血的临床表现及其诊治。方法对50例肝硬化上消化道出血的患者资料进行回顾性的临床分析。结果肝硬化患者出血的诱因以饮酒暴食最多，其次是服用非甾体类抗炎药，出血的病因以曲张静脉破裂为主，其次是门脉高压性胃病。综合治疗显效率20．0％，有效率66．0％，无效率14．0％（其中死亡2例），总有效率86．0％。结论避免饮酒及服用非甾类抗炎药，积极降低门脉压，改善肝功能对减少肝硬化患者发生上消化道出血具有重要意义。     

老年人上消化道出血114例临床分析

目的探讨老年人上消化道出血的临床特点。方法回顾性分析我院1997年1月-2006年12月收治的老年人上消化道出血114例的临床特点，并与同期中青年病例比较。结果老年人上消化道出血仍以消化性溃疡多见（43．5％），但胃溃疡出血发生率增加（22．58％），稍高于十二指肠溃疡发病率（20．97％），与中青年人以十二指肠溃疡为主有显著差异；胃癌出血发生率显著增加（18．28％），占病因第二位，与中青年人相比差异显著；老年患者合并症、并发症、再出血率和死亡率显著高于中青年组。结论老年人上消化道出血仍以消化性溃疡为多见，胃溃疡、胃癌出血发生率增加，并发症多，再出血率和死亡率高。     

肝硬化门静脉血栓形成的危险因素分析

目的分析肝硬化门静脉血栓(PVT)形成的独立危险因素,并建立实用性强、适用性广的无创预测模型以期为肝硬化PVT形成防治提供参考依据。方法回顾性分析西南医科大学附属医院2018年9月至2020年4月收治的肝硬化符合纳入排除标准者353例,60例合并PVT患者为PVT组,随机选择同期120例无PVT患者为对照组,对可能影响PVT形成的因素进行单因素分析及多因素Logistic回归分析,由此建立肝硬化PVT形成的无创预测模型。结果肝炎病毒及酒精是肝硬化的前两位病因,分别占63.89%、16.28%,其中乙型病毒性肝炎占57.78%,是肝硬化的最主要病因。多因素Logistic回归分析显示,血红蛋白(Hb)、D-二聚体、脾静脉内径是PVT形成的独立危险因素(P<0.01)。PVT形成的预测模型为logit P_(PVT)=-2.76+0.34×D₂+2.72×脾静脉内径-0.02×Hb。此外,PVT组上消化道出血发生率显著高于对照组(70.00%vs 37.50%,P<0.01),两组余临床表现及并发症发生率差异无统计学意义(P>0.05)。结论乙型病毒性肝炎仍是肝硬化的主要病因,其次为酒精。PVT患者上消化道出血风险明显增加,不利于胃食管静脉曲张出血防治。Hb降低、D-二聚体升高、脾静脉内径增宽是肝硬化门静脉血栓形成的独立危险因素,建议对肝硬化患者动态随访上述指标,必要时行进一步诊治。     

我国云南香格里拉地区104例肝硬化患者的病因及临床特征分析

目的:分析香格里拉地区肝硬化患者的主要病因及临床特征,为本地区肝硬化的防控提供信息。方法:收集2019年1月至2021年6月期间在云南迪庆藏族自治州人民医院就诊的所有肝硬化患者共104例,回顾性分析患者肝硬化病因的构成比以及主要临床特点等。结果:104例肝硬化患者的年龄为33~86岁,平均年龄为(59.5±11.3)岁;男女比例为9∶4藏族占62.5%,汉族占17.31%,和彝族占15.38%。乙肝Child-Pugh A级38例(37%),B级56例(54%),C级10例(9%);主要临床表现为腹胀。肝硬化病因构成比中,酒精性肝硬化占38%,乙肝肝硬化占48%,丙肝肝硬化占1%,混合性硬化占13%。香格里拉地区肝硬化患者的年龄低于全国其他地区,尤其是酒精性肝硬化患者的发病年龄较其他原因肝硬化年轻,且经规范治疗后疾病缓解率仅为1%。结论:病毒性肝炎仍是我国云南香格里拉地区导致肝硬化的主要病因,酒精性肝病次之,混合性肝硬化占比高。本地区需重视酒精对人体的危害宣教,同时加强病毒性肝炎的防治。     

岳阳地区1345例肝硬化患者的病因分析

【目的】探讨岳阳地区肝硬化病因的特点。【方法】对1345例肝硬化住院病人的资料进行回顾性分析。【结果】1345例中乙型病毒性肝炎（HB）肝硬化737例（54．80％），血吸虫性肝硬化291例（21.64％）。【结论】HB和血吸虫病是岳阳地区肝硬化的主要原因。     

Alcoholic liver disease in Scotland and northeastern England: presenting features in 510 patients

A study of 510 patients in Scotland and northeastern England with histological evidence of alcohol-induced liver disease showed no difference in the age of presentation between males and females. Single men and widowed females were particularly susceptible to alcoholic liver disease. The social class distribution was similar to the population in general. Women were more reluctant to volunteer a history of alcoholism than men, they had a higher incidence of previous psychiatric illness (usually due to alcohol abuse) and they developed liver disease at lower consumption thresholds of alcohol than men. Patients under 40 years of age were more likely to have alcoholic fatty liver and less likely to have active cirrhosis than those over 40. Most often, the presenting symptoms were non-specific and tended to be related to the gastrointestinal system, particularly in women. Five per cent of patients were asymptomatic and 14% came to hospital for conditions other than alcoholic liver disease. Important clues to asymptomatic alcoholic liver disease included hepatomegaly, clubbing of the fingers and abnormal liver function tests. Gastro-oesophageal varices accounted for 40% of instances of haemorrhage and the mortality from upper gastrointestinal bleeding was 17%. Anaemia was the most common haematological abnormality. Alcoholic hepatitis was observed more frequently in the Glasgow area then elsewhere.     

Pathogenesis, diagnosis, and treatment of alcoholic liver disease

Alcohol-related liver disease is a major cause of morbidity and mortality in the United States. Alcoholic liver disease encompasses a clinicohistological spectrum, including fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. Fatty liver is a benign and reversible condition, but progression to alcoholic hepatitis and cirrhosis is life-threatening. Alcoholic hepatitis is diagnosed predominantly on clinical history, physical examination, and laboratory testing, although liver biopsy is often necessary to secure the diagnosis. The major focus of management is abstinence from alcohol, supportive care, treatment of complications of infection and portal hypertension, and maintenance of positive nitrogen balance through nutritional support. Corticosteroid therapy is controversial but should be considered in patients with a discriminant function greater than 32 and/or presence of spontaneous hepatic encephalopathy in the absence of infection, gastrointestinal bleeding, and renal failure. The only curative therapy for advanced alcoholic cirrhosis is liver transplantation. Several recent advances in understanding the pathogenesis of alcoholic liver disease may lead to novel future treatment approaches, including inhibition of tumor necrosis factor a, antioxidant therapy, stimulation of liver regeneration, and stimulation of collagen degradation.     

Alcoholic Liver Disease

Alcoholic liver disease consists of well defined entities. Fatty liver is the commonest hepatic abnormality in alcoholics and in most cases it is reversible. Possibly a sustained fatty liver occasionally may induce fibrosis. Alcoholic hepatitis or subclinical necrosis may also proceed to hepatic fibrosis. The latter can regress if no further injury occurs or it may develop into frank cirrhosis in case of continuing liver injury. A general model of alcoholic liver disease is presented.     

Alcohol and the liver

Since ethanol metabolism predominantly takes place in the liver it is not surprising that hepatic intermediary metabolism is strikingly influenced. Alcohol is metabolized via three enzyme systems: alcohol dehydrogenase (ADH), microsome ethanol oxidizing system (MEOS) and catalase. The ADH reaction produces reducing equivalents as NADH which results in various metabolic disorders such as hyperproteinemia IV and V, hypoglycaemia, lactacidosis, hyperuricaemia, and certain forms of porphyria. The metabolism of hormones is also disturbed. Alcohol fatty liver is a direct consequence of NADH production. Alcoholic liver disease comprises of fatty liver, alcoholic hepatitis and cirrhosis. Risk factors of alcoholic liver disease are the amount of alcohol consumed, drinking pattern, female gender and certain genetic predispositions. Alcoholic hepatitis is characterized by a typical clinical and laboratory feature, and specific heaptic morphology. Poor prognostic factors are continuous alcohol consumption, cholestatis and perivenular fibrosis. Alcoholic cirrhosis has similar complications as cirrhosis of other etiology. Therapy includes abstinence, antioxidative drugs, steroids, and S-adenosylmethionine. Liver transplantation is of long-term benefit.     

Alcoholic liver disease

Alcoholic liver disease presents a wide spectrum of clinical manifestations ranging from mild asymptomatic fatty liver to alcoholic hepatitis and severe life-threatening liver failure with ascites, hemorrhaging esophageal varices, and encephalopathy. Although still poorly understood, the mechanism of this injury is probably the result of numerous direct toxic and metabolic effects of alcohol on the hepatocyte. Therapy consists primarily of abstinence and supportive care. However, several newer treatments are actively being studied. These include prednisolone, anabolic steroids, glucagon and insulin, propylthiouracil, and cyanidanol. Colchicine is promising as an agent to inhibit fibrosis. Complications of cirrhosis, including ascites and variceal hemorrhage, are the result of end stage disease. A return to old techniques of ascitic fluid management suggests that therapeutic large-volume paracentesis with albumin infusion is a safe and effective form of therapy. Variceal hemorrhage is best treated with sclerotherapy, vasoconstrictors, and balloon tamponade. Little has been done to alter the ultimately dismal prognosis and long-term survival of alcoholic liver disease.     

1-14C]Ethanol breath test in alcoholic liver disease

The activity of ethanol metabolising enzymes was assessed in 51 patients with alcoholic and non-alcoholic liver disease using tracer doses of [1-14C]ethanol and measuring 14CO2 excretion in the breath. Alcoholic patients with only fatty infiltration of the liver showed significantly increased activity compared with controls. Comparing alcoholic patients with cirrhosis and a serum albumin greater than 28 g/l, activity in those with a recent history of continued heavy drinking was significantly greater than in patients who had abstained from alcohol. In addition, both groups of alcoholic cirrhosis showed significantly more activity than patients with non-alcoholic cirrhosis. The activities of patients with acute alcoholic or viral hepatitis were normal when their prothrombin times were less than 7 sec prolonged, but were reduced when prolongation exceeded 7 sec. These results demonstrate that in chronic alcoholic liver disease, even with cirrhosis, alcohol can still increase the activity of ethanol oxidising enzymes provided hepatic function remains adequate. However, this response is lost in acute liver damage and in chronic alcoholic disease with severe hepatic dysfunction.     

Alcoholic liver disease

Aggressive management to prevent alcoholic cirrhosis should include the use of biopsy results to diagnose and to monitor alcoholic liver disease. Guidelines for the interpretation of the liver biopsy are highlighted. The diagnosis, course, and treatment of alcoholic hepatitis and cirrhosis are presented in detail.     

Recent developments in the treatment of alcoholic hepatitis

Alcoholic hepatitis is a form of acute injury to liver tissue that is also a precursor of cirrhosis, and carries significant morbidity and mortality. Severe alcoholic hepatitis in particular carries a high short-term mortality, and also places an enormous burden on stretched healthcare resources. Treatment of alcoholic hepatitis has been limited to supportive management and nutritional supplementation without clear improvements in outcome, and the timing and patient selection for hepatic transplantation is problematic. The use of corticosteroids has remained controversial for many years, but probably has a role in selected patients. Various other therapeutic strategies have been tested over the decades and none has shown any consistent benefit. Recently there have been major developments in our understanding of the mechanisms of alcoholic liver injury, including the role of cytokines and hepatocyte apoptosis. For the first time, there are exciting possibilities for specific therapies for this challenging and serious condition.     

Natural History of Alcoholic Hepatitis. IV. GLYCOSAMINOGLYCURONANS AND COLLAGEN IN THE HEPATIC CONNECTIVE TISSUE

The extractable and nonextractable collagen and glycosaminoglycuronans (GAG) were estimated and characterized in 32 dried, defatted human livers obtained at necropsy. 10 had normal livers. 22 of the 32 livers were from patients who drank in excess: 5 had fatty livers, 7 had alcholic hepatitis, and 10 had cirrhosis. Livers with alcoholic hepatitis or cirrhosis had significantly increased total and 1 N NaCl-extractable collagen. Only alcoholic hepatitis livers had significantly increased Tris-buffer-extractable GAG, but the amino acid composition of these GAG (proteoglycans) was no different from that of normal livers. The major fraction of these GAG had isoelectric pH (pI) 相似文献   

105例乙肝肝硬化内镜特点分析

目的了解乙型肝炎肝硬化内镜特点，准确预测判断上消化道出血的危险性，为临床诊治提供可靠依据。方法对该院收治的105例乙型肝炎肝硬化患者应用日本产Olympus GIF-XQ240电子内窥镜作胃十二指肠检查。结果食管胃底静脉曲张100例，其中食管静脉曲张(esophageal variceal，EV)82例，胃底静脉曲张(gastric variceal，GV)18例，EV并门脉高压性胃病(portal hypertensive gastropathy，PHG)64例，十二指肠球部溃疡(duodenal ulcer，DU)21例。结论食管静脉曲张是乙肝肝硬化最具有特征的内镜表现，门脉高压性胃病、十二指肠溃疡是乙型肝炎肝硬化门脉高压症的常见合并症。