Obesity and its nurturing effect on hepatitis C

McCullough, Arthur J.

doi:10.1053/jhep.2003.50413

Cited by 33 publications

(25 citation statements)

References 17 publications

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“…In addition, hepatic steatosis decreases contact between interferon and hepatocytes receptors [16] . Steatosis interferes with the signaling cascade of interferon [Janus Kinase (JAK) activate signal transduction and activator of transcription (STAT) which express IFN genes] [32] . On the other hand, the HCV core protein promotes insulin resistance via TNF-production and insulin resistance induces steatosis, fibrogenesis, and IFN-resistance [16,33,34] .…”

Section: How Does Concomitant Ms With Hcv Infection Impair the Responmentioning

confidence: 99%

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: How Does Concomitant Ms With Hcv Infection Impair the Responmentioning

confidence: 99%

Hepatitis C comorbidities affecting the course and response to therapy

El-Zayadi¹

2009

WJG

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“…HCV directly associates with IR independent of the visceral fat area in non-obese and non-diabetic patients [35] . In addition to IR, obesity and hepatic steatosis have been recognized as independent risk factors for a poor response to IFN-α therapy [72,73] . In obese individuals, subcutaneous fat could cause a reduction in the initial absorption and bioavailability of interferon given subcutaneously [72] .…”

Section: Response To Interferon Therapy In Hcv Infectionmentioning

confidence: 99%

“…In addition to IR, obesity and hepatic steatosis have been recognized as independent risk factors for a poor response to IFN-α therapy [72,73] . In obese individuals, subcutaneous fat could cause a reduction in the initial absorption and bioavailability of interferon given subcutaneously [72] . In the meantime, obesity and hepatic steatosis impair immune responses to HCV and increase fibrosis progression in obese patients [73] .…”

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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“…Possible explanations for the decreased response to interferon-based therapy in patients with coexistent CHC and steatosis or steatohepatitis include an altered immune response, fixed-drug dosing of interferon, and decreased bioavailability of drug. 33 Most patients with NAFLD are overweight or obese and typically are insulin resistant. Recently RomeroGomez et al 34 showed a significant reduction in SVR among patients with insulin resistance.…”

Section: Diminished Effectiveness Of Antiviral Therapymentioning

confidence: 99%

Steatosis and Chronic Hepatitis C Infection: Mechanisms and Significance

Harrison

2005

Clinical Gastroenterology and Hepatology

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Obesity and its nurturing effect on hepatitis C

Cited by 33 publications

References 17 publications

Hepatitis C comorbidities affecting the course and response to therapy

Hepatitis C comorbidities affecting the course and response to therapy

Hepatic steatosis: A benign disease or a silent killer

Steatosis and Chronic Hepatitis C Infection: Mechanisms and Significance

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