Abstract
Nonalcoholic fatty liver disease (NAFLD), tightly linked to the metabolic syndrome (MS), has emerged as a leading cause of chronic liver disease worldwide. Since it is potentially progressive towards non-alcoholic steatohepatitis (NASH) and hepatic fibrosis, up to cirrhosis and its associated complications, the need for predictive factors of NAFLD and of its advanced forms is mandatory. Despite the current “gold standard” for the assessment of liver damage in NAFLD being liver biopsy, in recent years, several non-invasive tools have been designed as alternatives to histology, of which fibroscan seems the most promising. Among the different serum markers considered, serum uric acid (SUA) and ferritin have emerged as possible predictors of severity of liver damage in NAFLD. In fact, as widely described in this review, they share common pathogenetic pathways and are both associated with hepatic steatosis and MS, thus suggesting a likely synergistic action. Nevertheless, the power of these serum markers seems to be too low if considered alone, suggesting that they should be included in a wider perspective together with other metabolic and biochemical parameters in order to predict liver damage.
Highlights
Nonalcoholic fatty liver disease (NAFLD), tightly linked to metabolic syndrome (MS), has emerged as a leading cause of chronic liver disease worldwide with a rapidly growing prevalence in the general population, ranging between 20% and 30%, and paralleling the epidemics of obesity and type 2 diabetes mellitus (T2DM) all over the world [1,2]
NAFLD encompasses a clinical-pathologic spectrum of liver diseases ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), the more aggressive form of NAFLD, which can progress to cirrhosis and its associated complications [3,4]
Its production is regulated by the endogenous and exogenous precursor proteins delivered to the liver, whereas its excretion is controlled by the kidneys through renal plasma flow, glomerular filtration and proximal tubular exchange
Summary
Nonalcoholic fatty liver disease (NAFLD), tightly linked to metabolic syndrome (MS), has emerged as a leading cause of chronic liver disease worldwide with a rapidly growing prevalence in the general population, ranging between 20% and 30%, and paralleling the epidemics of obesity and type 2 diabetes mellitus (T2DM) all over the world [1,2]. NAFLD encompasses a clinical-pathologic spectrum of liver diseases ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), the more aggressive form of NAFLD, which can progress to cirrhosis and its associated complications [3,4]. The only validated method to diagnose NASH, the potentially evolving form of NAFLD, is liver biopsy. This procedure is limited by intra and inter-observer variability, sampling errors and invasiveness, letting impossible its feasibility in such a large number of patients with NAFLD. Increasing evidence has shown that SUA levels as well as high ferritin are associated with the metabolic insulin resistance syndrome, higher body fat content and more severe liver damage
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