Loss to Specialized Cardiology Follow-Up in Adults Living with Congenital Heart Disease

Background:Much has been written about the loss to follow-up in the transition between pediatric and adult Congenital Heart Disease(CHD)care centers.Much less is understood about the loss to follow-up(LTF)after a successful transition.This is critical too,as patients lost to specialised care are more likely to experience mor-bidity and premature mortality.Aims:To understand the prevalence and reasons for loss to follow-up(LTF)at a large Australian Adult Congenital Heart Disease(ACHD)centre.Methods:Patients with moderate or highly complex CHD and gaps in care of>3 years(defined as LTF)were identified from a comprehensive ACHD data-base.Structured telephone interviews examined current care and barriers to clinic attendance.Results:Overall,407(22%)of ACHD patients(n=1842)were LTF.The mean age at LTF was 31(SD 11.5)years and 54%were male;311(76%)were uncontactable.Compared to adults seen regularly,lost patients were younger,with a greater socio-economic disadvantage,and had less complex CHD(p<0.05 for all).We interviewed 59 patients(14%).The top 3 responses for care absences were“feeling well”(61%),losing track of time(36%),and not needing fol-low-up care(25%).Conclusions:A large proportion of the ACHD population becomes lost to specialised cardiac care,even after a successful transition.This Australian study reports younger age,moderate complexity defects,and socio-economic disadvantage as predictive of loss to follow-up.This study highlights the need for novel approaches to patient-centered service delivery even beyond the age of transition and resources to maintain patient engagement within the ACHD service.

Use of iron in perinatal anaemia:Indications for women’s health care policies and procedure

This paper reviews management of obstetric anaemia and the role of intravenous iron for the treatment of obstetric anaemia.Red blood cell transfusions are routinely used for haemoglobin restoration in anaemic women.The decision for red blood cell transfusion is made on a combination of haemoglobin level and clinical status,and it is suggested that transfusions are not necessary in those who are well compensated or when alternative therapy is available.To reduce the risk,intravenous iron infusion is proposed as a bloodless therapeutic approach.There are a variety of iron preparations.Intravenous iron infusion can reduce the requirement for blood transfusion in hemodynamically stable women with perinatal anaemia,especially in resource-scarce settings.It a cost-effective bloodless approach for the treatment of anaemia than can enhance patient outcomes.According to the literature,when haemoglobin is greater than 90 g/L,blood transfusion is not often required.In perinatal women with anaemia,the decision whether to administer blood or iron is based on patient preferences,haemoglobin levels,clinical symptoms,past and present medical conditions and the clinician’s judgement.Nevertheless,due to the lack of rigid criteria for blood transfusions in the majority of clinical settings,it is considered the default treatment for anaemia in perinatal women.

Ventricular Arrhythmia in the Fontan Circulation:Prevalence,Risk Factors and Clinical Implications

Objective:Sudden cardiac death(SCD)and malignant ventricular arrhythmia(VA)are increasingly recognized as important issues for people living with a Fontan circulation,but data are lacking.We sought to characterize the cohort who had sudden cardiac death,most likely related to VA and/or documented VA in the Australia and New Zealand Fontan Registry including risk factors and clinical outcomes.Methods:A retrospective cohort study was performed.Inclusion criteria were documented non-sustained ventricular tachycardia,sustained ventricular tachycardia,ventricular fibrillation,resuscitated cardiac arrest or SCD>30 days post-Fontan completion.Results:Of 1611 patients,20(1.2%)had VA;14(1.0%)had VA without SCD and 6(<1%)had SCD(6%of all deaths recorded in Registry;5 of those had documented VA at the time of arrest and 1 was presumed to be VA-associated).The median age at first VA was 20.5(14–32)years,10(50%)were females,and the median age at Fontan operation was 8(4–17)years.On univariable analysis,hypoplastic left heart syndrome(p=0.03)and older age Fontan operation(p<0.001)were associated with VA.Earlier Fontan era(p<0.003),atriopulmonary Fontan(p<0.001),pre-Fontan atrioventricular valve repair(p=0.013)pre-or post-Fontan atrial arrhythmia(p=0.010)were associated with SCD.Patients with VA had a 3 times higher risk of death or heart transplant(HR 3.27(1.19,8.98),p=0.02).Conclusions:A proportion of people living with a Fontan circulation have malignant VA.Routine VA screening in this cohort is essential.More data are needed to aid risk stratification.

核心肽对类风湿关节炎滑膜细胞增殖与凋亡的影响

背景:前期研究发现,在类风湿关节炎关节腔中注入核心肽,可以明显抑制病情活跃度且抑制滑膜的浸润增生。但由于T细胞和滑膜细胞之间联系密切,核心肽是通过直接作用于滑膜细胞还是通过T细胞介导抑制滑膜细胞尚缺乏研究。目的:对比观察核心肽对类风湿关节炎和骨性关节炎滑膜细胞增殖与凋亡的影响。方法:采用酶消化法分离类风湿关节炎和骨性关节炎患者手术切取的病变滑膜组织滑膜细胞,MTT法检测滑膜细胞增殖率。取第3代类风湿性关节炎和骨性关节炎滑膜细胞分5组干预:空白对照组、甲氨蝶呤组、10,25,50μmol/L核心肽组。MTT法检测各组滑膜细胞增殖率变化;采用流式细胞仪检测各组滑膜细胞凋亡情况。结果与结论:类风湿关节炎滑膜细胞体外增殖速度较骨性关节炎滑膜细胞快(P<0.05)。3种剂量的核心肽均可抑制骨性关节炎滑膜细胞的增殖,诱导其凋亡,且具有剂量相关性,高剂量时,核心肽更明显表现出对骨性关节炎滑膜细胞凋亡的诱导作用。而对于类风湿关节炎滑膜细胞,只有中、高剂量核心肽显示出明显的诱导细胞凋亡作用,但未见明显的剂量依赖性。核心肽对类风湿关节炎滑膜细胞的凋亡诱导作用明显小于其对骨性关节炎细胞的凋亡诱导作用。结果提示核心肽对滑膜细胞具有一定的直接作用,高剂量核心肽在体外可抑制类风湿关节炎滑膜细胞的过度增殖,而中、高剂量核心肽可诱导类风湿关节炎滑膜细胞的凋亡。

瘦素基因G-2548A位点多态性与哮喘的相关性研究

目的:探讨瘦素基因启动子区G-2548A位点多态性与哮喘之间的相关性。方法:以外周血白细胞DNA组为模板,应用聚合酶链反应-限制性内切酶片段长度多态性(PCR-RFLP)方法对194例哮喘患者和214例健康个体瘦素基因启动子区G-2548A位点基因型进行分析。结果:哮喘组和健康组瘦素基因G-2548A位点等位基因A和G频率分布具有差异性,哮喘组A等位基因频率显著高于健康组(χ2=4.858,P=0.028,OR=1.456,95%CI=1.042-2.036);哮喘组和健康组基因型分布差异具有统计学意义,其中AA基因型患哮喘的风险较高,为GA+GG基因型的1.516倍(χ2=4.048,P=0.044,OR=1.516,95%CI=1.010-2.275)。结论:瘦素基因G-2548A位点多态性和哮喘的发病具有相关性,A等位基因是哮喘的遗传易感因子。

基因芯片技术对哮喘病人相关基因的筛选和分析

目的利用基因芯片技术寻找哮喘病患者与正常人外周血单核细胞之间差异表达基因,拟为哮喘的早期诊断及预防提供分子标记。方法用淋巴细胞分离液分别提取16例哮喘病患者与16例正常人外周血单核细胞,用QIAGEN RneasyKit提取纯化样本总RNA,并合成用荧光标记的cRNA,分别与含有41 000条基因序列的全基因芯片杂交,以基因表达倍数值≥2.0和基因表达倍数值≤-2.0为阈值来确定差异表达基因,然后用Genespring软件利用生物信息学方法对差异表达基因进行功能分类分析。结果按P<0.05差异显著性标准,从34 183条表达基因谱中,筛选出哮喘患者与正常对照差异表达2倍以上的基因有4177条,差异表达2倍以上已知与哮喘相关的基因有19条。经代谢途径分析发现这些差异基因主要涉及到炎症反应、免疫反应、防御反应、创伤反应、外部刺激反应等8大功能分类。结论哮喘的发生涉及众多基因表达的改变,芯片技术可以有效地筛选出哮喘患者与正常对照的差异表达基因,对进一步探索哮喘的发病机制、有效的干预或逆转哮喘具有重要意义。

双侧乳内动脉π型桥全动脉化冠状动脉旁路移植术

目的 研究 π型桥全动脉化心肌血运重建的临床应用。 方法 1994年 9月到 2 0 0 2年 8月对 2 2例患者根据冠状动脉病变解剖特点选用π型桥进行全动脉化心肌血运重建 ,即 3支血管病变合并对角支 /中间支中段病变时 ,采用由左侧乳内动脉小 Y型桥与前降支和对角支 /中间支吻合 ,与双侧乳内动脉 T型桥共同构成 π型桥。 结果本组无围术期死亡 ,无心肌梗死、脑血管意外和胸骨感染发生 ;1例患者术后二次开胸止血。随访 6 0 .7± 2 3.0个月 ,无心绞痛复发需要冠脉介入治疗或手术治疗者 ,也无冠心病导致的死亡发生。 结论 对 3支血管病变合并对角支 /中间支中段冠脉病变的患者 ,双侧乳内动脉 π型桥可以顺利完成全动脉化心肌血运重建 ,中期效果良好。

一氧化氮与门脉高压症

门脉高压症血流动力学改变的形成和发展主要与肝内循环阻力及内脏循环血流量两方面的变化有关。一氧化氮(NO)作为重要的调节因子,通过一氧化氮合成酶各亚型截然不同的调控机制和作用,参与了肝血窦收缩舒张、肝星状细胞激活、肝内氧化应激水平改变及门脉循环新生血管生成等病理改变并且在其中起着重要作用。NO作为药物治疗门脉高压的研究方兴未艾,旨在选择性利用其特性在降低门脉压力的同时不影响内脏循环血流动力学,从而达到治疗门脉高压症的目的。现就NO与门脉高压症之间的关系并针对以上所述几个方面的研究进展加以综述。

Current concepts on the role of nitric oxide in portal hypertension

Portal hypertension(PHT) is defined as a pathological increase in portal venous pressure and frequently accompanies cirrhosis.Portal pressure can be increased by a rise in portal blood flow,an increase in vascular resistance,or the combination.In cirrhosis,the primary factor leading to PHT is an increase in intra-hepatic resistance to blood flow.Although much of this increase is a mechanical consequence of architectural disturbances,there is a dynamic and reversible component that represents up to a third of the increased vascular resistance in cirrhosis.Many vasoactive substances contribute to the development of PHT.Among these,nitric oxide(NO) is the key mediator that paradoxically regulates the sinusoidal(intra-hepatic) and systemic/splanchnic circulations.NO deficiency in the liver leads to increased intra-hepatic resistance while increased NO in the circulation contributes to the hyperdynamic systemic/splanchnic circulation.NO mediated-angiogenesis also plays a role in splanchnic vasodilation and collateral circulation formation.NO donors reduce PHT in animals models but the key clinical challenge is the development of an NO donor or drug delivery system that selectively targets the liver.

Failed biliary cannulation: Clinical and technical outcomes after tertiary referral endoscopic retrograde cholangiopancreatography

AIM: Prospective evaluation of repeat endoscopic retrograde cholangiopancreatography (ERCP) for failed Schutz grade 1 biliary cannulation in a high-volume center. METHODS: Prospective intention-to-treat analysis of patients referred for biliary cannulation following recent unsuccessful ERCP. RESULTS: Fifty-one patients (35 female; mean age: 62.5 years; age range: 40-87 years) with previous failed biliary cannulation were referred for repeat ERCP. The indication for ERCP was primarily choledocholithiasis (45%) or pancreatic malignancy (18%). Successful biliary can- nulation was 100%. The precut needle knife sphincterotomy (NKS) rate was 27.4%. Complications occurred in 3.9% (post-ERCP pancreatitis). An identif iable reason for initial unsuccessful biliary cannulation was present in 55% of cases. Compared to a cohort of 940 nave pa-pilla patients (female 61%; mean age: 59.9 years; age range: 18-94 years) who required sphincterotomy over the same time period, there was no statistical difference in the cannulation success rate (100% vs 98%) or postERCP pancreatitis (3.1% vs 3.9%). Precut NKS use was more frequent (27.4% vs 12.7%) (P = 0.017). CONCLUSION: Referral to a high-volume center following unsuccessful ERCP is associated with high technical success, with a favorable complication rate, compared to routine ERCP procedures.

Effects of resveratrol in experimental and clinical non-alcoholic fatty liver disease

The prevalence of obesity and related conditions like non-alcoholic fatty liver disease(NAFLD) is increasing worldwide and therapeutic options are limited.Alternative treatment options are therefore intensively sought after.An interesting candidate is the natural polyphenol resveratrol(RSV) that activates adenosinmonophosphate-activated protein kinase(AMPK) and silent information regulation-2 homolog 1(SIRT1).In addition,RSV has known anti-oxidant and anti-inflammatory effects.Here,we review the current evidence for RSVmediated effects on NAFLD and address the different aspects of NAFLD and non-alcoholic steatohepatitis(NASH) pathogenesis with respect to free fatty acid(FFA) flux from adipose tissue,hepatic de novo lipogenesis,inadequate FFA β-oxidation and additional intra- and extrahepatic inflammatory and oxidant hits.We review the in vivo evidence from animal studies and clinical trials.The abundance of animal studies reports a decrease in hepatic triglyceride accumulation,liver weight and a general improvement in histological fatty liver changes,along with a reduction in circulating insulin,glucose and lipid levels.Some studies document AMPK or SIRT1 activation,and modulation of relevant markers of hepatic lipogenesis,inflammation and oxidation status.However,AMPK/SIRT1-independent actions are also likely.Clinical trials are scarce and have primarily been performed with a focus on overweight/obese participants without a focus on NAFLD/NASH and histological liver changes.Future clinical studies with appropriate design are needed to clarify the true impact of RSV treatment in NAFLD/NASH patients.

Surgical management of hepatocellular carcinoma

Hepatocellular carcinoma(HCC) is the second most common cause of death from cancer worldwide. Standard potentially curative treatments are either resection or transplantation. The aim of this paper is to provide an overview of the surgical management of HCC, as well as highlight current issues in hepatic resection and transplantation. In summary, due to the relationship between HCC and chronic liver disease, the management of HCC depends both on tumourrelated and hepatic function-related considerations. As such, HCC is currently managed largely through nonsurgical means as the criteria, in relation to the above considerations, for surgical management is still largelyrestrictive. For early stage tumours, both resection and transplantation offer fairly good survival outcomes(5 years overall survival of around 50%). Selection therefore would depend on the level of hepatic function derangement, organ availability and local expertise. Patients with intermediate stage cancers have limited options, with resection being the only potential for cure. Otherwise, locoregional therapy with transarterial chemoembolization or radiofrequency ablation are viable options. Current issues in resection and transplantation are also briefly discussed such as laparoscopic resection, ablation vs resection, anatomical vs non-anatomical resection, transplantation vs resection, living donor liver transplantation and salvage liver transplantation.

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.

Interaction between cyclooxygenase-2,Snail,and E-cadherin in gastric cancer cells

AIM:To investigate the mechanisms of how cyclooxygenase-2(COX-2)regulates E-cadherin in gastric cancer cells.METHODS:COX-2 expression in human gastric cancer cell lines SGC-7901,BGC-823,MGC-803 and AGS were measured at the mRNA and protein level.COX-2 rich cell line SGC-7901 was chosen for subsequent experiments.siRNA mediated gene knockdown was used to investigate the impact of COX-2 on nuclear factor-κB (NF-κB),Snail,and E-cadherin in gastric cancer cells.Gene expression was determined by Western blot and real-time polymerase chain reaction.To analyze whether NF-κB inhibition could interrupt the modulatory effect of COX-2 or prostaglandin E2(PGE2)on E-cadherin,gastric cancer cells were treated with celecoxib or PGE2,in the presence of NF-κB specific siRNA.RESULTS:Highest expression level of COX-2 was found in SGC-7901 cells,both at mRNA and protein levels.siRNA mediated down-regulation of COX-2 led to a reduced expression of NF-κB and Snail,but an increased expression of E-cadherin in SGC-7901 cells.siRNA mediated down-regulation of NF-κB also led to a reduced expression of E-cadherin and Snail in SGC-7901 cells.However,COX-2 expression did not alter after cells were treated with NF-κB specific siRNA in SGC-7901 cells.Treatment of SGC-7901 cells with celecoxib led to a reduced expression of Snail but an increased expression of E-cadherin.In contrast,treatment of SGC-7901 cells with PGE2 led to an increased Snail and a decreased E-cadherin.However,siRNAmediated knockdown of NF-κB partially abolished the effect of celecoxib and PGE2 on the regulation of E-cadherin and Snail in SGC-7901 cells.CONCLUSION:COX-2 likely functions upstream of NF-κB and regulates the expression of E-cadherin via NF-κB/Snail signaling pathway in gastric cancer cells.

Australian tertiary care outcomes of entecavir monotherapy in treatment naive patients with chronic hepatitis B

AIM:To evaluate the long-term treatment outcomes of entecavir monotherapy in treatment naive patients in an Australian tertiary care setting. METHODS:A retrospective analysis of treatment naive patients receiving entecavir monotherapy through Westmead Hospital was performed.Patients were excluded if they had received previous treatment with another nucleoside or nucleotide analogue,were pregnant or less than 18 years old. RESULTS:Out of 336 patients,163 patients fulfilled the selection criteria.Range of follow up was 3-46 mo (mean 26 mo).134 patients(82.2%)had pre-treatment biopsies,with 26 patients(16.0%)demonstrating F3-4 fibrosis.In total,153 patients(93.9%)achieved at least Partial Virological Suppression(PVS),with 134 patients (82.2%)achieving complete virological suppression. The cumulative CVS and PVS rates at 36 mo were 82.1%and 96.4%,respectively.3 patients(1.8%)failed to achieve PVS,while 5 patients(3.0%)developed virological rebound.128 patients(78.5%)maintained CVS throughout follow up.Predictors of CVS included lower baseline DNA level(P=0.001),hepatitis B virus e antigen negative status(P=0.001)and increasing age at treatment(log rank 0.001).No significant adverse effects were reported necessitating cessation of entecavir. CONCLUSION:Entecavir monotherapy is efficacious and safe in an Australian tertiary care setting.Resistance and rebound rates are very low.This is similar to data from controlled and uncontrolled trials around the world.

Significance of hepatitis virus infection in the oncogenicinitiation of hepatocellular carcinoma

Hepatocellular carcinoma(HCC) is one of the most common causes of cancer-related death worldwide. Chronic infection of hepatitis B virus(HBV) and/or hepatitis C virus(HCV) is a major risk factor in the development of the HCC, independently from excessive alcohol abuse and metabolic disease. Since the biology of HBV and HCV is different, their oncogenic effect may go through different mechanisms, direct and/or indirect. Viral hepatitis infection is associated with cellular inflammation, oxidative stress, DNA damage, that may lead to subsequent hepatic injuries such as chronic hepatitis, fibrosis, cirrhosis, and finally HCC. Direct oncogenic properties of these viruses are related with their genotypic characteristics and the ability of viral proteins to interact with host proteins, thus altering the molecular pathways balance of the cells. In addition, the integration of HBV DNA, especially the gene S and X, in a particular site of the host genome can disrupt chromosomal stability and may activate various oncogenic mechanisms, including those in hematopoietic cells. Recently, several studies also had demonstrated that viral hepatitis could trigger the population of hepatic cancer stem cells. This review summarize available pre-clinical and clinical data in literature regarding oncogenic properties of HBV and HCV in the early initiation of HCC.

Hepatocellular carcinoma and non-alcoholic steatohepatitis:The state of play

Hepatocellular carcinoma(HCC) is now the fifth cancer of greatest frequency and the second leading cause of cancer related deaths worldwide. Chief amongst the risks of HCC are hepatitis B and C infection, aflatoxin B1 ingestion, alcoholism and obesity. The latter can promote non-alcoholic fatty liver disease(NAFLD), that can lead to the inflammatory form non-alcoholic steatohepatitis(NASH), and can in turn promote HCC. The mechanisms by which NASH promotes HCC are only beginning to be characterized. Here in this review, we give a summary of the recent findings that describe and associate NAFLD and NASH with the subsequent HCC progression. We will focus our discussion on clinical and genomic associations that describe new risks for NAFLD and NASH promoted HCC. In addition, we will consider novel murine models that clarify some of the mechanisms that drive NASH HCC formation.

Update on global epidemiology of viral hepatitis and preventive strategies

Viral hepatitis is one of the major public health concerns around the world but until recently it has drawn little attention or funding from global health policymakers.Every year 1.4 million people die from viral hepatitisrelated cirrhosis and liver cancer.However,the majority of the infected population are unaware of their condition.This population have significant obstacles to overcome such as lack of awareness,vulnerability,increased migration,disease stigma,discrimination,as well as poor health resources,conflict in policy development and program implementation.Despite implementing infection control measures over the last few decades eradication or significant disease reduction remains elusive.This study aims to present the current global prevalence status and examines potential elimination strategies.The information for this research were obtained through a systematic review,published scientific literatures,the official websites of various government organisations,international public health organisations and internationally recognised regulatory bodies over a period of 40 years between 1978 and2018.

Notch2 regulates matrix metallopeptidase 9 via PI3K/AKT signaling in human gastric carcinoma cell MKN-45

AIM:To clarify the role of activated Notch2 in the invasiveness of gastric cancer.METHODS:To investigate the invasiveness of silencing Notch2 gene expression,we established a Notch2small interfering RNA(siRNA) transfected cell line using the MKN-45 gastric cancer cell line.After the successful transfection confirmed by real-time reverse transcription-polymerase chain reaction(RT-PCR) and Western blotting,migration and invasion assays were employed to evaluate the aggressiveness of the gastric cancer.RT-PCR and Western blottings were employed to confirm the down-regulation of Notch2 and to evaluate the expression of epithelial mesenchymal transition-related gene matrix metallopeptidase 9(MMP9),Akt,p-Akt.To confirm the relationship between PI3KAkt and MMP9,the PI3K inhibitor LY294002 was used to treat MKN-45 cells.RESULTS:Notch2 expression was dramatically decreased after Notch2 siRNA transfection(100.00% ± 9.74% vs 11.61% ± 3.85%,P < 0.01 by qRT-PCR).There was also a marked reduction of Notch target gene Hes1(100.00% ± 4.74% vs 61.61% ± 3.58%,P < 0.05) at the mRNA,indicating an inhibition of Notch signaling.Inhibition of Notch signaling was also confirmed by the marked reduction of Notch2 intracellular domain at the protein levels(100.00% ± 9.74% vs 65.61% ± 7.58%,P < 0.05).Down-regulation of Notch2 by siRNA enhanced tumor cell invasion(100.00% ± 21.64% vs 162.22% ± 16.84%,P < 0.05) and expression of MMP9(1.56 fold,P < 0.05),and activated the pro-MMP9 protein to its active form(1.48 fold,P < 0.05).There was no significant difference in the protein levels of Akt between the two groups(100.00% ± 10.87% vs 96.61% ± 7.33%,P > 0.05),while down-regulation of Notch2 elevated p-Akt expression(100.00% ± 9.87% vs 154.61% ± 13.10%,P < 0.05).Furthermore,p-Akt and MMP9 was down-regulated in response to the inhibitor LY294002(p-Akt 100.00% ± 8.87% vs 58.27% ± 5.01%,P < 0.05;MMP9 100.00% ± 9.17% vs 50.03% ± 4.88%,P < 0.05).CONCLUSION:Notch2 may negatively regulate cell invasion by inhibiting the PI3K-Akt signaling

Oily fish, coffee and walnuts: Dietary treatment for nonalcoholic fatty liver disease

Rates of non-alcoholic fatty liver disease(NAFLD) are increasing worldwide in tandem with the metabolic syndrome, with the progressive form of disease, nonalcoholic steatohepatitis(NASH) likely to become the most common cause of end stage liver disease in the not too distant future. Lifestyle modification and weight loss remain the main focus of management in NAFLD and NASH, however, there has been growing interest in the benefit of specific foods and dietary components on disease progression, with some foods showing protective properties. This article provides an overview of the foods that show the most promise and their potential benefits in NAFLD/NASH, specifically; oily fish/fish oil, coffee, nuts, tea, red wine, avocado and olive oil. Furthermore, it summarises results from animal and human trials and highlights potential areas for future research.