安络化纤丸治疗脂肪肝83例临床观察

脂肪肝在我国人群中的发病率高达10%.我院肝病科于2002年4月-2003年4月,采用安络化纤丸对83例脂肪肝患者进行前后治疗,对照观察如下:     

安络化纤丸治疗脂肪肝47例临床分析

2004年6月-2005年4月,我们采用安络化纤丸联合凯西莱治疗47例脂肪肝患者,疗效显著,现报告如下.     

还原型谷胱甘肽联合安络化纤丸治疗酒精性脂肪肝100例

目的探索还原型谷胱甘肽联合安络化纤丸治疗酒精性脂肪肝的疗效。方法将200例酒精性脂肪肝患者随机分为两组,100例用还原型谷胱甘肽联合安络化纤丸为治疗组,100例单用还原型谷胱甘肽为对照组,疗程均为1个月。结果治疗组有效率91.00%(91/100),对照组有效率70.00%(70/100),两组比较有显著性差异(P<0.001)。结论还原型谷胱甘肽联合安络化纤丸治疗酒精性脂肪肝有良好效果,值得临床推广应用。     

安络化纤丸治疗脂肪肝的临床研究

1．1 一般资料 随机按序选择我院2000年10月-2004年6月门诊和住院病例58例,分为冶疗组32例,对照组26例。其中男42例,女16例,年龄29～56岁,平均41岁。病程1．13年,平均4．6年。肥胖者12例,高脂血症5例,嗜酒（饮酒年数〉5年,饮酒量〉150g/d）21例,2组患者在年龄、性别、病程及肝功能等生化指标方面比较,无显著性差异（P〉0．05）。     

安络化纤丸治疗肝炎肝硬化70例临床观察

目的观察70例肝炎后肝硬化患者应用安络化纤丸治疗后临床症状、体征、肝功能、血清肝纤维化指标的恢复情况和肝脏影像学改变。方法治疗组70例患者服用安络化纤丸(森隆药业有限公司),剂量为6g／次,口服,3／d;对照组66例,接受丹参片治疗,3片／次,3／d。其他护肝降酶治疗2组相同,2组疗程均为3个月。结果安络化纤丸治疗后血清透明质酸酶(HA)、     

安络化纤丸治疗中晚期肝炎肝硬化70例临床观察

目的:观察肝炎肝硬化患者应用安络化纤丸治疗后临床症状、体征、肝功能、血清肝纤维化指标的恢复情况和肝脏脾脏影象学改变.方法:138名中晚期肝硬化患者分为两组,治疗组70例患者口服安络化纤丸,6g/次,3次/d;对照组68例接受丹参片治疗,3片/次,3次/d.两组疗程均为6个月.结果:安络化纤丸治疗后血清透明质酸酶(HA)、层粘蛋白(LN)和Ⅲ型前胶原(PC-Ⅲ)平均水平下降十分显著,HA尤为显著,HA尤为突出;肝脏影象学检查有显著改善.结论:安络化纤丸有较好的抗肝硬化效果.     

安络化纤丸治疗HBeAg阴性乙型肝炎肝硬化的临床观察

目的 观察安络化纤丸治疗HBeAg阴性乙型肝炎(乙肝)肝硬化(LC)患者的疗效.方法 随机将68例HBeAg阴性乙肝肝硬化患者分为治疗组38例、对照组30例,治疗组给予口服安络化纤丸,每次6 g、3/d;对照组给予护肝片,每次4片、3/d,疗程均为3个月.观察治疗前后临床症状、体征的变化以及肝脾影像学改变;肝功能、肝纤维化、病毒学指标的变化和药物的不良反应.结果 安络化纤丸临床使用安全、可靠;在肝功能改善、症状缓解,有一定效果;治疗组与对照组比较,脾厚测量平均值明显缩小,肝纤维化指标HA和Ⅳ-C明显下降,LN无明显改变.结论 安络化纤丸治疗HBeAg阴性乙肝肝硬化临床应用安全可靠,在保肝、脾脏回缩、抗纤维化方面具有一定疗效.     

拉米夫定联合安络化纤丸治疗乙型肝炎肝硬化30例临床观察

目的 探讨乙型肝炎肝硬化患者通过拉米夫定和安络化纤丸联合治疗的效果.方法 随机选择45例乙型肝炎肝硬化患者,分别给予拉米夫定联合安络化纤丸和拉米夫定治疗1年6个月.结果 治疗结束时,联合组的血清谷丙酶和透明质酸水平下降比单用拉米夫定组优;治疗组30例中17例(56.7%)HBV DNA阴转,17例HBeAg阴转,7例出现抗-HBc(+);对照组15例中8例HBV DNA阴转(53.3%),8例HBeAg阴转,2例出现抗-HBc(+).结论 拉米夫定联合安络化纤丸治疗慢性乙型肝炎肝硬化疗效确切,安络化纤丸有较好抗肝纤维化及改善肝功能,缓解临床症状作用.但抗乙型肝炎毒复制作用不突出.     

安络化纤丸治疗慢性肝炎的临床疗效观察

目的 观察安络化纤丸治疗慢性肝炎的临床疗效及对血清肝纤维化指标的影响。方法 随机将60例慢性肝炎患者分为安络化纤丸治疗组和一般保肝治疗组，对比分析治疗前和治疗6个月时血清丙氨酸氨基转移酶、白蛋白、透明质酸、Ⅲ型前胶原和层粘连蛋白水平的变化。结果 安络化纤丸治疗组在降低丙氨酸氨基转移酶和血清肝纤维化指标方面均优于一般保肝治疗组。结论 安络化纤丸具有较好的抗肝纤维化作用。     

安络化纤丸治疗慢性乙型肝炎肝纤维化疗效观察

目的观察安络化纤丸对慢性乙型肝炎(乙肝)患者的肝功能、血清肝纤维化指标的影响。方法将98例门诊慢性乙肝患者随机分为2组。对照组48例给予常规护肝治疗;治疗组50例,在对照组用药的基础上给予安络化纤丸6g,早晚各1次,服用6个月。对比分析治疗前后血清透明质酸(HA)、层粘连蛋白(LN)、Ⅲ型前胶原(PCⅢ)、Ⅳ型胶原(Ⅳ-C)水平的变化及肝功能变化。结果治疗组在降低血清肝纤维化指标方面均优于对照组;治疗组治疗后转氨酶明显降低。结论安络化纤丸能较好地促进肝功能的恢复,具有良好的抗肝纤维化作用。治疗期间未发现明显不良反应。     

非酒精性脂肪性肝病治疗研究进展

非酒精性脂肪性肝病是全球性的公共卫生问题。调整生活方式及保持健康心理状态是治疗非酒精性脂肪性肝病的基础。本文通过对其发病机理研究的梳理,重点介绍了近年来国内外关于非酒精性脂肪性肝病药物治疗的进展,包括氧化应激、炎症反应、脂质代谢、纤维形成和细胞凋亡等不同阶段靶向治疗药物应用的安全性和有效性。     

Treatment of fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is considered to be a hepatic manifestation of metabolic syndrome. The clinicopathologic spectrum ranges from simple steatosis to nonalcoholic steatohepatitis (NASH). Simple steatosis has a relatively benign clinical course, but NASH can progress to cirrhosis and hepatocellular carcinoma. As yet there is no convincingly effective treatment for NAFLD and the best option for these patients might be a multimodal treatment plan targeting obesity, insulin resistance, diabetes mellitus, hyperlipidemia and hypertension.     

登革病毒感染合并脂肪肝191例肝脏酶学分析

目的 探讨西双版纳州登革热合并脂肪肝病例的肝脏酶学变化特征,为制定当地登革热有效治疗方案提供依据。方法 对2013和2015年西双版纳州191例登革病毒感染合并脂肪肝病例临床资料和191例随机对照组进行登革病例主要肝脏酶学指标回顾性分析。结果 191例登革病毒感染合并脂肪肝患者丙氨酸氨基转氨酶增高率为84.8%,天门冬氨酸氨基转氨酶增高率为90.1%,γ-谷氨酰转移酶增高率76.8%和黄疸指数增高率20.4%,除黄疸指数外,其它3个指标均明显高于对照组(P<0.05)。结论 西双版纳州登革热病例中合并脂肪肝患者肝损伤严重,其中以丙氨酸氨基转氨酶、天门冬氨酸氨基转氨酶、γ-谷氨酰转移酶增高为主,提示一旦发现登革热患者合并脂肪肝时,临床医师应密切监测患者上述3种酶的变化并及时给予相关治疗。     

Treatment of nonalcoholic fatty liver disease

Opinion statement Nonalcoholic fatty liver disease (NAFLD) is very common in the United States, and in some patients it may lead to cirrhosis, liver failure, and liver cancer. NAFLD encompasses a spectrum of liver injury, ranging from steatosis to steatohepatitis, advanced fibrosis, and cirrhosis. Nonalcoholic steatohepatitis (NASH), an advanced form of NAFLD, histologically comprises steatosis, balloon degeneration, inflammation, and fibrosis in varying degrees. It is generally believed that simple steatosis is benign with minimal risk of progression, whereas NASH is progressive and can lead to cirrhosis. The commonly associated risk factors for NAFLD include obesity, hyperlipidemia, and diabetes mellitus. The pathogenesis of NAFLD and NASH is not fully known; however, current evidence suggests that insulin resistance and lipid peroxidation play a role in the pathogenesis of this condition. Currently, there are no proven effective therapies available for the treatment of NASH. Although there are numerous studies that have explored various treatments for NASH, these generally consist of small numbers of patients with suboptimal endpoints. Treatment strategies for NAFLD and NASH can be broadly divided into 1) treatment or control of underlying risk factors such as hyperlipidemia, diabetes mellitus, and obesity; and 2) specific pharmacologic therapy such as insulin sensitizers, antioxidants, or cytoprotective agents. Newer thiazolidinediones, such as rosiglitazone and pioglitazone, have shown promise in the treatment of NASH in pilot studies. However, these agents should not be used in clinical practice until their efficacy and safety are firmly established in larger studies. Despite encouraging initial studies, the recently completed multicenter, randomized, controlled trial failed to show any efficacy for ursodeoxycholic acid in the treatment of NASH. Other agents, such as vitamin E, betaine, probucol, and atorvastatin, have been explored as therapeutic agents for NASH. However, none of these studies have shown convincingly their utility in the treatment of NASH. Attempts to identify optimal therapy for patients with NASH are being vigorously pursued by the research community and important advances are expected within next several years. Until then, subjects should be advised to avoid alcohol, lose weight, and exercise regularly, and meticulous attention should be paid to the control of their risk factors such as diabetes and hyperlipidemia.     

Treatment of nonalcoholic fatty liver disease

Treatment of patients with nonalcoholic fatty liver disease (NAFLD) has typically been focused on the management of associated conditions such as obesity, diabetes mellitus and hyperlipidemia. NAFLD associated with obesity may resolve with weight reduction, although the benefits of weight loss have been inconsistent. Appropriate control of glucose and lipid levels is always recommended, but not always effective in reversing the liver condition. Results of pilot studies evaluating ursodeoxycholic acid, gemfibrozil, betaine, N-acetylcysteine, vitamin E (alpha-tocopherol), metformin and thiazolidinedione derivatives suggest that these medications may be of potential benefit for patients with NAFLD. These medications, however, need first to be tested in well-controlled trials with clinically relevant end-points and extended follow up. A better understanding of the pathogenesis and natural history of NAFLD will help to identify the subset of patients at risk of progressing to advanced liver disease, and hence, those patients who should derive the most benefit from medical therapy.     

Treatment of nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is the most common cause for elevated liver enzymes in the developed nations. Beyond prevention programs which are of particular interest because of the increasing number of overweight children, treatment should be focussed on the most important risk factors, obesity and insulin resistance. As a consequence of elucidating the pathomechanisms of NAFLD, the number of potential therapeutic options increased. However, many studies investigating the therapeutic effect show shortcomings in at least one of the following points: lack of a serial liver biopsy, short term of treatment and limited number of included patients. The second generation insulin sensitizer piogiitazone and rosiglitazone show the most promising improvements in NAFLD, but weight gain and potential hepatotoxicity calls for attention. In conclusion, a general recommendation for the application of specific drugs cannot be given. Besides controlled clinical trials, weight reduction and physical activity to improve insulin sensitivity in obese patients should be the priority objective.     

Treatment strategies in nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is an increasingly recognized health problem. Increased fat accumulation in the liver is observed in 20-30% of the population in the Western world, and in approximately 10% of this cohort it is associated with nonalcoholic steatohepatitis, which is characterized by inflammation and fibrosis. Disease presentation of NAFLD ranges from asymptomatic disease to cirrhosis with the complication of liver failure and hepatocellular carcinoma. NAFLD is suspected on the basis of various clinical aspects (an elevated alanine aminotransferase concentration, presence of obesity and diabetes) that alone are not sufficient to establish diagnosis or prognosis. The major diagnostic procedure is liver biopsy, which allows assessment of liver injury. In most cases, NAFLD is associated with insulin resistance, which is therefore the target of most current NAFLD treatment modalities. Various treatment strategies such as weight loss and/or exercise, thiazolidinediones, metformin, lipid-lowering agents and antioxidants have been studied. So far, no single intervention has convincingly improved liver histology. It is recommended that patients at high risk of developing advanced liver disease, and who are not part of controlled studies, should receive nutritional counseling and take physical exercise to achieve moderate weight loss and improve insulin sensitivity.     

Treatment of fibrosis in nonalcoholic fatty liver disease

Nonalcoholic steatohepatitis (NASH) is one of the most common liver disorders in North America. The mechanism of liver injury in NASH involves insulin resistance and oxidative stress as well as cytokine release. Therapeutic interventions aimed at enhancing insulin sensitivity or reducing oxidative stress have been studied. The role of peptide hormones secreted by adipose tissue—adipocytokines—in the potential pathogenesis of NASH is an area of intense research. As the function of adipokines in modulating hepatic inflammation and fibrosis is elucidated, the potential for novel treatment strategies in patients with NASH is likely to be realized.