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The NAFLD fibrosis score: A noninvasive system that identifies liver fibrosis in patients with NAFLD
TLDR
A simple scoring system accurately separates patients with nonalcoholic fatty liver disease with and without advanced fibrosis, rendering liver biopsy for identification ofAdvanced fibrosis unnecessary in a substantial proportion of patients.
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Nonalcoholic fatty liver disease: From steatosis to cirrhosis
TLDR
The present “gold standard” management of NASH is modest weight reduction, particularly correction of central obesity achieved by combining dietary measures with increased physical activity, which improves insulin resistance and reverses steatosis, hepatocellular injury, inflammation, and fibrosis.
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Lamivudine for patients with chronic hepatitis B and advanced liver disease.
TLDR
Continuous treatment with lamivudine delays clinical progression in patients with chronic hepatitis B and advanced fibrosis or cirrhosis by significantly reducing the incidence of hepatic decompensation and the risk of hepatocellular carcinoma.
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NASH and insulin resistance: Insulin hypersecretion and specific association with the insulin resistance syndrome
TLDR
There is a near‐universal association between NASH and IR irrespective of obesity, and most patients with NASH have IRS, according to the homeostasis model assessment.
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CYP2E1 and CYP4A as microsomal catalysts of lipid peroxides in murine nonalcoholic steatohepatitis.
TLDR
Results show that experimental NASH is strongly associated with hepatic microsomal lipid peroxidation, and CYP4A enzymes are identified as alternative initiators of oxidative stress in the liver.
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Epidemiology of non-alcoholic fatty liver disease in China.
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Hepascore: an accurate validated predictor of liver fibrosis in chronic hepatitis C infection.
TLDR
A model of 4 serum markers plus age and sex provides clinically useful information regarding different fibrosis stages among hepatitis C patients.
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Etiopathogenesis of nonalcoholic steatohepatitis.
TLDR
NASH can be regarded as the hepatic consequence of the metabolic syndrome (or syndrome X) and attention should now shift from steatosis, a generally benign process that is less evident in the advanced stages of cirrhosis, to the mechanisms for hepatocellular injury, inflammation, and hepatic fibrosis.
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Hepatic cytochrome P450 2E1 is increased in patients with nonalcoholic steatohepatitis
TLDR
It is concluded that hepatic CYP2E1 is increased in patients with NASH compared with normal livers, suggesting that the pathogenetic mechanisms for NASH may be similar and, like alcoholic steatohepatitis, may involve induction of CYP 2E1.
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Increased hepatocyte CYP2E1 expression in a rat nutritional model of hepatic steatosis with inflammation.
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