异丙嗪治疗急性轻度非嗜酒性酒精中毒疗效观察

[目的 ]探讨异丙嗪治疗急性轻度非嗜酒性酒精中毒的临床治疗效果。 [方法 ]72例分 A、B两组 ,A组 4 0例 ,B组32例 ,A组常规治疗 +肌注异丙嗪 2 5～ 5 0 mg,B组常规治疗 +肌注纳络酮 0 .4～ 0 .8mg。 [结果 ]A组病例临床症状消除情况明显优于 B组。 [结论

胰岛素抵抗和非酒精性脂肪性肝病研究进展

非酒精性脂肪性肝病(NAFLD)是现在临床上最为常见的肝病之一,其病因及发病机制均相当复杂,至今尚未完全阐明.目前认为,胰岛素抵抗(IR)不仅是NAFLD的触发因素,而且还可能间接促进单纯性脂肪肝向脂肪性肝炎(NASH)乃至肝纤维化转变的过程.至于IR是否直接参与NASH的发生、发展尚存在争议.此外,NAFLD本身也可能诱发及加重IR,比如肝细胞内蓄积的脂肪、TNF-α、瘦素抵抗等都参与这一过程.随着二者关系及相关因素的发展,NAFLD在诊疗方面也取得了较大的进展.近年来,有关这方面的研究很多,本文对此作阐述.

肝苏颗粒治疗非酒精性脂肪性肝炎临床观察

目的:探讨肝苏颗粒治疗非酒精性脂肪性肝炎的疗效。方法:对169例非酒精性脂肪性肝炎随机分为两组,治疗组用肝苏颗粒,对照组用熊去氧胆酸和复方益肝灵片。观察两组治疗前后的症状、体重、生化指标ALT、AST、γ-GT、TC、TG、GS的变化。结果:治疗后治疗组降低体重、ALT、AST、γ-GT、GS恢复,显效率、总有效率优于对照组(P<0．05或P<0．01),TG、TC两组比较P>0．05,但治疗前后比较P<0．05。结论:肝苏颗粒治疗非酒精性肝炎疗效明显,对改善脂质代谢、下调血糖、下降体重,均有较好的作用。

非酒精性脂肪肝的中西医研究进展

非酒精性脂肪肝是一种无过量饮酒史,以肝实质细胞脂肪变性和脂肪贮积为特征的临床病理综合征。非酒精性脂肪肝属于祖国传统医学中"肝癖""积证""胁痛""痰证"等范畴。本文综合分析了中西医对非酒精性脂肪肝的病因病机及治疗原则的研究现状,为临床上治疗本病提供了一定的理论依据。

疏肝和胃调脂方治疗非酒精性脂肪肝41例临床观察

目的:观察自拟方疏肝和胃调脂方对非酒精性脂肪肝的疗效。方法:将非酒精性脂肪肝患者82例随机分为对照组及治疗组,对照组在以饮食及运动疗法的基础上服用易善复,而治疗组在饮食及运动疗法的基础上,予以自拟的疏肝和胃调脂方(柴胡、黄芩、党参、法夏、党参、决明子、山楂、内金、泽泻、菖蒲、郁金、苏叶等)每日一剂,共治疗八周,治疗前后检测患者血脂四项、肝功五项及肝胆B超。结果:治疗组痊愈19例,显效13例,有效6例,无效3例,总有效率为92.7%;对照组痊愈12例,显效10例,有效9例,无效10例,总有效率为75.6%。两组疗效比较差异具有统计学意义(p<0.05)。结论:疏肝和胃调脂方对非酒精性脂肪肝有良好的疗效,其具体作用机制有待于进一步研究。

非酒精性脂肪肝患者血清酶学和血脂及肝纤维化指标分析

目的探讨血液生化和肝纤维化指标在非酒精性脂肪肝患者临床诊断中的意义。方法对符合B超诊断的286例非酒精性脂肪肝患者进行血液生化指标(TG、TC、HDL-c、ALT、AST、LDL-c、ALT、AST、GGT、ALP)和肝纤维化指标(PCⅢ、HA、CIV、LN)检测,并以体检健康者作为对照。结果非酒精性脂肪肝患者TG和TC水平均高于健康对照组(P<0.01),HDL-c和LDL-c与对照组相比分别呈下降和升高的趋势;重度非酒精性脂肪肝组ALT、AST和GGT明显升高(P<0.01),ALP升高不显著(P>0·05),PCⅢ、HA、CIV、LN均高于健康组(P<0.05),重度组与轻、中度组之间PCⅢ、HA,,CIV和LN差异均有显著性(P<0.01),中度脂肪肝与轻度脂肪肝之间PCⅢ、HA、CIV和LN差异无显著性(P>0·05)。结论非酒性脂肪肝患者多项血液生化指标异常,重度非酒性脂肪肝患者尚存在不同程度的肝纤维化趋向。多项血液生化指标的检测可作为非酒精性脂肪肝筛查的重要依据,而肝纤维化指标的检测可进一步作为非酒精性脂肪肝病情监控和疗效评估的重要依据。

286例非酒精性脂肪肝患者血液生化指标和肝纤维化指标的分析

目的:探讨血液生化和肝纤维化指标在非酒精性脂肪肝患者临床诊断中的意义。方法:对符合B超诊断的286例非酒精性脂肪肝患者进行血液生化指标(TG、TC、HDL-c、LDL-c、ALT、AST、GGT、ALP)和肝纤维化指标(PCⅢ、HA、CⅣ、LN)检测,并以体检健康者作为对照。结果:非酒精性脂肪肝患者TG和TC水平均高于对照组(P<0.01),HDL-c和LDL-c与对照组相比分别呈下降和升高的趋势;重度非酒精性脂肪肝组ALT、AST和GGT明显升高(P<0.01),ALP升高不显著(P>0.05);非酒精性脂肪肝患者PCⅢ、HA、CⅣ和LN均高于健康组(P<0.05),重度组与轻、中度组之间PCⅢ、HA、CⅣ和LN差异均有显著性(P<0.01),中度脂肪肝与轻度脂肪肝之间PCⅢ、HA、CⅣ和LN差异无显著性(P>0.05)。结论:非酒性脂肪肝患者多项血液生化指标异常,重度非酒性脂肪肝患者尚存在不同程度的肝纤维化趋向。多项血液生化指标的检测可作为非酒精性脂肪肝筛查的重要依据,而肝纤维化指标的检测可进一步作为非酒精性脂肪肝病情监控和疗效评估的重要依据。

Comprehensive Understanding of Immune Cells in The Pathogenesis of Non-alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease(NAFLD)is the most common chronic liver disease,defined by several phases,ranging from benign fat accumulation to non-alcoholic steatohepatitis(NASH),which can lead to liver cancer and cirrhosis.Although NAFLD is a disease of disordered metabolism,it also involves several immune cell-mediated inflammatory processes,either promoting and/or suppressing hepatocyte inflammation through the secretion of pro-inflammatory and/or anti-inflammatory factors to influence the NAFLD process.However,the underlying disease mechanism and the role of immune cells in NAFLD are still under investigation,leaving many open-ended questions.In this review,we presented the recent concepts about the interplay of immune cells in the onset and pathogenesis of NAFLD.We also highlighted the specific non-immune cells exhibiting immunological properties of therapeutic significance in NAFLD.We hope that this review will help guide the development of future NAFLD therapeutics.

Olive oil consumption and non-alcoholic fatty liver disease

The clinical implications of non-alcoholic fatty liver diseases(NAFLD)derive from their potential to progress to fibrosis and cirrhosis.Inappropriate dietary fat intake,excessive intake of soft drinks,insulin resistance and increased oxidative stress results in increased free fatty acid delivery to the liver and increased hepatic triglyceride(TG)accumulation.An olive oil-rich diet decreases accumulation of TGs in the liver,improves postprandial TGs,glucose and glucagonlike peptide-1 responses in insulin-resistant subjects, and upregulates glucose transporter-2 expression in the liver.The principal mechanisms include:decreased nuclear factor-kappaB activation,decreased lowdensity lipoprotein oxidation,and improved insulin resistance by reduced production of inflammatory cytokines(tumor necrosis factor,interleukin-6)and improvement of jun N-terminal kinase-mediated phosphorylation of insulin receptor substrate-1.The beneficial effect of the Mediterranean diet is derived from monounsaturated fatty acids,mainly from olive oil.In this review,we describe the dietary sources of the monounsaturated fatty acids,the composition of olive oil,dietary fats and their relationship to insulin resistance and postprandial lipid and glucose responses in non-alcoholic steatohepatitis,clinical and experimental studies that assess the relationship between olive oil and NAFLD,and the mechanism by which olive oil ameliorates fatty liver,and we discuss future perspectives.

Nonalcoholic fatty liver disease: An overview of current insights in pathogenesis, diagnosis and treatment

Estimates of people suffering from overweight (one billion) and obesity (300 million) are increasing. The accumulation of triglycerides in the liver, in the absence of excess alcohol intake, has been described in the early sixties. It was not until 1980, however, that Ludwig et al named this condition nonalcoholic steatohepatitis (NASH). Subsequently, nonalcoholic fatty liver disease (NAFLD) has been used as a general name for conditions ranging from simple steatosis through steatohepatitis to end-stage liver disease (cirrhosis). Many studies have demonstrated the significant correlation with obesity and insulin resistance. Other studies have revealed a signifi- cant correlation between hepatic steatosis, cardiovascu- lar disease and increased intima-media thickness. WHO estimated that at least two million patients will develop cirrhosis due to hepatic steatosis in the years to come. Longitudinal cohort studies have demonstrated that those patients with cirrhosis have a similar risk to devel- op hepatocellular carcinoma as those with other causes of cirrhosis. Taken all together, NAFLD has become the third most important indication for liver transplantation. There- fore, training programmes in internal medicine, gastroen- terology and hepatology should stress the importance of diagnosing this entity and treat properly those at risk for developing complications of portal hypertension and con- comittant cardiovascular disease. This review will focus on the clinical characteristics, pathophysiology, imaging tech- niques and the readily available therapeutic options.

Expression of p53,Bax and Bcl-2 proteins in hepatocytes in non-alcoholic fatty liver disease

AIM: To analyze the protein expression essential for apoptosis in liver steatosis. METHODS: The expression of proapoptotic proteins p53, Bax, and antiapoptotic Bcl-2 in hepatocytes with steatosis (SH) and without steatosis (NSH) was evaluated in 84 patients at various stages of non-alcoholic fatty liver disease (NAFLD). RESULTS: Immunohistochemical staining of liver tissue showed the activation of p53 protein in SH and NSH with increased liver steatosis, diminished Bcl-2 and slightly decreased Bax protein. Positive correlation was found between the stage of liver steatosis with p53 expression in SH (r = 0.54, P < 0.01) and NSH (r = 0.49, P < 0.01). The antiapoptotic protein Bcl-2 was diminished together with the advancement of liver steatosis, especially in non-steatosed hepatocytes (r =0.43, P < 001). CONCLUSION: Apoptosis is one of the most important mechanisms leading to hepatocyte elimination in NAFLD. The intensification of inflammation in NAFLD induces proapoptotic protein p53 with the inhibition of antiapoptotic Bcl-2.

Liver histology according to the presence of metabolic syndrome in nonalcoholic fatty liver disease cases

AIM:To investigate the histologic features of the liver in nonalcoholic fatty liver disease (NAFLD) cases according to the presence of metabolic syndrome or its individual components. METHODS:We enrolled 81 patients (40 male,41 fe-male) who were diagnosed with fatty liver by ultraso-nographic scan and fulfi lled the inclusion criteria. First anamnesis,anthropometric,clinical,laboratory and imaging features of all participants were recorded and then liver biopsy was performed after gaining consent from patients. Diagnosis of metabolic syndrome was dependent on patients having 3 or more out of 5 risk criteria defined by the WHO. Biopsy specimens were assessed according to Brunt et al's classification. RESULTS:Sixty-nine of the 81 patients had nonalco-holic steatohepatitis (NASH),11 had simple fatty liver and 1 had cirrhosis according to histologic evaluation. Comparisons were made between two groups of NASH patients,those with and without metabolic syndrome. We did not detect statistically significant differences in liver histology between NASH patients with and wit-hout metabolic syndrome. CONCLUSION:NASH can progress without metabolic risk factors or the presence of metabolic syndrome.

Non-alcoholic fatty liver disease and the metabolic syndrome:An update

Sedentary lifestyle and poor dietary choices are leading to a weight gain epidemic in westernized countries, subsequently increasing the risk for developing the metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). NAFLD is estimated to affect approximate 30% of the general US population and is considered the hepatic manifestation of the metabolic syndrome. Recent findings linking the components of the metabolic syndrome with NAFLD and the progression to nonalcoholic steatohepatitis (NASH) will be reviewed; in particular, the role of visceral adipose tissue, insulin resistance, and adipocytokines in the exacerbation of these conditions. While no therapy has been proven effective for treating NAFLD/NASH, common recommendations will be discussed.

Role of peroxisome proliferators-activated receptors in the pathogenesis and treatment of nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease （NAFLD） is highly prevalent and can result in nonalcoholic steatohepatitis （NASH） and progressive liver disease including cirrhosis and hepatocellular carcinoma. A growing body of literature implicates the peroxisome proliferators- activated receptors （PPARs） in the pathogenesis and treatment of NAFLD. These nuclear hormone receptors impact on hepatic triglyceride accumulation and insulin resistance. The aim of this review is to describe the data linking PPARα and PPART to NAFLD/NASH and to discuss the use of PPAR ligands for the treatment of NASH.

Nonalcoholic fatty liver disease is a novel predictor of cardiovascular disease

AIM:To clarify whether nonalcoholic fatty liver disease(NAFLD)increases the risk of cardiovascular disease.METHODS:We carried out a prospective observational study with a total of 1637 apparently healthy Japanese men and women who were recruited from a health check-up program.NAFLD was diagnosed by abdominal ultrasonography.The metabolic syndrome(MS)was defined according to the modified National Cholesterol Education Program(NCEP)ATP Ⅲ criteria.Five years after the baseline evaluations,the incidence of cardiovascular disease was assessed by a self-administered questionnaire.RESULTS:Among 1221 participants available for outcome analyses,the incidence of cardiovascular disease was higher in 231 subjects with NAFLD at baseline(5 coronary heart disease,6 ischemic stroke,and 1 cerebral hemorrhage)than 990 subjects without NAFLD(3 coronary heart disease,6 ischemic stroke,and 1 cerebral hemorrhage).Multivariate analyses indicated that NAFLD was a predictor of cardiovascular disease independent of conventional risk factors(odds ratio 4.12,95% CI,1.58 to 10.75,P = 0.004).MS was alsoindependently associated with cardiovascular events.But simultaneous inclusion of NAFLD and MS in a multivariate model revealed that NAFLD but not MS retained a statistically significant correlation with cardiovascular disease.CONCLUSION:Although both of them were predictors of cardiovascular disease,NAFLD but not MS retained a statistically significant correlation with cardiovascular disease in a multivariate model.NAFLD is a strong predictor of cardiovascular disease and may play a central role in the cardiovascular risk of MS.

Serum leptin and soluble leptin receptor in non-alcoholic fatty liver disease

AIM: To determine the role of leptin system in non-al- coholic fatty liver disease (NAFLD) development by deli- neating the changes in serum levels of leptin and soluble leptin receptor (sOB-R). METHODS: Blood samples were collected from 30 consecutive patients with liver-biopsy-proven NAFLD and 30 patients with cholecystolithiasis (stationary phase) as controls. Serum leptin levels were determined by radio- immunoassay and concentration of sOB-R was measured by ELISA. Body mass index (BMI) was calculated for all subjects, and serum insulin, C-peptide, and lipoprotein levels were also detected. RESULTS: Mean serum leptin level and BMI in the NAFLD group were significantly higher than in the con- trols (both P < 0.001), but mean sOB-R level was lower in the NAFLD group when compared to the controls. Both men and women in the NAFLD group had higher mean serum leptin levels and lower sOB-R levels than did the men and women in the control group (all P < 0.001). The- re was a significant negative correlation between serum leptin and sOB-R levels (r = -0.725, P < 0.001). Multiva- riate analysis showed that the percentage of hepatocyte steatosis, sex, BMI, and homeostasis model assessment of insulin resistance (HOMA IR) were independently rela- ted to serum leptin levels. CONCLUSION: Elevated serum leptin seems to be afeature of steatosis, and serum leptin seems to increase as hepatocyte steatosis develops. An enhanced release of leptin is accompanied by an decrease in sOB-R con- centration, which suggests higher resistance of periphe- ral tissues towards the action of leptin.

Nonalcoholic fatty liver disease and mitochondrial dysfunction

Nonalcoholic fatty liver disease (NAFLD) includes hepatic steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. NAFLD is the most common liver disorder in the United States and worldwide. Due to the rapid rise of the metabolic syndrome, the prevalence of NAFLD has recently dramatically increased and will continue to increase. NAFLD has also the potential to progress to hepatocellular carcinoma (HCC) or liver failure. NAFLD is strongly linked to caloric overconsumption, physical inactivity, insulin resistance and genetic factors. Although significant progress in understanding the pathogenesis of NAFLD has been achieved in years, the primary metabolic abnormalities leading to lipid accumulation within hepatocytes has remained poorly understood. Mitochondria are critical metabolic organelles serving as "cellular power plants". Accumulating evidence indicate that hepatic mitochondrial dysfunction is crucial to the pathogenesis of NAFLD. This review is focused on the significant role of mitochondria in the development of NAFLD.

Effect of insulin-sensitizing agents in combination with ezetimibe, and valsartan in rats with non-alcoholic fatty liver disease

AIM： To assess whether treatment with insulinsensitizing agents （ISAs） in combination with ezetimibe and valsartan have greater effect on hepatic fat content and lipid peroxidation compared to monotherapy in the methionine choline-deficient diet （MCDD） rat model of non-alcoholic fatty liver disease （NAFLD）. METHODS： Rats （n = 6 per group） were treated with different drugs, including MCDD only, MCDD diet with either metformin （200 mg/kg）, rosiglitazone （3 mg/kg）, metformin plus rosiglitazone （M＋R）, ezetimibe （2 mg/ kg）, valsartan （2 mg/kg）, or combination of all drugs for a total of 15 wk. Liver histology, lipids, parameters of oxidative stress and TNF-alpha were measured. RESULTS： Fatty liver （FL） rats demonstrated severe hepatic fatty infiltration （〉 91% fat）, with an increase in hepatic TG （＋1263%, P 〈 0.001）, hepatic cholesterol （＋245%, P 〈 0.03）, hepatic MDA levels （＋225%, P 〈 0.001）, serum TNF-alpha （17.8 ＋ 10 vs 7.8 ＋ 0.0, P 〈 0.001）, but a decrease in hepatic alpha tocopherol （-74%, P 〈 0.001） as compared to the control rats. Combination therapy with all drugs produced a significant decrease in liver steatosis （-54%）, hepatic TG （-64%）, hepatic cholesterol （-31%） and hepatic MDA （-70%）, but increased hepatic alpha tocopherol （＋443%） as compared to FL rats. Combination therapy with ISA alone produced a smaller decrease in liver steatosis （-32% vs -54%, P 〈 0.001） and in hepatic MDA levels （-55% vs -70%, P 〈 0.01）, but a similar decrease in hepatic lipids when compared with the all drugs combination. TNF-alpha levels decreased significantly in all treatment groups except in ISA group. CONCLUSION： Combination therapies have a greater effect on liver fat content as compared to monotherapy. Rosiglitazone appears to improve hepatic steatosis to a greater extent than metformin.