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.
Highlights
Related to the 21st century epidemic of obesity and type 2 diabetes, the prevalence of non-alcoholic fatty liver disease (NAFLD) continues to increase with almost 1 billion people being affected globally [1]
The close association between changes in the fibrosis stage and the baseline activity scores or changes in the disease activity during follow-up is seen in non-alcoholic steatohepatitis (NASH) clinical trials: patients achieving NASH resolution or a decrease in the activity grade had some degree of fibrosis regression [10,11]. These results provide the rationale for developing drugs that targets disease activity and indirectly reverses fibrosis
It is accepted that NAFLD is a multi-systemic disease situated in the center of the metabolic syndrome and insulin resistance, and involves the liver and the extrahepatic organs
Summary
Related to the 21st century epidemic of obesity and type 2 diabetes, the prevalence of non-alcoholic fatty liver disease (NAFLD) continues to increase with almost 1 billion people being affected globally [1]. Contrary to other chronic liver diseases where the etiological agent is either modifiable (e.g., alcohol consumption) or accessible to a targeted specific treatment (viral or autoimmune hepatitis), multiple factors (genetic, epigenetic, environmental, clinical) are driving the disease progression in NAFLD, resulting in a variety of clinical phenotypes that require an individual therapeutic approach. For these reasons, it is important to understand the natural history of NAFLD and identify the factors that can modify the disease course. We would like to critically analyze (1) the factors that drive the natural history of NAFLD, (2) the specific liver and metabolic clinical phenotypes and (3) their impact on the clinical practice and therapeutic advances globally and at the individual level
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