非酒精性脂肪性肝病血清标志物研究进展

目的 非酒精性脂肪性肝病(NAFLD)是目前全球最流行的慢性肝脏疾病,其主要发生机制包括胰岛素抵抗和氧化应激等.不同血清标志物与NAFLD发病机制密切相关,但尚无明确的定论.本文主要就NAFLD发生发展过程中不同血清标志物的作用作一综述.     

非酒精性脂肪性肝病的病因及治疗

非酒精性脂肪性肝病(NAFLD)主要包括单纯性脂肪肝、非酒精性脂肪性肝炎(NASH)和脂肪性肝硬化。该病通常原发于与胰岛素抵抗(IR)相关的超重、肥胖、2型糖尿病和高脂血症等代谢紊乱，是胰岛素抵抗综合征的组成部分。NAFLD不仅可导致肝病相关残疾和死亡，而且与动脉粥样硬化性心、脑血管事件的高发密切相关。现就其病因和治疗作一综述。     

非酒精性脂肪性肝病患者血清LncRNA H19表达变化及临床意义

目的:检测长链非编码RNA H19(lncRNA H19)在非酒精性脂肪性肝病(NAFLD)患者血清中表达情况,探讨LncRNA H19在NAFLD中的临床意义.方法:选择2019年1月-2020年12月收治的NAFLD患者137例作为研究对象,根据CT影像学表现将NAFLD患者分为轻度脂肪肝组(57例),中度脂肪肝组...     

非酒精性脂肪性肝病患者血清PTX3的水平及临床意义

目的探讨非酒精性脂肪肝病患者血清五聚蛋白(PTX)3水平及其临床意义。方法选取2013年2月至2015年2月非酒精性脂肪肝性病患者130例(研究组),根据是否合并肝炎分为肝炎组(n=48例)和非肝炎组(n=82例),另选健康体检者130例(对照组),应用Spearman分析PTX3的参数,应用Logistic回归分析危险因子、ROC对脂肪肝炎的诊断价值。结果研究组血清中PTX3水平显著低于对照组,且肝炎组显著低于非肝炎组(P0.05);Spearman分析显示:胰岛素抵抗指数(HOMA-IR)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、腹腔内脂肪面积(VAT)、腹壁皮下脂肪面积(SAT)以及超敏C反应蛋白(hs-CRP)均为PTX3的相关因素;Logistic回归分析显示:PTX3是非酒精性脂肪肝的保护因素,而HOMA-IR、hs-CRP以及SAT为非酒精性脂肪性肝病的危险因素;血清PTX3诊断非酒精性脂肪性肝病ROC下面积为0.962,鉴别肝炎合并非酒精性脂肪性肝病和单纯性非酒精性脂肪性肝病的最佳截点为1.45 ng/ml。结论血清PTX3为非酒精性脂肪肝病的保护因素,能鉴别非酒精性脂肪性肝病是否合并肝炎。     

血清omentin-1和vaspin在非酒精性脂肪性肝病患者中的表达及意义

目的 探讨脂肪因子网膜蛋白-1(omentin-1)、内脏脂肪组织来源的丝氨酸蛋白酶抑制剂(visceral adipose tissue-derived serine protease inhibitor,vaspin)在非酒精性脂肪性肝病(nonalcoholic fatty liver disease,NAFLD...     

酒精性与非酒精性脂肪性肝病

脂肪性肝病(FLD)根据有无过量饮酒史,分为酒精性肝病(ALD)和非酒精性脂肪性肝病(NAFLD)两大类。两者享有FLD的许多共性特征,但又各有其独特之处。 1.酒精性与非酒精性FLD的异同:NAFLD的肝组织学改变与ALD相似,包括单纯性脂肪肝、脂肪性肝炎及肝硬化。我国及日本学者认为ALD还应包括轻症ALD、酒精性重型肝炎及酒精性肝纤维化,事实上NAFLD均有其相对应的临床病理类     

非酒精性脂肪性肝病病理学研究进展

非酒精性脂肪性肝病(NAFLD)是包括单纯性脂肪肝、非酒精性脂肪性肝炎(NASH)、非酒精性脂肪性肝纤维化/肝硬化三个病变过程的临床病理综合征.美国的流行病学调查结果表明NAFLD发病率接近20%[1,2],远远超过丙型肝炎或酒精性肝病的发病率[3],NAFLD现已成为欧美等国慢性肝病中的第一大病种.我国目前尚无确切的NAFLD发病率数据,已有的流行病学研究结果显示,我国NAFLD的发病率约为5%～12%[4],随着我国肥胖人群的不断增加,NAFLD的发病率有可能更高.病理组织学检查被认为是NAFLD诊断的"金标准",自1980年Ludwig等[5]首次命名NASH以来,随着研究的广泛深入,NAFLD病理学研究也取得了很大进展.     

MicroRNAs as controlled systems and controllers in non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is a multi-faceted condition including simple steatosis alone or associated with inflammation and ballooning (non-alcoholic steatohepatitis) and eventually fibrosis. The NAFLD incidence has increased over the last twenty years becoming the most frequent chronic liver disease in industrialized countries. Obesity, visceral adiposity, insulin resistance, and many other disorders that characterize metabolic syndrome are the major predisposing risk factors for NAFLD. Furthermore, different factors, including genetic background, epigenetic mechanisms and environmental factors, such as diet and physical exercise, contribute to NAFLD development and progression. Several lines of evidence demonstrate that specific microRNAs expression profiles are strongly associated with several pathological conditions including NAFLD. In NAFLD, microRNA deregulation in response to intrinsic genetic or epigenetic factors or environmental factors contributes to metabolic dysfunction. In this review we focused on microRNAs role both as controlled and controllers molecules in NAFLD development and/or their eventual value as non-invasive biomarkers of disease.     

Management of non-alcoholic fatty liver disease in 2015

There is no single pharmacologic therapy that has been approved to treat nonalcoholic fatty liver disease in the general population. The backbone of therapy currently includes intensive lifestyle modification with established targets for diet and weight loss. The use of unsweetened, unfiltered coffee along with limiting high fructose corn syrup have emerged as beneficial dietary recommendations. The use of empiric oral hypoglycemic agents and vitamin E, however, has not been widely accepted. Developing bariatric surgical techniques are promising, but additional studies with long-term follow up are needed before it can be widely recommended. Finally, liver transplantation is an increasingly frequent consideration once complications of end-stage disease have developed. The future treatment of those with nonalcoholic fatty liver disease will likely involve a personalized approach. The importance of the gut microbiome in mediating hepatocyte inflammation and intestinal permeability is emerging and may offer avenues for novel treatment. The study of anti-fibrotic agents such as pentoxifylline and FXR agonists hold promise and new pathways, such as hepatocyte cannabinoid receptor antagonists are being studied. With the incidence of obesity and the metabolic syndrome increasing throughout the developed world, the future will continue to focus on finding novel agents and new applications of existing therapies to help prevent and to mediate the progression of nonalcoholic fatty liver disease.     

Liver transplantation and non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is an important health problem worldwide. NAFLD encompasses a histological spectrum ranging from bland liver steatosis to severe steatohepatitis (nonalcoholic steatohepatitis, NASH) with the potential of progressing to cirrhosis and its associated morbidity and mortality. NAFLD is thought to be the hepatic manifestation of insulin resistance (or the metabolic syndrome); its prevalence is increasing worldwide in parallel with the obesity epidemic. In many developed countries, NAFLD is the most common cause of liver disease and NASH related cirrhosis is currently the third most common indication for liver transplantation. NASH related cirrhosis is anticipated to become the leading indication for liver transplantation within the next one or two decades. In this review, we discuss how liver transplantation is affected by NAFLD, specifically the following: (1) the increasing need for liver transplantation due to NASH; (2) the impact of the increasing prevalence of NAFLD in the general population on the quality of deceased and live donor livers available for transplantation; (3) the long term graft and patient outcomes after liver transplantation for NASH, and finally; and (4) the de novo occurrence of NAFLD/NASH after liver transplantation and its impact on graft and patient outcomes.     

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 glucagon- like peptide-1 responses in insulin-resistant subjects, and upregulates glucose transporter-2 expression in the liver. The principal mechanisms include： decreased nuclear factor-kappa B activation, decreased low- density 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.     

Circulating microRNAs in patients with non-alcoholic fatty liver disease

AIM: To identify novel non-invasive biomarkers for non-alcoholic fatty liver disease(NAFLD). METHODS: Twenty patients with histologically proven NAFLD and 20 controls were included. All NAFLD cases were scored using the NAFLD activity score. The rela-tive expressions of miR-197, miR-146 b, miR-10 b, miR-181d, miR-34 a, miR-122, miR-99 a and miR-29 a were analyzed using real-time polymerase chain reaction. RESULTS: Serum levels of miR-181 d, miR-99 a, miR-197 and miR-146 b were significantly lower in biopsy-proven NAFLD patients than in the healthy controls. Serum lev-els of miR-197 and miR-10 b were inversely correlated with degree of inflammation and miR-181 d and miR-99 a were inversely correlated with serum gamma glu-tamyl transferase levels in non-alcoholic steatohepatitis patients. CONCLUSION: NAFLD is associated with altered se-rum miRNA expression pattern. This study provides clues for defining the non-invasive diagnosis of NAFLD.     

Coronavirus disease 2019 and non-alcoholic fatty liver disease

The coronavirus disease 2019(COVID-19) pandemic may present with a broad range of clinical manifestations, from no or mild symptoms to severe disease. Patients with specific pre-existing comorbidities, such as obesity and type 2 diabetes, are at high risk of coming out with a critical form of COVID-19. Nonalcoholic fatty liver disease(NAFLD) is the most common chronic liver disease, and, because of its frequent association with metabolic alterations including obesity and type 2 diabetes, it has recently been re-named as metabolic-associated fatty liver disease(MAFLD). Several studies and systematic reviews pointed out the increased risk of severe COVID-19 in NAFLD/MAFLD patients. Even though dedicated mechanistic studies are missing, this higher probability may be justified by systemic low-grade chronic inflammation associated with immune dysregulation in NAFLD/MAFLD, which could trigger cytokine storm and hypercoagulable state after severe acute respiratory syndrome coronavirus 2 infection. This review focuses on the predisposing role of NAFLD/MAFLD in favoring severe COVID-19, discussing the available information on specific risk factors, clinical features, outcomes, and pathogenetic mechanisms.     

Risk factors for hepatic steatosis in adults with cystic fibrosis: Similarities to non-alcoholic fatty liver disease

AIM To investigate the clinical, biochemical and imaging characteristics of adult cystic fibrosis(CF) patients with hepatic steatosis as compared to normal CF controls.METHODS We performed a retrospective review of adult CF patients in an academic outpatient setting during 2016. Baseline characteristics, genetic mutation analysis as well as laboratory values were collected. Abdominal imaging(ultrasound, computed tomography, magnetic resonance) was used to determine presence of hepatic steatosis. We compare patients with hepatic steatosis to normal controls.RESULTS Data was collected on 114 patients meeting inclusion criteria. Seventeen patients(14.9%) were found to have hepatic steatosis on imaging. Being overweight(BMI 25)(P = 0.019) and having a higher pp FEV1(75 vs 53, P = 0.037) were significantly associated with hepatic steatosis. Patients with hepatic steatosis had a significantly higher median alanine aminotransferase level(27 vs 19, P = 0.048). None of the hepatic steatosis patients had frank CF liver disease, cirrhosis or portal hypertension. We found no significant association with pancreatic insufficiency or CF related diabetes.CONCLUSION Hepatic steatosis appears to be a clinically and phenotypically distinct entity from CF liver disease. The lack of association with malnourishment and the significant association with higher BMI and higher pp FEV1 demonstrate similarities with non-alcoholic fatty liver disease. Long term prospective studies are needed to ascertain whether CF hepatic steatosis progresses to fibrosis and cirrhosis.     

脂肪因子与非酒精性脂肪肝

非酒精性脂肪性肝病的发病机制目前尚不十分清楚,脂代谢异常(尤其是TG)与胰岛素抵抗(IR)可能是其病因的关键环节,瘦素、脂联素、抵抗素、肿瘤坏死因子等多种脂肪因子在非酒精性脂肪肝的形成、炎性改变及纤维化的过程中发挥了重要作用.