scholarly journals Non-alcoholic fatty liver disease and hepatocellular carcinoma: Clinical challenges of an intriguing link

2022 ◽  
Vol 28 (3) ◽  
pp. 310-331
Lampros Chrysavgis ◽  
Ilias Giannakodimos ◽  
Panagiota Diamantopoulou ◽  
Evangelos Cholongitas
Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 790
Monica Lupsor-Platon ◽  
Teodora Serban ◽  
Alexandra Iulia Silion ◽  
George Razvan Tirpe ◽  
Alexandru Tirpe ◽  

Global statistics show an increasing percentage of patients that develop non-alcoholic fatty liver disease (NAFLD) and NAFLD-related hepatocellular carcinoma (HCC), even in the absence of cirrhosis. In the present review, we analyzed the diagnostic performance of ultrasonography (US) in the non-invasive evaluation of NAFLD and NAFLD-related HCC, as well as possibilities of optimizing US diagnosis with the help of artificial intelligence (AI) assistance. To date, US is the first-line examination recommended in the screening of patients with clinical suspicion of NAFLD, as it is readily available and leads to a better disease-specific surveillance. However, the conventional US presents limitations that significantly hamper its applicability in quantifying NAFLD and accurately characterizing a given focal liver lesion (FLL). Ultrasound contrast agents (UCAs) are an essential add-on to the conventional B-mode US and to the Doppler US that further empower this method, allowing the evaluation of the enhancement properties and the vascular architecture of FLLs, in comparison to the background parenchyma. The current paper also explores the new universe of AI and the various implications of deep learning algorithms in the evaluation of NAFLD and NAFLD-related HCC through US methods, concluding that it could potentially be a game changer for patient care.

Metabolites ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 54
Benjamin Buchard ◽  
Camille Teilhet ◽  
Natali Abeywickrama Samarakoon ◽  
Sylvie Massoulier ◽  
Juliette Joubert-Zakeyh ◽  

Non-Alcoholic Fatty Liver Disease (NAFLD) is considered as the forthcoming predominant cause for hepatocellular carcinoma (HCC). NAFLD-HCC may rise in non-cirrhotic livers in 40 to 50% of patients. The aim of this study was to identify different metabolic pathways of HCC according to fibrosis level (F0F1 vs. F3F4). A non-targeted metabolomics strategy was applied. We analyzed 52 pairs of human HCC and adjacent non-tumoral tissues which included 26 HCC developed in severe fibrosis or cirrhosis (F3F4) and 26 in no or mild fibrosis (F0F1). Tissue extracts were analyzed using 1H-Nuclear Magnetic Resonance spectroscopy. An optimization evolutionary method based on genetic algorithm was used to identify discriminant metabolites. We identified 34 metabolites differentiating the two groups of NAFLD-HCC according to fibrosis level, allowing us to propose two metabolomics phenotypes of NAFLD-HCC. We showed that HCC-F0F1 mainly overexpressed choline derivatives and glutamine, whereas HCC-F3F4 were characterized by a decreased content of monounsaturated fatty acids (FA), an increase of saturated FA and an accumulation of branched amino acids. Comparing HCC-F0F1 and HCC-F3F4, differential expression levels of glucose, choline derivatives and phosphoethanolamine, monounsaturated FA, triacylglycerides were identified as specific signatures. Our metabolomics analysis of HCC tissues revealed for the first time two phenotypes of HCC developed in NAFLD according to fibrosis level. This study highlighted the impact of the underlying liver disease on metabolic reprogramming of the tumor.

2013 ◽  
Vol 72 (4) ◽  
pp. 412-419 ◽  
Christopher D. Byrne

Non-alcoholic fatty liver disease (NAFLD) is now recognised as the hepatic component of metabolic syndrome (MetS). NAFLD is an example of ectopic fat accumulation in a visceral organ that causes organ-specific disease, and affects risk of other related diseases such as type 2 diabetes and CVD. NAFLD is a spectrum of fat-associated liver conditions that can culminate in end stage liver disease, hepatocellular carcinoma and the need for liver transplantation. Simple steatosis, or fatty liver, occurs early in NAFLD and may progress to non-alcoholic steatohepatitis, fibrosis and cirrhosis with increased risk of hepatocellular carcinoma. Prevalence estimates for NAFLD range from 2 to 44% in the general population and it has been estimated that NAFLD exists in up to 70% of people with type 2 diabetes. Although many obese people have NAFLD, there are many obese people who do not develop ectopic liver fat. The aim of this review which is based on a presentation at the Royal Society of Medicine, UK in December 2012 is to discuss development of NAFLD, ectopic fat accumulation and insulin resistance. The review will also describe the relationships between NAFLD, type 2 diabetes and CVD.

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