代谢相关脂肪性肝病生活方式干预治疗进展

代谢相关脂肪性肝病(MAFLD)全球患病率高达25%～30%,MAFLD与肝硬化、肝细胞癌、肝外恶性肿瘤、糖尿病、心血管疾病的发病率和死亡率密切相关，带来了巨大的疾病负担。生活方式的改变，包括饮食和体育锻炼来实现减重，仍是现阶段MAFLD的一线治疗措施。本文拟综述生活方式干预治疗MAFLD的进展，旨在为MAFLD的治疗提供借鉴。     

代谢相关脂肪性肝病基于中国居民膳食指南的个体化干预研究

背景 代谢相关脂肪性肝病(metabolic associated fatty liver disease, MAFLD)在全球范围内广泛流行,不良的饮食生活习惯与其发生发展密切相关,通过饮食运动及生活方式干预是防治MAFLD的重要措施之一,但目前关于MAFLD的饮食运动及生活方式的干预策略尚无定论,其方式方法仍需要进一步研究.目的 基于中国居民膳食指南为MAFLD患者制定个体化膳食及运动处方,探索个体化限制能量平衡膳食联合运动指导的干预方式对改善MAFLD的作用.方法 根据是否接受个体化饮食运动干预分为干预组和对照组,分别在入组时(T0)收集患者的人体测量指标、实验室检测指标,通过问卷调查了解患者的一般信息、家族史、膳食及生活习惯、食物频率等,根据患者实际情况给予干预组患者个体化膳食处方和运动处方,对照组给予常规健康宣教, 6 mo后(T1)再次收集患者的资料,比较干预前后人体测量指标和实验室检测指标的变化.结果 127例MAFLD患者(对照组32例,干预组95例)中,汽车出行者占62.99%,久坐者(>8 h/d)占48.82%,饮食口味重者占比>50%,爱加餐者占37...     

基于“脾主为胃行其津液”理论以行气祛湿活血法论治代谢相关脂肪性肝病

<正>于2020年国际专家共识声明将代谢相关脂肪性肝病(MAFLD)定义为肝脂肪沉积并伴有超重/肥胖、存在2型糖尿病或合并代谢紊乱^[1]。在术语上批准由代谢相关脂肪性肝病(MAFLD)取代之前的非酒精性脂肪性肝病(NAFLD)，强调了代谢失调是本病不容忽视的环节，本文以MAFLD替代NAFLD进行阐述。近年来，随着人们生活方式及饮食结构的改变，MAFLD影响世界上超过四分之一的人口，造成了严重的健康及经济负担。MAFLD包括一系列组织学异常，可由单纯肝脂肪变性逐步向肝纤维化及肝硬化进展；另则MAFLD有促进2型糖尿病、心血管疾病及慢性肾病等全身系统并发症的风险，是常见的慢性肝脏疾病之一，西医单一靶点药物治疗有其局限性^[2,3]。中医药因其多成分、多途径、多靶点特点，在对本病防治上有其优势。     

健康教育和健康促进在脂肪肝防治中的作用

正脂肪肝,现被命名为"代谢相关脂肪性肝病(MAFLD)",是全球最常见的慢性肝病,人群患病率为6.3%～45.0%,其中10%～30%为非酒精性脂肪性肝炎(NASH),在我国已经成为第一大肝病~([1-3])。脂肪肝至今仍无特效的治疗药物,其最基础、最有效的治疗是生活方式的改变与调整。而健康教育和健康促进在生活方式的调整中发挥着非常重要的作用。健康教育的定义是:通过有计划、有组织、有系统的社会教育活动,使人们自觉地采纳有益于健康的行为和生活方式,消除或减轻影响健康的危险因素,预     

常占杰教授“清源澄流”辨治代谢相关脂肪性肝病经验

<正>代谢相关脂肪性肝病(MAFLD)以肝细胞脂肪过度储存、变性为特征^[1]，是一种代谢应激性肝损伤^[2]。目前MAFLD已成为我国第一大慢性肝病，可逐渐进展为肝硬化、肝癌^[3]。MAFLD强调综合干预，其基础用药主要为降血脂药物，包括他汀类和贝特类药物等，长期使用均有潜在肝毒性^[4]。中医药在治疗MAFLD具有调节脂质代谢、改善肝功能、改善患者症状体征等优势^[5]。常占杰教授是全国老中医药专家学术经验继承工作指导教师、陕西省名中医，悬壶40余年，造诣颇丰，其在MAFLD的治疗上，提出“清源澄流”的辨治思想，研发临床验方消木丹等，疗效确切。笔者有幸从师侍诊，受益匪浅。本文对常占杰教授治疗MAFLD的学术经验掇菁撷华，以飨同道。     

维生素D缺乏与代谢相关脂肪性肝病的关系

代谢相关脂肪性肝病(MAFLD)为全球第一大慢性肝病，但发病机制仍不明确，尚缺乏有效的治疗药物。介绍了MAFLD患者常伴有维生素D缺乏，维生素D可能通过影响糖脂代谢、炎症信号通路、免疫调节、肠道微生态等多种途径参与MAFLD的发生发展。提出维生素D有望成为MAFLD的治疗药物，临床上需关注MAFLD患者维生素D水平的监测和管理，但其内在机制、具体补充剂量及疗程亟待深入探索。     

代谢性脂肪性肝病表观遗传学当前的挑战与展望

代谢性脂肪性肝病(MAFLD)是全球范围内日益严重的健康问题，其特点是肝脏脂肪沉积、炎症和纤维化，最终可能发展为肝硬化和肝细胞癌。近年来的研究发现，MAFLD中存在多种关键的表观遗传学改变，如异常的DNA甲基化模式、组蛋白修饰和microRNA及长非编码RNA的调控异常等。这些改变可能影响到MAFLD关键生物学过程，进一步促进疾病发展。此外，表观遗传学调控还与遗传、环境及生活方式等多种因素相互作用，共同影响MAFLD的发生和发展。本综述总结MAFLD表观遗传学研究的最新进展，并探讨该领域所面临的挑战及未来研究方向，旨在为未来MAFLD的诊治提供新思路。     

鼠李糖乳杆菌干预肠道菌群及脂质代谢治疗代谢相关性脂肪性肝病的研究进展

代谢相关性脂肪性肝病(metabolic associated fatty liver disease, MAFLD)现已成为全世界最常见的慢性肝病,发病率在逐年增加,目前无临床特效药,其发病机制复杂,主要涉及肥胖、肠道菌群、胰岛素抵抗、环境、遗传等。近年来,益生菌在预防和治疗MAFLD中被广泛研究,鼠李糖乳杆菌(Lactobacillus rhamnosus, LGG)属乳杆菌属的经典益生菌菌株。大量研究证明,LGG可通过调节肠道菌群、改善肠黏膜屏障及降低胆固醇改善MAFLD。本文主要阐述LGG干预MAFLD的相关可能机制。     

甘草酸二铵脂质配位体治疗高脂饮食大鼠非酒精性脂肪性肝病疗效观察

非酒精性脂肪性肝病（NAFLD）的诊断和治疗是目前肝病研究的重点和热点之一,但由于其病因繁多且发病机制尚不十分明确,目前临床上尚无治疗此病的满意药物。甘草酸二铵脂质配位体已初步应用于临床辅助治疗多种慢性肝病,但关于其治疗MAFLD的研究报道少见,本研究通过建立高脂饮食大鼠NAFLD模型,观察甘草酸二铵脂质配位体对大鼠NAFLD的治疗效果。     

刘光伟教授运用二陈丸治疗代谢相关脂肪性肝病经验撷英

<正>代谢相关脂肪性肝病(MAFLD)属于代谢应激肝损伤性疾病，与胰岛素抵抗(IR)及遗传易感性密切相关。根据肝脏不同病理改变，MAFLD可分为单纯性脂肪肝、脂肪性肝炎、脂肪性肝硬化、脂肪性肝细胞癌^[1]。近20年来由于人们生活方式的改变，MAFLD已成为中国最普遍的肝脏病种及21世纪全球重要的公共健康问题之一。相关研究表明，生活方式、环境因素及经济水平是该病进展的关键因素^[2]。中医药具有整体观念及辩证论治的特色治疗优势，在该病的长期的临床实践中发挥出重大作用。刘光伟，主任医师，博士研究生导师，河南中医药大学第一附属医院国家区域肝病诊疗中心主任。刘师从事肝病中西医结合科研、临床工作多年，提倡中西医结合防治消化系统疾病，在长期的医疗实践中积累了丰富的临床经验。吾辈有幸随师侍诊，受益匪浅，现将刘教授治疗MAFLD临证经验整理如下，以飨同道。     

代谢相关脂肪性肝病饮食干预新策略的研究进展

不良的饮食习惯是导致代谢相关脂肪性肝病(MAFLD)呈全球性流行的重要原因,而膳食模式调整更是MAFLD管理的基石。近年来大量新的治疗性膳食模式被提出并尝试应用于MAFLD的治疗,包括限制能量均衡饮食、低碳饮食、低血糖生成指数饮食、低游离糖饮食、轻断食饮食、高蛋白饮食、地中海饮食等,这些新方法在临床上应用的治疗效果不一。介绍了这些膳食治疗新策略的治疗理念、实践方法以及在国内外MAFLD人群治疗中的获益证据,为临床医生指导患者实现个体化的营养治疗提供新视角。     

代谢相关脂肪性肝病肝外并发症研究进展与现状

代谢相关脂肪性肝病(metabolic associated fatty liver disease,MAFLD)是作为描述这种疾病的一个更合适的总括述语,新的定义将代谢功能障碍列为肝病的重要病因,论证了MAFLD的高异质性,加快了向新治疗的转化路径.MAFLD的肝外并发症其发生率和相关疾病,远远超过肝病本身,严重威脅着人类健康.鉴于当前人们对其严重性认识不足,且对肝外并发病的疾病范围、发病机制、诊断的研究还不完善,尤其当前对其缺乏有效的药物治疗,有鉴于此本文就MAFLD肝外并发症研究现状与进展作一介绍与述评,与广大读者共享.     

代谢相关性脂肪性肝病无创诊断方法研究进展

据估计,全球约有25%的成年人患有代谢相关性脂肪性肝病(metabolic associated fatty liver disease,MAFLD),且发病率逐年上升。肝脏活检仍是诊断MAFLD的金标准。近年来,无创诊断方法发展比较迅速。本文针对MAFLD的无创诊断研究进展进行了较为系统的综述。     

Macrophages in metabolic associated fatty liver disease

Metabolic associated fatty liver disease(MAFLD), formerly named non-alcoholic fatty liver disease is the most common liver disorder in many countries. The inflammatory subtype termed steatohepatitis is a driver of disease progression to cirrhosis, hepatocellular carcinoma, liver transplantation, and death, but also to extrahepatic complications including cardiovascular disease, diabetes and chronic kidney disease. The plasticity of macrophages in response to various environmental cues and the fact that they can orchestrate cross talk between different cellular players during disease development and progression render them an ideal target for drug development. This report reviews recent advances in our understanding of macrophage biology during the entire spectrum of MAFLD including steatosis, inflammation, fibrosis, and hepatocellular carcinoma, as well as for the extra-hepatic manifestations of MAFLD. We discuss the underlying molecular mechanisms of macrophage activation and polarization as well as cross talk with other cell types such as hepatocytes, hepatic stellate cells, and adipose tissue. We conclude with a discussion on the potential translational implications and challenges for macrophage based therapeutics for MAFLD.     

Blood pressure stratification for predicting liver fibrosis risk in metabolic dysfunction associated fatty liver disease

Introduction and objectivesThe optimal blood pressure (BP) range for patients with metabolic dysfunction-associated fatty liver disease (MAFLD) is currently unknown. This study aimed to explore the relationship between stratified BP levels and MAFLD progression.Patients and MethodsThe data of adults who underwent yearly health check-ups were screened to establish both a cross-sectional and a 6-year longitudinal cohort of individuals with MAFLD. BP was classified into the following categories optimal, normal, high-normal, and hypertension. Liver fibrosis was diagnosed with fibrosis-4 (FIB-4) score, nonalcoholic fatty liver disease fibrosis score (NFS), and aspartate aminotransferase-to-platelet ratio index (APRI).ResultsA total of 10,232 individuals were included in the cross-sectional cohort. In the MAFLD population, individuals with liver fibrosis had significantly higher BP levels and hypertension prevalence (P < 0.001) than those without. Furthermore, liver fibrosis score was significantly associated with BP levels (P < 0.001). In the 6-year longitudinal cohort of 3661 individuals with MAFLD without liver fibrosis, the incidence rates of liver fibrosis increased with increasing BP levels as follows optimal=11.20%, normal=13.9%, high-normal=19.5%, hypertension=26.20% (log-rank 22.205; P < 0.001). Cox regression analysis showed that both baseline high-normal BP (hazard ratio [HR], 1.820; P=0.019) and hypertension (HR, 2.656; P < 0.001) were predictive of liver fibrosis.ConclusionsBP stratification may be useful in predicting the progression of MAFLD. Individuals having MAFLD with concurrent hypertension or high-normal BP are at a higher risk of liver fibrosis. These findings may provide a criteria for early intervention of MAFLD to prevent liver fibrosis.     

Drug-induced Fatty Liver Disease: Pathogenesis and Treatment

Metabolic dysfunction-associated fatty liver disease (commonly known as MAFLD) impacts global health in epidemic proportions, and the resulting morbidity, mortality and economic burden is enormous. While much attention has been given to metabolic syndrome and obesity as offending factors, a growing incidence of polypharmacy, especially in the elderly, has greatly increased the risk of drug-induced liver injury (DILI) in general, and drug-induced fatty liver disease (DIFLD) in particular. This review focuses on the contribution of DIFLD to DILI in terms of epidemiology, pathophysiology, the most common drugs associated with DIFLD, and treatment strategies.     

药物性肝病的诊断与治疗进展

药物性肝病(DILD)是指在使用某种或几种药物后,由药物或其代谢产物引起的肝脏损害。随着新药不断研发和应用于临床,药物性肝病的发病率也在逐年增高,引起人们对药物性肝损伤的重视及研究。此文主要就药物性肝病的诊断与治疗进展作一综述。     

Type 2 diabetes mellitus in metabolic-associated fatty liver disease vs. type 2 diabetes mellitus non-alcoholic fatty liver disease: a longitudinal cohort analysis

Introduction and ObjectivesType 2 Diabetes Mellitus (T2DM) is comorbidity commonly presenting with fatty liver. A recently proposed definition of "metabolic associated fatty liver disease" (MAFLD) is thought to replace non-alcoholic fatty liver disease (NAFLD). Yet, despite the significant prevalence of T2DM among fatty liver, there remains limited evidence on the impact of the change in the definition of T2DM.Materials and MethodsThe current study uses data from the United States National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018. Survival analysis was conducted with a cox regression and sub-distribution hazard ratio for competing risk events.Results6727 patients had a diagnosis of T2DM. 4982 individuals with T2DM had MAFLD and 2032 were MAFLD(+)/NAFLD(-), while 2950 patients were MAFLD(+)/NAFLD(+). The new definition increased fatty liver diagnosis by 68.89%. Patients who were classified as MAFLD(+)/NAFLD(-) were at a higher risk of major adverse cardiovascular events, advanced fibrosis, all-cause and cardiovascular-related mortality compared to MAFLD(+)/NAFLD(+). In MAFLD(+)/NAFLD(-), viral hepatitis significantly increases the odds of advanced fibrosis (OR: 6.77, CI: 3.92 to 11.7, p < 0.001) and all-cause mortality (HR: 1.75, CI: 1.29 to 2.40, p < 0.001).ConclusionsThe identification and treatment of NAFLD in patients with T2DM is a major concern and the premature change to MAFLD results in an over-diagnosis of fatty liver, exaggerated mortality, and morbidity in patients with T2DM. The definition of MAFLD causes further heterogeneity in fatty liver disease/NAFLD.     

Metabolic-associated fatty liver disease from childhood to adulthood: State of art and future directions

In 2020, an international group of experts proposed to replace the term of nonalcoholic fatty liver disease with metabolic-associated fatty liver disease (MAFLD). This recent proposal reflects the close association of fatty liver with metabolic derangements, as demonstrated by previous robust data. Several factors [including genetics, inflammation, metabolic abnormalities, insulin resistance (IR), obesity, prenatal determinants, and gut–liver axis] have been found to be involved in MAFLD pathophysiology, but this tangled puzzle remains to be clearly understood. In particular, IR has been recognized as a key player in metabolic impairments development in children with fatty liver. On this ground, MAFLD definition focuses on the pathophysiological basis of the disease, by emphasizing the crucial role of metabolic impairments in this condition. Although primarily developed for adults, MAFLD diagnostic criteria have been recently updated with an age-appropriate definition for sex and age percentiles, because of the increasing attention to cardiometabolic risk in childhood. To date, accumulating evidence is available on the feasibility of MAFLD definition in clinical practice, but some data are still conflicting in highly selected populations. Considering the growing prevalence worldwide of fatty liver and its close relationship with metabolic dysfunction both in children and adults with subsequent increased cardiovascular risk, early strategies for MAFLD identification, treatment and prevention are needed. Novel therapeutic insights for MAFLD based on promising innovative biological techniques are also emerging. We aimed to summarize the most recent evidence in this intriguing research area both in children and adults.