Review Article: Drug Therapy for NAFLD
Non-alcoholic fatty liver disease represents a spectrum of liver diseases, characterized mainly by macrovesicular steatosis in the absence of significant alcohol ingestion. Non-alcoholic fatty liver disease includes both non-alcoholic fatty liver and non-alcoholic steatohepatitis.
Non-alcoholic steatohepatitis once considered a benign process is now known to lead to progressive fibrosis and cirrhosis. Histologically indistinguishable from alcoholic liver disease, the exact aetiology of non-alcoholic fatty liver disease remains unknown, but the fundamental pathophysiological process appears to be insulin resistance and oxidative stress related to the metabolic syndrome.
Therapy has focused on risk factors, weight reduction and pharmacological intervention. Promising pharmacological treatments have been demonstrated with antioxidants, insulin sensitizers, hepatoprotectants and lipid-lowering agents. However, without larger randomized studies, no pharmacological treatments can be recommended at this time.
Non-alcoholic fatty liver disease (NAFLD) represents a spectrum of liver diseases characterized mainly by macrovesicular steatosis in the absence of significant alcohol ingestion. The hepatic histology can vary from steatohepatitis to isolated hepatic steatosis, referred to as non-alcoholic steatohepatitis (NASH) or its precursor non-alcoholic fatty liver disease (NAFL), respectively. NASH once considered a benign process has been found to lead to progressive fibrosis and cirrhosis. The transition of NAFL to NASH is not clearly demarcated; however, histologically, NASH will show the presence of cytological ballooning, Mallory's hyaline, scattered inflammation and pericellular fibrosis. Because the presence of inflammation and fibrosis is distinctive features in NASH, a liver biopsy is often needed to differentiate NAFL from NASH.
It is estimated that 12–15% of the general population has NAFL while 3–4% have NASH. While a majority of cases occur in females between the ages of 40 and 60, reports in children are well documented. NAFLD association with the metabolic syndrome is also well documented ( Table 1 ). All subjects with the metabolic syndrome are potentially at risk for having NAFLD. An estimated 70–80% of obese individuals have NAFL while 1520% have NASH. Approximately 50–100% of subjects with NASH are overweight, 50–60% are hypertensive and 50–60% have dyslipidemias. While the exact aetiology of NAFLD remains unknown, the fundamental pathophysiologic process that connects the diverse conditions associated with NAFLD seems to be insulin resistance. Insulin resistance is present in approximately 98% of individuals with NAFLD and over 80% of subjects meet the criteria for the metabolic syndrome.
Summary and Introduction
Summary
Non-alcoholic fatty liver disease represents a spectrum of liver diseases, characterized mainly by macrovesicular steatosis in the absence of significant alcohol ingestion. Non-alcoholic fatty liver disease includes both non-alcoholic fatty liver and non-alcoholic steatohepatitis.
Non-alcoholic steatohepatitis once considered a benign process is now known to lead to progressive fibrosis and cirrhosis. Histologically indistinguishable from alcoholic liver disease, the exact aetiology of non-alcoholic fatty liver disease remains unknown, but the fundamental pathophysiological process appears to be insulin resistance and oxidative stress related to the metabolic syndrome.
Therapy has focused on risk factors, weight reduction and pharmacological intervention. Promising pharmacological treatments have been demonstrated with antioxidants, insulin sensitizers, hepatoprotectants and lipid-lowering agents. However, without larger randomized studies, no pharmacological treatments can be recommended at this time.
Introduction
Non-alcoholic fatty liver disease (NAFLD) represents a spectrum of liver diseases characterized mainly by macrovesicular steatosis in the absence of significant alcohol ingestion. The hepatic histology can vary from steatohepatitis to isolated hepatic steatosis, referred to as non-alcoholic steatohepatitis (NASH) or its precursor non-alcoholic fatty liver disease (NAFL), respectively. NASH once considered a benign process has been found to lead to progressive fibrosis and cirrhosis. The transition of NAFL to NASH is not clearly demarcated; however, histologically, NASH will show the presence of cytological ballooning, Mallory's hyaline, scattered inflammation and pericellular fibrosis. Because the presence of inflammation and fibrosis is distinctive features in NASH, a liver biopsy is often needed to differentiate NAFL from NASH.
It is estimated that 12–15% of the general population has NAFL while 3–4% have NASH. While a majority of cases occur in females between the ages of 40 and 60, reports in children are well documented. NAFLD association with the metabolic syndrome is also well documented ( Table 1 ). All subjects with the metabolic syndrome are potentially at risk for having NAFLD. An estimated 70–80% of obese individuals have NAFL while 1520% have NASH. Approximately 50–100% of subjects with NASH are overweight, 50–60% are hypertensive and 50–60% have dyslipidemias. While the exact aetiology of NAFLD remains unknown, the fundamental pathophysiologic process that connects the diverse conditions associated with NAFLD seems to be insulin resistance. Insulin resistance is present in approximately 98% of individuals with NAFLD and over 80% of subjects meet the criteria for the metabolic syndrome.
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