Steatosis affects chronic hepatitis C progression in a genotype specific way

Rubbia‐Brandt, Laura

doi:10.1136/gut.2003.018770

Cited by 258 publications

(233 citation statements)

References 26 publications

(14 reference statements)

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“…Older age at infection and chronic excessive alcohol intake are consistently considered primary determinants of fibrosis progression, 4,6,7,20,23,24 and the relationship between fibrosis stage and necroinflammatory grade has been documented in both longitudinal and cross-sectional studies. 3,12,25,26 Steatosis is also a recognized factor associated with severe fibrosis 11,27,28 and emerged as an independent predictor of FPR in our study, while being close to significance for the prediction of severe fibrosis. An impact of genotype 3 was found in analyses based on FPR, independently of steatosis, and was absent when considering fibrosis stage.…”

Section: Discussionmentioning

confidence: 66%

Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C

Hézode¹,

Roudot‐Thoraval²,

Nguyen³

et al. 2005

Hepatology

259

191

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Cannabinoids present in Cannabis sativa (marijuana) exert biological effects via cannabinoid receptors CB1 and CB2. We recently demonstrated that CB1 and CB2 receptors regulate progression of experimental liver fibrosis. We therefore investigated the impact of cannabis smoking on fibrosis progression rate in patients with chronic hepatitis C (CHC). Two hundred seventy consecutive untreated patients with CHC of known duration undergoing liver biopsy were studied. Demographic, epidemiological, metabolic, and virological data were recorded, and detailed histories of cannabis, alcohol, and tobacco use over the span of hepatitis C virus infection were obtained.

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Section: Discussionmentioning

confidence: 66%

Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C

Hézode¹,

Roudot‐Thoraval²,

Nguyen³

et al. 2005

Hepatology

259

191

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“…3,4 However, whether this association is directly mediated by the virus through the increased steatosis observed in patients with HCV genotype 3 or is a consequence of other external factors is still debated. 27,28 In our models, we included an interaction term between viral genotype and steatosis to account for the reasonable different influence of steatosis according to HCV genotype. Indeed, correcting for steatosis, we still detected an effect for the HCV 3 genotype, suggesting that the faster fibrosis progression observed in genotype 3 patients appears to be not completely explained by the presence of steatosis.…”

Section: Discussionmentioning

confidence: 99%

Genetic variation in the interleukin -28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection

et al. 2011

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Polymorphisms in the interleukin-28B (IL28B) region are associated with spontaneous and treatment-induced viral clearance in hepatitis C virus (HCV) infection. Nevertheless, it is unknown whether genetic variation at the IL28B locus influences the natural history of chronic HCV infection. Thus, we asked whether an association between IL28B polymorphisms and liver fibrosis progression existed. We studied 247 consecutive patients with chronic HCV, an accurate estimate of the date of infection, and a liver biopsy performed before any treatment. No patient had a history of alcohol abuse or coinfection with other viruses. We assessed the role of rs8099917 and rs12979860 polymorphisms and the effect of host and environmental factors on fibrosis progression. Blood transfusion (75%) was the main modality of infection. Median age at infection was 21 years, and median interval between infection and liver biopsy was 25 years. One hundred twenty-nine patients (52%) were infected by HCV-1, 74 (30%) by HCV-2, 34 (14%) by HCV-3, and 10 (4%) by HCV-4. Bridging fibrosis/cirrhosis (Ishak !4) was detected in 24% of patients. Age at infection had a marked effect on fibrosis progression by both a linear model and Cox proportionalhazard regression (P < 2E-16). A 12.1% increase in the hazard of advanced fibrosis was estimated for each additional year at infection, suggesting that this was the major explanatory variable in this cohort. Male gender (P < 0.05), HCV genotype 3 (P < 0.001) and steatosis (P < 0.05) were also associated with faster fibrosis progression. Conversely, the two IL28B polymorphisms had no impact on fibrosis progression. Conclusion: In HCV patients with a known date of infection, IL28B genotype was not associated with fibrosis progression rate or with the risk of developing advanced liver fibrosis.

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“…30 In the clinical setting, one must consider the role of other insults such as alcohol in the development of steatosis. Studies have provided conflicting data regarding the contribution of alcohol to steatosis in chronic HCV, 10,15,31 perhaps in part because of the difficulty in obtaining a reliable history of alcohol consumption.…”

Section: Steatosis Influences the Progression Of Fibrosis In Chronic Hcvmentioning

confidence: 99%

Steatosis: Co-factor in other liver diseases

2005

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The prevalence of fatty liver is rising in association with the global increase in obesity and type 2 diabetes. In the past, simple steatosis was regarded as benign, but the presence of another liver disease may provide a synergistic combination of steatosis, cellular adaptation, and oxidative damage that aggravates liver injury. In this review, a major focus is on the role of steatosis as a co-factor in chronic hepatitis C (HCV), where the mechanisms promoting fibrosis and the effect of weight reduction in minimizing liver injury have been most widely studied. Steatosis, obesity, and associated metabolic factors may also modulate the response to alcohol-and drug-induced liver disease and may be risk factors for the development of hepatocellular cancer. The pathogenesis of injury in obesity-related fatty liver disease involves a number of pathways, which are currently under investigation. Enhanced oxidative stress, increased susceptibility to apoptosis, and a dysregulated response to cellular injury have been implicated, and other components of the metabolic syndrome such as hyperinsulinemia and hyperglycemia are likely to have a role. Fibrosis also may be increased as a by-product of altered hepatocyte regeneration and activation of bipotential hepatic progenitor cells. In conclusion, active management of obesity and a reduction in steatosis may improve liver injury and decrease the progression of fibrosis. (HEPATOLOGY 2005;42:5-13.)

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Steatosis affects chronic hepatitis C progression in a genotype specific way

Cited by 258 publications

References 26 publications

Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C

Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C

Genetic variation in the interleukin -28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection

Steatosis: Co-factor in other liver diseases

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