scholarly journals Cardiovascular Diseases and Non-Alcoholic Fatty Liver Disease: Relationship and Pathogenetic Aspects of Pharmacotherapy

2022 ◽  
Vol 17 (6) ◽  
pp. 880-888
Author(s):  
A. V. Nelidova ◽  
M. A. Livzan ◽  
N. A. Nikolaev ◽  
T. S. Krolevets

The association of non-alcoholic fatty liver disease (NAFLD) and cardiovascular risk is currently one of the actively studied areas. The incidence of non-alcoholic fatty  liver disease continues to grow worldwide. In the structure of mortality rate of patients with non-alcoholic fatty  liver disease,  the first place is occupied by cardiovascular events: stroke and myocardial infarction. Studies have shown that the presence of severe liver fibrosis (F3-4) in NAFLD not only increases the risk of cardiovascular diseases (CVD), but also increases the risk  of  overall  mortality  by  69%  due  to mortality from cardiovascular causes. The degree of increased risk is associated with the degree of activity of non-alcoholic steatohepatitis (NASH). Despite the large number of works on this topic, we do not have a clear opinion on the impact on cardiovascular risk, interaction and the contribution of various factors, as well as algorithms for managing patients with non-alcoholic fatty liver disease to reduce the risk of cardiovascular diseases. This article describes the pathogenetic factors of formation of cardiovascular risks in patients with non-alcoholic fatty liver disease, proposed the idea of stratification of cardiovascular risks in these patients, taking into account changes in the structure of the liver (fibrosis) and function (clinical and biochemical activity) and also it describes the main directions of drug therapy, taking into account the common pathogenetic mechanisms for non-alcoholic fatty liver disease and cardiovascular diseases. The role of obesity, local fat depots, adipokines, and endothelial dysfunction as the leading pathogenetic factors of increased cardiovascular risk in patients with NAFLD is discussed. Among pathogenetically justified drugs in conditions of poly and comorbidity, hypolipidemic (statins, fibrates), angiotensin II receptor antagonists, beta-blockers, etc. can be considered. According to numerous studies, it becomes obvious that the assessment of cardiovascular risks in patients with NAFLD will probably allow prescribing cardiological drugs, selecting individualized therapy regimens, taking into account the form of NAFLD, and on the other hand, building curation taking into account the identified cardiovascular risks.

2020 ◽  
pp. 1-12
Author(s):  
Feng Gao ◽  
Kenneth I. Zheng ◽  
Pei-Wu Zhu ◽  
Yang-Yang Li ◽  
Hong-Lei Ma ◽  
...  

Abstract The FNDC5 gene encodes the fibronectin type III domain-containing protein 5 that is a membrane protein mainly expressed in skeletal muscle, and the FNDC5 rs3480 polymorphism may be associated with liver disease severity in non-alcoholic fatty liver disease (NAFLD). We investigated the influence of the FNDC5 rs3480 polymorphism on the relationship between sarcopenia and the histological severity of NAFLD. A total of 370 adult individuals with biopsy-proven NAFLD were studied. The association between the key exposure sarcopenia and the outcome liver histological severity was investigated by binary logistic regression. Stratified analyses were undertaken to examine the impact of FNDC5 rs3480 polymorphism on the association between sarcopenia and the severity of NAFLD histology. Patients with sarcopenia had more severe histological grades of steatosis and a higher prevalence of significant fibrosis and definite non-alcoholic steatohepatitis than those without sarcopenia. There was a significant association between sarcopenia and significant fibrosis (adjusted OR 2·79, 95 % CI 1·31, 5·95, P = 0·008), independent of established risk factors and potential confounders. Among patients with sarcopenia, significant fibrosis occurred more frequently in the rs3480 AA genotype carriers than in those carrying the FNDC5 rs3480 G genotype (43·8 v. 17·2 %, P = 0·031). In the association between sarcopenia and liver fibrosis, there was a significant interaction between the FNDC5 genotype and sarcopenia status (P value for interaction = 0·006). Sarcopenia is independently associated with significant liver fibrosis, and the FNDC5 rs3480 G variant influences the association between sarcopenia and liver fibrosis in patients with biopsy-proven NAFLD.


2021 ◽  
Vol 2 (8) ◽  
pp. 12-19
Author(s):  
Natalia M. Vorobyeva ◽  
◽  
Olga N. Tkacheva ◽  

Syndrome of increased epithelial permeability occurs due to a decrease in the barrier function of the gastrointestinal mucosa due to impaired intercellular interactions, resulting in bacterial translocation (i. e. penetration of bacteria and toxins from the gastrointestinal lumen into the bloodstream), which can initiate an inflammatory process in various diseases. Syndrome of increased epithelial permeability plays an important role in the pathogenesis of many chronic diseases, including cardiovascular and non-alcoholic fatty liver disease (NAFLD). In turn, the presence of NAFLD is associated with an increase in cardiovascular morbidity and mortality. The use of ursodeoxycholic acid in NAFLD allows reducing both hepatological and cardiovascular risks. Gastro- and enteroprotector rebamipide not only eliminates increased epithelial permeability and acts at all three levels of protection of the mucosepithelial barrier, but also has multiple pleiotropic effects, which opens up wide prospects for its use in cardiovascular diseases and NAFLD. The hepatoprotective and anti-sclerotic effects of rebamipide identified in experimental studies need further study in clinical trials in NAFLD patients.


2017 ◽  
Author(s):  
Kenzo Motohashi ◽  
Ahmad Moolla ◽  
Tom Marjot ◽  
Mark Ainsworth ◽  
Jeremy Tomlinson ◽  
...  

Choonpa Igaku ◽  
2020 ◽  
Vol 47 (6) ◽  
pp. 241-248
Author(s):  
Hirohito TAKEUCHI ◽  
Katsutoshi SUGIMOTO ◽  
Hisashi OSHIRO ◽  
Kunio IWATSUKA ◽  
Shin KONO ◽  
...  

Metabolites ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 54
Author(s):  
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.


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