Progression from isolated steatosis to steatohepatitis and fibrosis in nonalcoholic fatty liver disease

Pais, Raluca; Pascale, Alina; Fedchuck, L.; Charlotte, Frédéric; Poynard, Thierry; Ratziu, Vlad

doi:10.1016/j.gcb.2010.06.004

Cited by 60 publications

(48 citation statements)

References 14 publications

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“…Concomitant liver steatosis and fibrosis are frequently observed in liver fibrosis patients, particularly those with nonalcoholic and alcoholic liver diseases and viral hepatitis C and B (28,29 /s was observed in patients with a signal fat fraction of 10%-20%; however, in a study between the two similar groups by d`Assignies et al (31), there was no significant change in the ADC value. The source of discrepancy in the ADC value between those two prior studies is unclear.…”

Section: Discussionmentioning

confidence: 93%

Does steatosis affect the performance of diffusion-weighted MRI values for fibrosis evaluation in patients with chronic hepatitis C genotype 4?

Besheer¹,

Razek²,

Bendary³

et al. 2017

Turk J Gastroenterol

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Section: Discussionmentioning

confidence: 93%

Does steatosis affect the performance of diffusion-weighted MRI values for fibrosis evaluation in patients with chronic hepatitis C genotype 4?

Besheer¹,

Razek²,

Bendary³

et al. 2017

Turk J Gastroenterol

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“…67 It has also been reported in small case series that uncontrolled metabolic risk factors were the driving forces for many patients in progression from simple steatosis to NASH. 68 A few genomics studies, to date, have also implicated genetic factors associated with the progression of NAFLD, although these factors lack clinical application at this time. 69 As noted previously, it is also interesting to note that while hepatic injury induced by NASH is similar to that seen in patients with alcoholic liver disease, NASH does appear to progress more slowly and is less severe on histology than steatohepatitis caused by alcohol.…”

Section: Non-alcoholic Steatohepatitis (Nash) and Non-nashmentioning

confidence: 99%

“…71 In another study, after 5 years of follow-up, both inflammation and ballooning, and mild fibrotic changes were seen in patients with simple steatosis. 68 In a small series of 52 patients with NAFLD, who were evaluated 3 years after the initial diagnosis, among the patients that only had simple…”

Section: Non-alcoholic Steatohepatitis (Nash) and Non-nashmentioning

confidence: 99%

Epidemiology and Natural History of Non-alcoholic Fatty Liver Disease

Mishra¹,

Younossi²

2012

Journal of Clinical and Experimental Hepatology

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Non-alcoholic fatty liver disease (NAFLD) is an important cause of liver disease burden across the world. By definition, although the histopathologic features of NAFLD are identical to that of alcoholic liver disease, its diagnosis requires absence of significant alcohol use and absence of other causes of chronic liver disease. We now know that NAFLD is not simply a disease of the Western world. It is manifested across the world, in varying rates, across gender, across varying ethnicities, and in its association with other host factors. In this review article, the definition of NAFLD, its spectrum, ranging from mild steatosis to hepatocellular injury and inflammation defined as non-alcoholic steatohepatitis (NASH) is discussed. Mild steatosis is generally a stable disease whereas NASH can be progressive. Based on current published literature, current incidence and prevalence of NAFLD and NASH are discussed. It is also accepted that these processes will continue to increase in prevalence with the rise of obesity, type II diabetes, and associated metabolic syndrome. Some of the risk factors have been well-established and are discussed. In addition, this review also presents emerging associations with other risk factors for NAFLD. Natural history of NAFLD is variable depending upon the histologic subtypes and other underlying comorbidities and is discussed in this review as well. (J CLIN EXP HEPATOL 2012;2:135-144)

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“…5 Recent studies have shown that a certain proportion of non-alcoholic fatty liver disease (NAFLD) can progress to hepatic fibrosis (cirrhosis) and liver failure, 6 and the extent of hepatic steatosis is associated with fibrosis in chronic hepatitis C 7 and NAFLD. 8 In addition, AT 1 receptor blockade has an anti-fibrotic effect in the liver. 9,10 These studies suggest the possible role of excessive lipids accumulated in the liver in the development and promotion of liver fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Liver lipid content is reduced in rat given 7-day administration of angiotensin II

Ishizaka

Hongo

Sakamoto

et al. 2011

J Renin Angiotensin Aldosterone Syst

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Activation of the renin-angiotensin system may be involved in the development of hepatic steatosis, a condition that is associated with insulin resistance. We showed that in rats, angiotensin II induced accumulation of triglycerides in the renal tubular and cardiac cells, although it significantly reduced the weight of the rats. Here we investigated the liver lipid content of rats given long-term angiotensin II administration. Angiotensin II (0.7 mg/kg/day) was infused into the rats for 7 days via an osmotic minipump. Some rats also received hydralazine or losartan concomitantly. It was shown that angiotensin II reduced oil red O-stainable lipid droplets (6% of the control value) and liver triglyceride content (angiotensin II: 4.6 ± 0.8 mg/mg, control: 11.7 ± 1.1 mg/mg). Both of these phenomena were blocked by losartan, but not by hydralazine. Angiotensin II infusion reduced the expression and activity of AMP-activated protein kinase. In addition, angiotensin II decreased the mRNA expression of peroxisome proliferator-activated receptor-a and genes related to β-oxidation, although mRNA expression of genes related to lipogenesis were not affected. Angiotensin II reduced triglyceride content in the liver, unlike in the kidney or heart, via an AT1 receptor-dependent mechanism.

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Progression from isolated steatosis to steatohepatitis and fibrosis in nonalcoholic fatty liver disease

Cited by 60 publications

References 14 publications

Does steatosis affect the performance of diffusion-weighted MRI values for fibrosis evaluation in patients with chronic hepatitis C genotype 4?

Does steatosis affect the performance of diffusion-weighted MRI values for fibrosis evaluation in patients with chronic hepatitis C genotype 4?

Epidemiology and Natural History of Non-alcoholic Fatty Liver Disease

Liver lipid content is reduced in rat given 7-day administration of angiotensin II

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