Mechanisms of Synergy Between Alcohol and Hepatitis C Virus

Singal, Ashwani K.; Anand, B S

doi:10.1097/mcg.0b013e3180381584

Cited by 129 publications

(112 citation statements)

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“…This synergism affects both fibrosis progression and the development of hepatocellular carcinoma. The relationship between ALD and HCV was first described in populations of alcoholic individuals with liver disease (2) and confirmed later by investigators who compared the prevalence of HCV markers in alcoholic individuals with and without liver disease and found a significantly higher prevalence in those with liver disease (2)(3)(4).…”

Section: Introductionmentioning

confidence: 88%

“…Valeria R Mas, 1 Ryan Fassnacht, 1 Kellie J Archer, 1,2 and Daniel Maluf spond to ethanol or differ across animal strains with differing responses to ethanol. In similar research, many studies have been performed to evaluate the gene expression patterns associated with chronic HCV infection (15)(16)(17).…”

Section: O L M E D 1 6 ( 7 -8 ) 2 8 7 -2 9 7 J U L Y -A U G U S Tmentioning

confidence: 99%

“…Even though the coexistence of HCV and alcoholism has been associated with accelerated hepatic injury, the pathogenesis is not fully understood but is suspected to be multifactorial (1)(2)(3)(4). Liver biopsy samples in HCV-infected patients with reported alcohol consumption characteristically show a pattern of hepatic injury consistent with chronic viral hepatitis, indicating that the alcohol plays a role in potentiating the effects of HCV, rather than causing traditional alcoholrelated liver injury (5,6).…”

Section: Introductionmentioning

confidence: 99%

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Molecular Mechanisms Involved in the Interaction Effects of Alcohol and Hepatitis C Virus in Liver Cirrhosis

Mas

Fassnacht

Archer

et al. 2010

Mol Med

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The mechanisms by which alcohol consumption accelerates liver disease in patients with chronic hepatitis C virus (HCV) are not well understood. To identify the characteristics of molecular pathways affected by alcohol in HCV patients, we fit probe-set level linear models that included the additive effects as well as the interaction between alcohol and HCV. The study included liver tissue samples from 78 patients, 23 (29.5%) with HCV-cirrhosis, 13 (16.7%) with alcohol-cirrhosis, 23 (29.5%) with HCV/alcohol cirrhosis and 19 (24.4%) with no liver disease (no HCV/no alcohol group). We performed gene-expression profiling by using microarrays. Probe-set expression summaries were calculated by using the robust multiarray average. Probe-set level linear models were fit where probe-set expression was modeled by HCV status, alcohol status, and the interaction between HCV and alcohol. We found that 2172 probe sets (1895 genes) were differentially expressed between HCV cirrhosis versus alcoholic cirrhosis groups. Genes involved in the virus response and the immune response were the more important upregulated genes in HCV cirrhosis. Genes involved in apoptosis regulation were also overexpressed in HCV cirrhosis. Genes of the cytochrome P450 superfamily of enzymes were upregulated in alcoholic cirrhosis, and 1230 probe sets (1051 genes) had a significant interaction estimate. Cell death and cellular growth and proliferation were affected by the interaction between HCV and alcohol. Immune response and response to the virus genes were downregulated in HCV-alcohol interaction (interaction term alcohol*HCV). Alcohol*HCV in the cirrhotic tissues resulted in a strong negative regulation of the apoptosis pattern with concomitant positive regulation of cellular division and proliferation.

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Section: Introductionmentioning

confidence: 88%

Section: O L M E D 1 6 ( 7 -8 ) 2 8 7 -2 9 7 J U L Y -A U G U S Tmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Molecular Mechanisms Involved in the Interaction Effects of Alcohol and Hepatitis C Virus in Liver Cirrhosis

Mas

Fassnacht

Archer

et al. 2010

Mol Med

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“…They have a lower rate of response to drug treatment with interferon as a result of nonadherence (29).…”

Section: What Are the Contraindications To Drug Therapy For Hepatitismentioning

confidence: 99%

Hepatitis C

Jou¹,

Muir²

2008

Ann Intern Med

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Chronic hepatitis C virus (HCV) infection is the most common blood-borne infection in the United States, with an estimated overall prevalence of 3.2 million persons (1.3%) and prevalence peaks between age 40 to 49 years (1). The worldwide prevalence of HCV infection is even higher at 2.0%, corresponding to 140 million persons (2).In terms of complications, cirrhosis due to HCV disease is the most frequent indication for liver transplantation in the United States (3), and the overall incidence of hepatocellular carcinoma, a complication of HCV cirrhosis, continues to increase at alarming rates. In an evaluation of population-based registries of the Surveillance, Epidemiology, and End Results (SEER) program in the United States, the overall age-adjusted incidence rates of hepatocellular carcinoma increased from 1.4 per 100 000 in 1975 to 1977 to 3.0 per 100 000 in 1996 to 1998 (4). Prevention What factors increase the risk for hepatitis C virus (HCV) infection?The predominant risk factor for the transmission of HCV is percutaneous exposure to infected blood, which most commonly takes place through remote or chronic injection drug use. Transmission of HCV historically occurred with transfusion of blood products before screening of the blood supply in the United States before 1992. There seems to be no increased risk for HCV transmission through cosmetic procedures, such as tattooing and piercings, unless infection control measures are not followed (5).Transmission of HCV in health care workers after a needle-stick exposure occurs in up to 10% of cases (6). Additionally, the prevalence of HCV infection in hemodialysis patients isThe content of In the Clinic is drawn from the clinical information and education resources of the American College of Physicians (ACP), including PIER (Physicians' Information and Education Resource) and MKSAP (Medical Knowledge and Self-Assessment Program). Annals of Internal Medicine editors develop In the Clinic from these primary sources in collaboration with the ACP's Medical Education and Publishing Division and with the assistance of science writers and physician writers. Editorial consultants from PIER and MKSAP provide expert review of the content. Readers who are interested in these primary resources for more detail can consult http://pier.acponline.org and other resources referenced in each issue of In the Clinic. The information contained herein should never be used as a substitute for clinical judgment. For More Information Centers for Disease Control and Prevention (CDC)Hepatitis C Prevention www.cdc.gov/ncidod/diseases/hepatitis/c/hepcprev.htm Viral Hepatitis C www.cdc.gov/ncidod/diseases/hepatitis/c/index.htm National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Chronic Hepatitis C: Current Disease Management digestive.niddk.nih.gov/ddiseases/pubs/chronichepc/index.htm What I Need to Know about Hepatitis C digestive.niddk.nih.gov/ddiseases/pubs/hepc_ez/index.htm (English) digestive.niddk.nih.gov/ spanish/pubs/hepc_ez/index.htm (Spanish)

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“…Alcohol use and concomitant HCV infection act synergistically to cause more frequent and faster progression of fibrosis. 5 With the epidemic of obesity in the United States, prevalence rates of metabolic syndrome and visceral adiposity are increasing among alcoholics contributing to more prevalent and severe liver disease. 6 Alcohol remains the third most common preventable cause of death after smoking and hypertension.…”

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confidence: 99%

Recent trends in the epidemiology of alcoholic liver disease

Singal¹,

Anand²

2013

Clinical Liver Disease

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Alcohol has been the most frequently abused drug for centuries, but it was not until the 1960s that it was recognized as a direct hepatotoxin. 1 Chronic excessive use of alcohol can lead to fatty liver, alcoholic hepatitis, alcoholic cirrhosis, and liver cancer. Whereas fatty liver is a reversible process upon cessation of drinking alcohol, other pathologies are usually progressive despite abstinence. In the United States, approximately 60% of people in the general population report some drinking of alcohol with approximately 8% to 10% reporting heavy drinking (two or more drinks per day) where one drink is equivalent to 12 ounces of beer (4%-5% wt/vol), 6 ounces of wine (8%-10% wt/vol), and 2 ounces of hard liquor or whiskey (45% wt/vol). 2 Alcohol remains the second most common cause of liver cirrhosis after hepatitis C virus (HCV) infection in the United States, contributing to approximately 20% to 25% cases of liver cirrhosis and about half of all admissions among patients with cirrhosis. Of the various factors responsible for liver disease, duration and amount of drinking alcohol is the most important factor. Pooled data from many epidemiological studies show a minimum intake of 30 g/day of alcohol in women and 50 g/day in men consumed over at least 5 years to cause liver cirrhosis. 3 Prevalence and mortality rates from cirrhosis parallel alcohol consumption prevalence rates in the population globally. Within Europe, which has the highest rate of consumption per capita in the implementation of policies on alcohol sale has resulted in changing epidemiology in different parts of Europe. Alcohol consumption rates have decreased in southern Europe, whereas they have increased in eastern Europe and some areas of northern Europe (including Ireland and the United Kingdom). 4 Because only 10% to 15% of people engaged in heavy drinking develop liver cirrhosis, other factors such as host factors and comorbidities are clearly important (Fig. 1). Women are more prone to the hepatotoxic effect of alcohol compared with men and are prone to develop liver cirrhosis at a lower amount of alcohol consumption. Type of alcohol consumed, binge drinking (five or more drinks at one time), drinking on an empty stomach, and participation in alcohol rehabilitation programs such as Alcoholic Anonymous are some of the other factors. Alcohol use and concomitant HCV infection act synergistically to cause more frequent and faster progression of fibrosis. 5 With the epidemic of obesity in the United States, prevalence rates of metabolic syndrome and visceral adiposity are increasing among alcoholics contributing to more prevalent and severe liver disease. 6 Alcohol remains the third most common preventable cause of death after smoking and hypertension. Alcohol-related mortality affects young and middle-aged population with loss of productive life years. Liver-related mortality from alcohol contributes to 4% of mortality and 5% of disability adjusted life years (DALY) globally, with highest impact in Europe, where these same figures are 7% ...

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Mechanisms of Synergy Between Alcohol and Hepatitis C Virus

Abstract: Alcoholics with HCV infection have more severe liver disease compared with nondrinkers. Patients should be encouraged to enroll in rehabilitation programs so as to improve treatment adherence and response.

Cited by 129 publications

References 107 publications

Molecular Mechanisms Involved in the Interaction Effects of Alcohol and Hepatitis C Virus in Liver Cirrhosis

Molecular Mechanisms Involved in the Interaction Effects of Alcohol and Hepatitis C Virus in Liver Cirrhosis

Hepatitis C

Recent trends in the epidemiology of alcoholic liver disease

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