Chronic hepatitis C: Effect of alcohol on hepatic activity and viral titre

Cromie, Suzanne L.; Jenkins, Peter; Bowden, D. Scott; Dudley, F. J.

doi:10.1016/s0168-8278(96)80284-4

Cited by 113 publications

(73 citation statements)

References 20 publications

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“…In line with this observation, a decrease of alcohol consumption prior treatment of hepatitis C significantly reduced viral load. In addition, Cromie et al [24] showed that viral load decreased highly significantly within 4 mo when patients cut down on alcohol consumption from 39-100 g/d to 0-50 g/d. More recent data, however, clearly suggest that the poor response of alcoholics towards interferon therapy is more likely due to reduced compliance.…”

Section: Alcohol Consumption Hcv Replication and Response To Hcv Thementioning

confidence: 99%

Evaluation of standard liver volume formulae for Chinese adults

Shi¹,

Yan²,

Li³

et al. 2009

WJG

105

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Alcoholic liver disease (ALD) and hepatitis C virus (HCV) infection represent, either alone or in combination, more than two thirds of all patients with liver disease in the Western world. This review discusses the epidemiology and combined impact of ALD and HCV on the progression of liver disease. ALD and HCV affect the progression of liver disease to liver cirrhosis and hepatocellular carcinoma (HCC) in a synergistic manner. Thus, the risk for HCC increases five times with a daily alcohol consumption of 80 g; in the presence of HCV it is increased 20-fold, and a combination of both risk factors leads to a more than 100-fold risk for HCC development. Alcohol consumption also decreases the response to interferon treatment which is probably due to a lack of compliance than a direct effect on HCV replication. Several molecular mechanisms are discussed that could explain the synergistic interaction of alcohol and HCV on disease progression. They include modulation of the immune response and apoptosis, increased oxidative stress via induction of CYP2E1 and the hepatic accumulation of iron. Thus, both HCV and alcohol independently cause hepatic iron accumulation in > 50% of patients probably due to suppression of the liver-secreted systemic iron hormone hepcidin. A better understanding of hepcidin regulation could help in developing novel therapeutic approaches to treat the chronic disease in the future. For now, it can be generally concluded that HCV-infected patients should abstain from alcohol and alcoholics should be encouraged to participate in detoxification programs.

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Section: Alcohol Consumption Hcv Replication and Response To Hcv Thementioning

confidence: 99%

Evaluation of standard liver volume formulae for Chinese adults

Shi¹,

Yan²,

Li³

et al. 2009

WJG

105

View full text Add to dashboard Cite

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“…HCV titer is significantly greater in patients consuming greater than 10g of alcohol per day [187]. Habitual drinkers also showed higher levels of HCV RNA than non-habitual drinkers [182].…”

Section: Alcohol Reactive Species and Hcv Replicationmentioning

confidence: 95%

“…Habitual drinkers also showed higher levels of HCV RNA than non-habitual drinkers [182]. Abstinence or moderation of alcohol consumption could result in a substantial drop in the HCV RNA levels in some patients [141,186,187]. Whether heavy, moderate, and light alcohol intake leads to consistent elevations in serum as well as intrahepatic HCV RNA is still unclear [188][189][190][191].…”

Section: Alcohol Reactive Species and Hcv Replicationmentioning

confidence: 99%

Redox regulation of hepatitis C in nonalcoholic and alcoholic liver

Seronello

Sheikh²,

Choi

2007

Free Radical Biology and Medicine

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Hepatitis C virus (HCV) is an RNA virus of the Flaviviridae family that is estimated to have infected 170 million people worldwide. HCV can cause serious liver disease in humans such as cirrhosis, steatosis, and hepatocellular carcinoma. HCV induces a state of oxidative/nitrosative stress in patients through multiple mechanisms, and this redox perturbation has been recognized as a key player in the HCV-induced pathogenesis. Studies have shown that alcohol synergizes with HCV in the pathogenesis of liver disease, and part of these effects may be mediated by reactive species that are generated during hepatic metabolism of alcohol. Furthermore, reactive species and alcohol may influence HCV replication and the outcome of interferon therapy. Alcohol consumption has also been associated with increased sequence heterogeneity of the HCV RNA sequences, suggesting multiple modes of interaction between alcohol and HCV.This review summarizes current understanding of oxidative and nitrosative stress during HCV infection and possible combined effects of HCV, alcohol, and reactive species in the pathogenesis of liver disease.

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“…In a "perfect" world patients would have a single aetiology for their end-stage liver disease, unfortunately in the real world patients may undergo LT for ALD in the presence of other comorbidities, which can significantly affect the result. The most common is HCV, where there have been data of a more rapid progression of the liver disease in immunocompetent patients with the combination of ALD and HCV (Cromie et al, 1996;Pessione et al, 1998). However, other, more recent studies have shown that patients transplanted for ALD plus HCV had a better survival than patients with HCV alone and similar survival to those with ALD alone (Aguilera et al, 2009).…”

Section: Outcome Of Lt For Ald and Ethical Issues 31 Outcome Of Lt Fmentioning

confidence: 99%