The histologic spectrum of nonalcoholic fatty liver disease

Contos, Melissa J.; Choudhury, Jayanta; Mills, A. Scott; Sanyal, Arun J.

doi:10.1016/j.cld.2004.04.013

Cited by 63 publications

(38 citation statements)

References 64 publications

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“…NAFLD is a pathological entity encompassing a whole histological spectrum ranging from simple steatosis to steatohepatitis, with inflammation and fibrosis, to cirrhosis (Contos et al, 2004). Cirrhosis, which is irreversible, can further progress to hepatocellular carcinoma (Farazi and DePinho, 2006).…”

Section: Diagnosis and Pathogenesis Of Mets And Nafldmentioning

confidence: 99%

Metabolic syndrome and nonalcoholic fatty liver disease: Is insulin resistance the link?

Asrih

Jornayvaz

2015

Molecular and Cellular Endocrinology

278

196

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Section: Diagnosis and Pathogenesis Of Mets And Nafldmentioning

confidence: 99%

Metabolic syndrome and nonalcoholic fatty liver disease: Is insulin resistance the link?

Asrih

Jornayvaz

2015

Molecular and Cellular Endocrinology

278

196

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“…In the presence of cirrhosis, steatosis with varying combinations of cytological ballooning, Mallory bodies and inflammation were used as histological evidence of concurrent NASH. 17,18 With progression toward cirrhosis, central-to-central and central-to-portal bridges develop, distorting the hepatic lobular architecture. 19 Zone III pericellular fibrosis is therefore difficult to define in patients with cirrhosis and was not considered an independent criterion for NASH and cirrhosis.…”

Section: Methodsmentioning

confidence: 99%

Similarities and differences in outcomes of cirrhosis due to nonalcoholic steatohepatitis and hepatitis C†

et al. 2006

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The objective of this study was to prospectively define outcomes of cirrhosis due to nonalcoholic steatohepatitis (NASH) and compare them with those associated with hepatitis C virus (HCV) infection. We compared 152 patients with cirrhosis due to NASH with 150 matched patients with cirrhosis due to HCV. Over 10 years, 29/152 patients with cirrhosis due to NASH died compared with 44/150 patients with HCV (P < .04). This was mainly due to the lower mortality rate in patients with Child class A cirrhosis due to NASH versus HCV (3/74 vs. 15/75; P < .004). There were no significant across-group differences in mortality in patients with Child class B or C cirrhosis. Sepsis was the most common cause of death in both groups; patients with NASH had a higher cardiac mortality (8/152 vs. 1/150; P < .03). Patients with Child class A cirrhosis due to NASH also had a significantly lower risk of decompensation, defined by a 2-point increase in Child-Turcotte-Pugh score (P < .007). Cirrhosis due to NASH was associated with a lower rate of development of ascites (14/101 vs. 40/97 patients at risk; P < .006). NASH also had a significantly lower risk of development of hepatocellular carcinoma (10/149 vs. 25/147 patients at risk; P < .01). In conclusion, compensated cirrhosis due to NASH is associated with a lower mortality rate compared with that due to HCV. It is also associated with a lower rate of development of ascites, hyperbilirubinemia, and hepatocellular carcinoma. However, cardiovascular mortality is greater in patients with NASH. (HEPATOLOGY 2006;43:682-689.)

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“…NAFLD encompass histological features ranging from hepatic steatosis, steatohepatitis, fibrosis and cryptogenic cirrhosis [4]. HCC might occur as a likely end stage of NAFLD.…”

Section: Introductionmentioning

confidence: 99%

Unsaturated fatty acids promote hepatoma proliferation and progression through downregulation of the tumor suppressor PTEN

Vinciguerra

Carrozzino

Peyrou

et al. 2009

Journal of Hepatology

114

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The histologic spectrum of nonalcoholic fatty liver disease

Cited by 63 publications

References 64 publications

Metabolic syndrome and nonalcoholic fatty liver disease: Is insulin resistance the link?

Metabolic syndrome and nonalcoholic fatty liver disease: Is insulin resistance the link?

Similarities and differences in outcomes of cirrhosis due to nonalcoholic steatohepatitis and hepatitis C†

Unsaturated fatty acids promote hepatoma proliferation and progression through downregulation of the tumor suppressor PTEN

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