Non-alcoholic fatty liver disease: Severity of fibrosis and its relationships with clinical and biological variables

Corrao, Salvatore; Rinollo, Carmelina; Scaglione, Rosario

doi:10.1016/j.jhep.2015.01.010

Cited by 4 publications

(1 citation statement)

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“…Furthermore, EAT may play a pivotal role in the development and progression of both diastolic and systolic heart failure[ 17 – 19 ]. It is possible that epicardial adipose tissue (EAT) which secretes vasoactive molecules that regulate coronary arterial tone, and modulate inflammation [ 20 – 24 ], interferes with the autonomic nervous system determining both cardiovascular and liver damage [ 25 , 26 ].…”

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confidence: 99%

Epicardial Adipose Tissue (EAT) Thickness Is Associated with Cardiovascular and Liver Damage in Nonalcoholic Fatty Liver Disease

et al. 2016

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Background and AimsEpicardial adipose tissue (EAT) has been proposed as a cardiometabolic and hepatic fibrosis risk factor in patients with non alcoholic fatty liver disease (NAFLD). Aim of this study was to evaluate the role of EAT in NAFLD by analyzing 1) the association between EAT, the other metabolic parameters and the severity of steatosis 2) the relationship between cardiovascular (cIMT, cplaques, E/A), liver (presence of NASH and significant fibrosis) damage and metabolic risk factors including EAT 3) the relationship between EAT and genetic factors strongly influencing liver steatosis.MethodsIn a cross-sectional study, we considered 512 consecutive patients with NAFLD (confirmed by biopsy in 100). EAT, severity of steatosis, carotid intima-media thickness (cIMT) and plaques were evaluated by ultrasonography and results analysed by multiple linear and logistic regression models. Variables independently associated with EAT (mm) were female gender (p = 0.003), age (p = 0.001), BMI (p = 0.01), diastolic blood pressure (p = 0.009), steatosis grade 2 (p = 0.01) and 3 (p = 0.04), fatty liver index (p = 0.001) and statin use (p = 0.03). Variables independently associated with carotid IMT were age (p = 0.0001), hypertension (p = 0.009), diabetes (p = 0.04), smoking habits (p = 0.04) and fatty liver index (p = 0.02), with carotid plaques age (p = 0.0001), BMI (p = 0.03), EAT (p = 0.02),) and hypertension (p = 0.02), and with E/A age (p = 0.0001), diabetes (p = 0.005), hypertension (p = 0.04) and fatty liver index (p = 0.004). In the 100 patients with available liver histology non alcoholic steatohepatitis (NASH) was independently associated with EAT (p = 0.04) and diabetes (p = 0.054) while significant fibrosis with EAT (p = 0.02), diabetes (p = 0.01) and waist circumference (p = 0.05). No association between EAT and PNPLA3 and TM6SF2 polymorphisms was found.ConclusionIn patients with NAFLD, EAT is associated with the severity of liver and vascular damage besides with the known metabolic risk factors.

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Section: Introductionmentioning

confidence: 99%

Epicardial Adipose Tissue (EAT) Thickness Is Associated with Cardiovascular and Liver Damage in Nonalcoholic Fatty Liver Disease

et al. 2016

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Cardiometabolic Risk and Epicardial Adipose Tissue

Iacobellis

Fricke

2020

Epicardial Adipose Tissue

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Epicardial fat in patients with non-alcoholic fatty liver disease

Petta

Craxı̀

2015

Journal of Hepatology

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We recently reported that epicardial fat thickness is significantly associated with the severity of liver fibrosis in patients with nonalcoholic fatty liver disease (NAFLD), and that in this clinical setting, morphological and functional cardiac alterations by echocardiography are inversely related with the severity of liver damage [1]. Of note, these associations were maintained after correction for both cardiometabolic and hepatic confounders including visceral adiposity.In their letter [10], Corrao and colleagues suggest that some cytokines/adipocytokines as well as adiponectin, transforming growth factor b1, e-selectin, endothelin, and fibroblast growth factor 21 could explain the link we observed between the severity of liver disease and the presence of cardiac alterations. In this line in our paper we already suggested that ''the inflammatory state that characterize NAFLD/NASH might be able to act systemically, affecting the homeostasis of different organs, including the heart, as already demonstrated for systemic atherosclerosis [2] and kidney damage [3]''. Therefore we are planning to study the relationship between cytokines/adipocytokines levels, liver damage and cardiac alterations in NAFLD, as well as the role of genetic variants associated with NAFLD and its severity on the presence of cardiac alterations. We recently reported that gene variants in the PNPLA3 and TMS6F2 genes, can modulate the risk of atherosclerosis as well as the occurrence of cardiovascular events in patients with NAFLD or at high NAFLD risk [4,5].Corrao and colleagues also question the approach we used for the multivariate model, assessing variables independently associated with severe liver fibrosis. Specifically, they raised concerns about the inclusion in the model of both visceral obesity and epicardial fat, because considered as a phenomenon of collinearity. We thank the authors to correctly explain this phenomenon and the implication that it can produce on data interpretation. However, we respectfully think that our analysis is not biased by collinearity. Epicardial fat [6], as well as other ectopic fat depots like liver or dorsocervical fat [7], are obviously strongly related to visceral obesity. However, they do not depend on visceral obesity only, because they can have an independent role in affecting liver and systemic damage. In this line, cross-sectional and prospective studies showed that both liver and visceral fat are independent risk factors for presence and occurrence of cardiovascular events [8,9]. So, we included both visceral and epicardial fat in the model for fibrosis to demonstrate that the effect of epicardial fat is independent of that of visceral fat.Finally, in response to Ulucan and colleagues [11] we agree with the authors that the interference of epicardial fat with the autonomic nervous system could be one of the mechanisms linking this ectopic fat to liver damage. Accordingly, further clinical and experimental studies are needed in this topic.

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Non-alcoholic fatty liver disease: Severity of fibrosis and its relationships with clinical and biological variables

Cited by 4 publications

References 10 publications

Epicardial Adipose Tissue (EAT) Thickness Is Associated with Cardiovascular and Liver Damage in Nonalcoholic Fatty Liver Disease

Epicardial Adipose Tissue (EAT) Thickness Is Associated with Cardiovascular and Liver Damage in Nonalcoholic Fatty Liver Disease

Cardiometabolic Risk and Epicardial Adipose Tissue

Epicardial fat in patients with non-alcoholic fatty liver disease

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