体检人群非酒精性脂肪肝危险因素对照分析

目的通过体检调查,对非酒精性脂肪肝危险因素进行对照分析,为防治及医疗决策提供依据。方法收集2014年7月~2016年1月于笔者所在医院进行常规体检的1004人完整资料,根据是否患有NAFLD,将患者分为病例组295例与对照组709例两组。采用问卷调查与健康体检两部分收集调查对象的年龄、性别、职业、既往病史等一般特征及NAFLD临床诊断。对比分析两组研究对象BMI、收缩压、舒张压、PBG、TG、TC、ALT与UA水平。结果在1004例研究对象中,共检出NAFLD 295人,其发生率为29.38%。两组研究对象在年龄、空腹血糖差异无统计学意义(P0.05)。病例组患者BMI、收缩压、舒张压、PBG、TG、TC、ALT与UA水平,均明显高于对照组,差异显著具有统计学意义(P0.05)。以NAFLD为应变量,性别、年龄、BMI、空腹血糖、舒张压、胆固醇、甘油三酯和丙氨酸氨基转移酶为自变量进行Logistic回归分析,脂肪肝危险因素依次为甘油三酯、胆固醇、空腹血糖、BMI、舒张压、ALT、年龄和男性。结论烟台地区NAFLD患病率较高,高脂血症、超重及肥胖、糖尿病、高血压、高丙氨酸转氨酶、年龄、男性等为非酒精性脂肪肝的危险因素。合理控制体重,适当锻炼,做好高血压、糖尿病、肥胖的控制,可积极预防NAFLD的发生。     

非酒精性脂肪肝相关危险因素140例分析

目的探讨非酒精性脂肪肝(NAFLD)的相关危险因素及防治。方法回顾性分析140例NAFLD住院患者的临床资料,总结与之相关的危险因素。结果男性NAFLD患病率相比女性患病率高,女性NAFLD患病率随年龄增长呈升高趋势。NAFLD危险因素主要有胰腺炎,胆道感染,肿瘤,糖尿病相关外周血管病变和年龄。结论 NAFLD形成的主要危险因素与多种疾病密切相关,伴发疾病是导致病情进展及死亡的重要因素,采取有效干预措施、科学控制BMI、合理膳食、加强体育锻炼可以预防和控制NAFLD的发生和发展。     

某地区儿童非酒精性脂肪肝危险因素的调查

目的调查分析本地儿童非酒精性脂肪肝(NAFLD)的危险因素,为儿童非酒精性脂肪肝的预防、治疗提供参考。方法对本地2所中小学中,年龄6¹2岁患有非酒精性脂肪肝的1623例儿童进行问卷调查、体格检查、血脂、空腹胰岛素、三酰甘油检测B超检查及体质量指数(BMI),并与健康儿童进行比较,分析空腹胰岛素、三酰甘油、血压与非酒精性脂肪肝发生的相关性。结果 100例患有NAFLD的患儿中,发病年龄分布无统计学差异(P>0.05);三酰甘油及体质量指数(BMI)是NAFLD发病的高危因素(P<0.05),而空腹胰岛素水平与NAFLD发生无明显相关关系(P>0.05)。结论 NAFLD的发生与多种因素有关,三酰甘油与体质量指数是NAFLD发生的主要危险因素。     

非酒精性脂肪肝相关危险因素分析

目的分析非酒精性脂肪肝（NAFLD）患者临床指标,探讨其相关危险因素。方法 180例体检患者按有无NAFLD分为正常对照组（86例）和NAFLD组（94例）,对两组各临床指标进行统计分析。结果与对照组比较,NAFLD组体质量指数（BMI）、腰围、丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、γ-谷氨酰转肽酶（GGT）、血脂总胆固醇（TC）、甘油三酯（TG）、非高密度脂蛋白胆固醇（non-HDL-C）、空腹血糖（FBG）、尿酸、收缩压（SBP）、舒张压（DBP）均显著升高,而高密度脂蛋白胆固醇（HDL-C）显著降低（P〈0.05）。Logistic回归分析显示BMI、腰围、TG可较好地预测NAFLD,是NAFLD的独立危险因素（P〈0.05）。结论 NAFLD患者具有中心性肥胖、高血糖、高血压、脂代谢紊乱（高TC、高TG、低HDL-C）、高尿酸的特征,且肝酶升高。BMI、腰围、TG是发生NAFLD的独立危险因素。     

武汉某社区老年人群非酒精性脂肪性肝病的患病率及危险因素分析

目的调查分析老年人群非酒精性脂肪性肝病的患病率及危险因素,为老年性非酒精性脂肪性肝病的预防提供对策。方法选取武汉某社区的926例60—90岁老年人作为研究对象,调查非酒精性脂肪性肝病的患病率并分析其相关危险因素。结果926例老年人群中NAFLD共273例,患病率为29．5％。经多元Logistic回归分析,血脂异常、肥胖、高血压、糖尿病为老年人群中NAFLD的主要危险因素。结论老年人群非酒精性脂肪性肝病患病率较高,血脂异常、肥胖症、糖尿病和高血压为NAFLD的主要危险因素。     

焦作市3800名健康查体者非酒精性脂肪肝危险因素调查

<正>随着人们物质生活水平的不断提高,代谢性疾病对人类危害性也日益增大。肥胖、高脂血症、糖尿病、高血压病等已逐步显现出与脂肪肝的联系。为了探索诸多危险因子与脂肪肝发病的联系程度,笔者进行了本项研究。非酒精性脂肪肝是近年来被人们广泛认识的一种慢性肝脏疾病,表现为单纯脂肪变性到非酒精性肝炎,最终形成肝硬化。因此,脂肪肝已     

糖耐量减低患者非酒精性脂肪肝危险因素分析

目的:探讨糖耐量减低(IGT)患者非酒精性脂肪肝(NAFL)的特点、相关危险因素及临床意义。方法:随机选取IGT患者根据是否合并NAFL分为IGT合并NAFL组和IGT无NAFL组,测量身高、体重、腰围、臀围、空腹血清胆固醇(TC)、甘油三酯(TG)、空腹血糖(FPG)。分析IGT期NAFL的危险因素。结果:IGT患者合并NAFL的发病率为68.75%;IGT伴NAFL的体重指数(BM I)、腰臀比(WHR)和血脂水平高于IGT不伴NAFL组(P<0.05)。结论:血脂异常、肥胖、高血压是IGT伴NAFL患者的独立危险因素。     

非酒精性脂肪肝病危险因素及防控对策研究

目的通过对非酒精性脂肪肝病危险因素的分析,提出防控该病的对策。方法收集2005年1月至2008年12月来本院健康体检客人的一般资料、血糖、血脂、血压、血尿酸、肝脏超声、体重指数等数据,并进行统计分析。结果观察组舒张压、甘油三脂、BMI的平均值明显高于对照组（P〈0.05）,收缩压、空腹血糖、胆固醇、低密度脂蛋白及高密度脂蛋白较对照组略有升高（P〉0.05）,舒张压、甘油三脂、胆固醇、低密度脂蛋白、血尿酸、体重指数与非酒精性脂肪肝的发生呈正相关（P〈0.05）。结论高血压、血脂异常、BMI异常、血尿酸与非酒精性脂肪肝病的发生密切相关,控制这些指标可以降低非酒精性脂肪肝的发病率。     

青岛市城阳区非酒精性脂肪肝患病率及危险因素分析

目的了解健康人群中非酒精性脂肪肝病(NAFLD)患病率及相关危险因素,为防治NAFLD提供依据。方法以城阳人民医院健康体检的745例人群为研究对象,以是否患NAFLD将其分为NAFLD组和对照组,收集相关资料进行显著性分析。结果 NAFLD总检出率23.0%,有明显的家族史、性别、年龄差异;NAFLD组各危险因素检出率均高于对照组;除HDL,NAFLD组各临床指标均值均高于对照组;Logistic回归分析显示家族史、年龄、BMI、SBP、TG、UA、FINS、CHD、HT、HDL与NAFLD的发生密切相关。结论家族史、肥胖、年龄、高血压、TG、UA、FINS、CHD、HT升高是NAFLD的危险因素,HDL是其保护因素。     

The natural history and risk factors for progression of non-alcoholic fatty liver disease and steatohepatitis

Nonalcoholic fatty liver disease (NAFLD) is a condition of increasing incidence in western Countries seldom associated to other diseases of high prevalence in general population (i.e. diabetes and obesity). NAFLD ranges from simple fatty liver to steatohepatitis (NASH), which may lead to cryptogenic cirrhosis and in some cases hepatocellular carcinoma (HCC). Natural history of NAFLD in humans is poorly understood and progression of liver disease seems to be due to interaction between hosting (i.e. genetic, gut flora, insulin resistance) and environmental factors (social and eating behaviours) that should be responsible of increased oxidative stress within hepatocytes. Even if we need non-invasive markers able to describe the progression of liver disease, only meaning of liver biopsy is useful to characterize the stigmata of worsening such as inflammation and fibrosis.     

Models for non-alcoholic fatty liver disease: a link with vascular risk

Non alcoholic fatty liver disease (NAFLD) is often part of the metabolic syndrome which includes central obesity, dyslipidaemia, insulin resistance/type 2 diabetes mellitus and hypertension. In turn, NAFLD may be associated with an increased vascular risk. Several experimental models which express histological steatosis or steatohepatitis with fibrosis have been described. This review identifies those models of NAFLD with features of vascular risk.     

Current best treatment for non-alcoholic fatty liver disease

Treatment of patients with non-alcoholic fatty liver disease (NAFLD) has typically been focused on the management of associated conditions such as obesity, diabetes mellitus and hyperlipidaemia. NAFLD associated with obesity may be resolved by weight reduction, although the benefits of weight loss have been inconsistent. Improving insulin sensitivity with lifestyle modifications or medications usually improves glucose and lipid levels in patients with diabetes and hyperlipidaemia. Improving insulin sensitivity is expected to improve the liver disease but in many diabetic/hyperlipidaemic patients with NAFLD, the appropriate control of glucose and lipid levels is not always accompanied by improvement of the liver condition. Results of pilot studies evaluating ursodeoxycholic acid, gemfibrozil, betaine, N-acetylcysteine, αtocopherol, metformin and thiazolidinedione derivatives suggest that these medications may be of potential benefit. This article reviews the treatment modalities currently available for patients with NAFLD, including emerging data from clinical trials evaluating promising medications as well as possibilities for the future.     

Adipokines and cytokines in non-alcoholic fatty liver disease

Background  Several adipocytokines have been implicated in the pathogenesis non-alcoholic fatty liver disease (NAFLD).
Aim  To assess adipocytokines in NAFLD patients and controls.
Methods  A total of 95 patients (26 non-alcoholic steatohepatitis (NASH), 19 simple steatosis (SS), 38 obese controls and 12 non-obese controls) were included. Fasting serum insulin, glucose, visfatin, resistin, adiponectin, tumour necrosis factor-α (TNF-α), interleukin-8 (IL-8) and IL-6 were determined. Univariate and multivariate analyses were used to compare groups and determine associations.
Results  Serum TNF-α and IL-8 were higher in NAFLD patients when compared with both obese and non-obese controls. Analysis involving all patients revealed a significant correlation between serum TNF-α and IL-8 ( P  < 6.319e−08), and between IL-6 and IL-8 ( P  < 5.271e−15). Homeostatic model assessment scores negatively correlated with adiponectin in NAFLD ( P  < 0.0032). Serum visfatin was higher in all three obese groups than in non-obese controls ( P  < 0.02, P  < 0.002 and P  < 0.008). Visfatin in NASH patients was lower than SS and obese controls. Although TNF-α was associated with NAFLD ( P  < 0.02), it was interdependent on visfatin. In comparison to SS, four factors were independently associated with NASH: age, alanine aminotransferase, IL-8 and adiponectin ( P  < 0.05). Multivariate analysis indicated that TNF-α was the only independent predictor of fibrosis in NASH ( P  < 0.0004).
Conclusion  These findings support a complex interaction between adipocytokines and the pathogenesis of NAFLD.