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Abstract
Non alcoholic steatohepatitis (NASH) is the inflammatory reaction of the liver to excessive accumulation of lipids in the hepatocytes. NASH can progress to cirrhosis and hepatocellular carcinoma (HCC). Fatty liver is the hepatic manifestation of metabolic syndrome. A subclinical inflammatory state is present in patients with metabolic alterations like insulin resistance, type-2 diabetes, obesity, hyperlipidemia, and hypertension. Platelets participate in immune cells recruitment and cytokines-induced liver damage. It is hypothesized that lipid toxicity cause accumulation of platelets in the liver, platelet adhesion and activation, which primes the immunoinflammatory reaction and activation of stellate cells. Recent data suggest that antiplatelet drugs may interrupt this cascade and prevent/improve NASH. They may also improve some metabolic alterations. The pathophysiology of inflammatory liver disease and the implication of platelets are discussed in details.
Highlights
The term non-alcoholic fatty liver disease (NAFLD) was coined by Ludwig and colleagues (Ludwig et al, 1980) to describe fatty liver disease arising in the absence of significant alcohol intake.NAFLD is histologically characterized by macrovesicular steatosis and further categorized into non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH) a more severe and evolutive disease, including inflammation and balooning.The definition by EASL Guidelines for the management of non-alcoholic fatty liver disease is the following: NAFLD characteristic is the excessive hepatic fat accumulation, which is associated with insulin resistance
A clinical trial in NAFLD and NASH patients analysing electron microscopy of hepatocytes, demonstrated that significant mitochondrial abnormalities were present in patients with NASH, but not in those with hepatic steatosis, suggesting that peripheral insulin resistance could lead only to the development of fatty liver disease, not to inflammation as seen in steatohepatitis (Sanyal et al, 2001)
Scientific evidence supports the hypothesis that platelets are implicated in the pathophysiology of NAFLD/NASH, mostly by exerting proinflammatory and profibrotic activities, rather than exerting their thrombogenic activities
Summary
The term non-alcoholic fatty liver disease (NAFLD) was coined by Ludwig and colleagues (Ludwig et al, 1980) to describe fatty liver disease arising in the absence of significant alcohol intake.NAFLD is histologically characterized by macrovesicular steatosis and further categorized into non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH) a more severe and evolutive disease, including inflammation and balooning.The definition by EASL Guidelines for the management of non-alcoholic fatty liver disease is the following: NAFLD characteristic is the excessive hepatic fat accumulation, which is associated with insulin resistance. A clinical trial in NAFLD and NASH patients analysing electron microscopy of hepatocytes, demonstrated that significant mitochondrial abnormalities were present in patients with NASH, but not in those with hepatic steatosis, suggesting that peripheral insulin resistance could lead only to the development of fatty liver disease, not to inflammation as seen in steatohepatitis (Sanyal et al, 2001).
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