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Review
. 2021 Mar 10;10(6):1161.
doi: 10.3390/jcm10061161.

Natural History of NAFLD

Affiliations
Review

Natural History of NAFLD

Raluca Pais et al. J Clin Med. .

Abstract

The epidemiology and the current burden of chronic liver disease are changing globally, with non-alcoholic fatty liver disease (NAFLD) becoming the most frequent cause of liver disease in close relationship with the global epidemics of obesity, type 2 diabetes and metabolic syndrome. The clinical phenotypes of NAFLD are very heterogeneous in relationship with multiple pathways involved in the disease progression. In the absence of a specific treatment for non-alcoholic steatohepatitis (NASH), it is important to understand the natural history of the disease, to identify and to optimize the control of factors that are involved in disease progression. In this paper we propose a critical analysis of factors that are involved in the progression of the liver damage and the occurrence of extra-hepatic complications (cardiovascular diseases, extra hepatic cancer) in patients with NAFLD. We also briefly discuss the impact of the heterogeneity of the clinical phenotype of NAFLD on the clinical practice globally and at the individual level.

Keywords: fatty liver; fibrosis; insulin resistance; metabolic syndrome.

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Conflict of interest statement

The authors declare they have no competing interest.

Figures

Figure 1
Figure 1
The severity of the liver damage in non-alcoholic fatty liver disease (NAFLD) is determined by the interaction of multiple risk factors combined in a well-determined clinical phenotype. Some of these factors (i.e., age, gender, genetics, etc.) cannot be modified, while others (obesity, type 2 diabetes, high blood pressure, sleep apnea) can be modified through specific interventions (general lifestyle measures or targeted control of comorbidities). Because of a unique clinical phenotype of each patient, NAFLD therapeutic interventions should be tailored on a clinical-based personalized approach for the selection of the best non-pharmacological approach or drug candidates to target a specific physiopathogenic pathway.
Figure 2
Figure 2
T2DM and NAFLD are linked through a bidirectional relationship: NAFLD increases the risk of T2DM occurrence and T2DM is a risk factor for NAFLD development and fibrosis progression. Total sugar intake and T2DM are independent risk factors for hepatocellular carcinoma (HCC).
Figure 3
Figure 3
Mechanisms of carcinogenesis according to the presence/absence of cirrhosis and disease modifiers involved NAFLD-related HCC.

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