Liver biopsy is a useful predictor of response to interferon therapy in chronic hepatitis C

Kaserer, Klaus; Fiedler, R.; Steindl, Petra; Müller, Christian; Wrba, Friedrich; Ferenci, Péter

doi:10.1046/j.1365-2559.1998.00413.x

Cited by 76 publications

(46 citation statements)

References 38 publications

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“…Several studies have recently confirmed that the SVR [7] is impaired in patients with high body mass index and for those with hepatic steatosis. These data indicate that HCV carriers should avoid weight gain by diet and physical exercise before initiation of antiviral therapy, all efforts should be made to improve the metabolic steatosis of the patient.…”

Section: Insulin Resistancementioning

confidence: 91%

“…When treating chronic hepatitis C (CHC), many clinicians do not take into consideration the presence of other comorbid conditions that lead to more progressive liver disease, such as cirrhosis and hepatocellular carcinoma (HCC) [3][4][5] . In recent studies, it has been proved that such comorbidities might reduce the response rate to PEGylated interferon (PEG-IFN)/ribavirin (RBV) therapy in HCV patients [6,7] . Eventually amelioration of these comorbidities before embarking on IFN-based therapy would improve the sustained virological response (SVR) and impair progression to cirrhosis and HCC.…”

Section: Introductionmentioning

confidence: 99%

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Hepatitis C comorbidities affecting the course and response to therapy

El-Zayadi¹

2009

WJG

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Several studies have demonstrated that the outcome of chronic hepatitis C (CHC) infection is profoundly influenced by a variety of comorbidities. Many of these comorbidities have a significant influence on the response to antiviral therapy. These comorbidities negatively affect the course and outcome of liver disease, often reducing the chance of achieving a sustained virological response with PEGylated interferon and ribavirin treatments. Comorbidities affecting response to antiviral therapy reduce compliance and adherence to inadequate doses of therapy. The most important comorbidities affecting the course of CHC include hepatitis B virus coinfection, metabolic syndrome, and intestinal bacterial overgrowth. Comorbidities affecting the course and response to therapy include schistosomiasis, iron overload, alcohol abuse, and excessive smoking. Comorbidities affecting response to antiviral therapy include depression, anemia, cardiovascular disease, and renal failure.

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Section: Insulin Resistancementioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Hepatitis C comorbidities affecting the course and response to therapy

El-Zayadi¹

2009

WJG

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“…8 The development of cirrhosis in patients with HCV may be associated with regression of steatosis, 21 as has previously been documented in non-alcoholic steatohepatitis (NASH). 22,23 The mechanisms leading to a reduction in steatosis in the liver with cirrhosis remain Mihm et al 99 Yes Ratziu et al 18 Yes Fartoux et al 19 Yes Czaja et al 9 Yes Yes Yes Hourigan et al 10,11 Yes Yes Yes Adinolfi et al 12 Yes Yes Yes Yes Westin et al 13 Yes Weak Yes Yes Castera et al 14 Yes Yes Monto et al 15 Yes Yes Yes Kumar et al 100 Yes Camps et al 101 Yes (BMI) Kaserer et al 102 Yes Bressler et al 60 Yes (BMI) Rubbia-Brandt et al 28 Yes Yes Poynard et al 16 Yes Yes Yes Yes Yes Patton et al 17 Yes Yes Yes Yes Yes Nair et al 70 No* Marrero et al 103 Yes Ohata et al 74 Yes *Steatosis was a risk for HCC in alcoholic and cryptogenic cirrhosis only. Abbreviation: BMI, body mass index.…”

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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“…Further more, hyperleptinemia in obese is an independent risk factor for non-response to antiviral therapy [74] . Hyperferritinemia downregulates the response to interferon therapy [75,76] . From this review, we have noted that steatosis, either metabolic or cytopathic, contributes to the development of NASH and progression to fibrosis, cirrhosis and HCC.…”

Section: Response To Interferon Therapy In Hcv Infectionmentioning

confidence: 99%

Hepatic steatosis: A benign disease or a silent killer

El-Zayadi¹

2008

WJG

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Steatosis is a common feature of many liver diseases, namely non-alcoholic steatohepatitis (NASH) and hepatitis C virus (HCV) infection, but the pathogenic mechanisms differ. Insulin resistance (IR), a key feature of metabolic syndrome, is crucial for NASH development, associated with many underlying genetically determined or acquired mitochondrial and metabolic defects and culminates to inflammation and progression to fibrosis. This may have potential implications for new drug therapy. In HCV-related disease, steatosis impacts both fibrosis progression and response to treatment. Steatosis in HCV-related disease relates to both viral factors (HCV genotype 3), and host factors (alcohol consumption, overweight, hyperlipidemia, diabetes). Among others, IR is a recognized factor. Hepatic steatosis is reported to be associated with disturbance in the signaling cascade of interferon and downregulation of its receptors. Thus, hepatic steatosis should not be considered a benign feature, but rather a silent killer.

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Liver biopsy is a useful predictor of response to interferon therapy in chronic hepatitis C

Abstract: Liver biopsy provides useful information for selection of patients with hepatitis C for IFN therapy.

Cited by 76 publications

References 38 publications

Hepatitis C comorbidities affecting the course and response to therapy

Hepatitis C comorbidities affecting the course and response to therapy

Steatosis: Co-factor in Other Liver Diseases *

Hepatic steatosis: A benign disease or a silent killer

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