It is well known that heavy alcohol consumption can lead to severe liver disease including cirrhosis and hepatocellular carcinoma, but the effects of alcohol on HCV and its treatment are less well studied. As described in the December 15, 2008 Journal of Infectious Diseases, E. McCartney and colleagues performed a laboratory study using cultured Huh-7 cells to examine the effects of alcohol metabolism on HCV replication and the antiviral activity of interferon. They found that exposing the cells to ethanol significantly increased HCV replication, which was dependent on oxidative stress; when the researchers added NAC to the cell cultures, ethanol no longer increased HCV replication. Furthermore, the anti-HCV activity of interferon was also reduced in the presence of ethanol. "These in vitro results mimic what is often noted clinically," the researchers concluded, supporting the recommendation that people with chronic hepatitis C should avoid alcohol or consume only small amounts.

Effects of Alcohol on HCV Replication and Treatment Response

Alcohol Use as a Risk Factor for Poor Adherence and Treatment Failure

ALCOHOL AND ITS EFFECTS ON HEPATITIS C

Effects of Alcohol on HCV Replication and Treatment Response

By Liz Highleyman

It is well known that heavy alcohol consumption can lead to advanced liver disease, including cirrhosis and hepatocellular carcinoma, but the effects of alcohol on hepatitis C virus (HCV) infection and its treatment are not fully understood.

As reported in the December 15, 2008 Journal of Infectious Diseases, Erin McCartney from the University of Adelaide in Australia and colleagues conducted a laboratory study to determine the effect of alcohol metabolism on HCV replication and the antiviral activity of interferon.

The researchers used Huh-7 cells that allow for in vitro HCV replication and metabolize ethanol via the introduced expression of cytochrome P450 2E1 (Cyp2e1). Cell cultures were exposed to ethanol and "treated" with interferon alfa.

Results

Exposing the cells to ethanol (0-100 mmol/L) significantly increased HCV replication.

This effect was dependent on Cyp2e1 expression and alcohol-metabolized oxidative stress.

This was demonstrated by the fact that the antioxidant N-acetylcysteine blocked the effect.

The anti-HCV action of interferon alfa was reduced in the presence of ethanol, most likely via attenuation of Stat1 tyrosine-701 phosphorylation.

"These in vitro results mimic what is often noted clinically," the researchers concluded. "[F]urther dissection of this model system will aid in our understanding of interactions between HCV and alcohol metabolism."

These findings serve to underline the recommendation that people with chronic hepatitis C or other types of liver disease should avoid alcohol entirely or consume it only in small amounts.

Infectious Diseases Laboratories, Institute of Medical and Veterinary Science, and School of Molecular and Biomedical Sciences, University of Adelaide, Adelaide, Australia; Digestive Diseases Laboratory, Northern Clinical School, University of Sydney, Sydney, Australia; Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX.

1/13/09

Reference
EM McCartney, L Semendric, KJ Helbig, and others. Alcohol Metabolism Increases the Replication of Hepatitis C Virus and Attenuates the Antiviral Action of Interferon. Journal of Infectious Diseases 198(12): 1766-1775. December 15, 2008. (Abstract).

http://www.hivandhepatitis.com/hep_c/news/2009/011309_a.html

Alcohol Use as a Risk Factor for Poor Adherence and Treatment Failure

Past research has produced conflicting data on the role of alcohol consumption in the progression of HIV disease.

As reported in the December 1, 2006 Journal of Acquired Immune Deficiency Syndromes, researchers examined the independent effect of alcohol and the combined effects of alcohol and illicit drug use on antiretroviral therapy utilization, adherence, and virological suppression in an urban cohort of HIV positive individuals.

In this observational clinical cohort, alcohol use, active drug use, and adherence were prospectively assessed at 6-month intervals. The investigators classified "hazardous alcohol use" as more than 7 drinks per week or more than 3 drinks on one occasion for women, and more than 14 drinks per week or more than 4 drinks on one occasion for men. Active drug use was defined as any use within the previous 6 months. Outcomes included utilization of antiretroviral therapy, 2-week adherence, and virological suppression. Analyses were adjusted for age, sex, race, years on antiretroviral therapy, and clinic enrollment time.

Results

• Between 1998 and 2003, 1711 individuals participated in 5028 interviews.

• 1433 of these patients (accounting for 3761 interviews) were on antiretroviral therapy.

•The prevalence of any alcohol use at the first interview was 45%, with 10% classified as hazardous drinkers.

•One-third of the sample used illicit drugs.

• In multivariate analyses adjusting for age, sex, race, active drug use, years on antiretroviral therapy, and clinic enrollment time, hazardous alcohol use, compared with no alcohol use, was independently associated with:

- decreased antiretroviral therapy utilization (AOR 0.65; 95% CI 0.51 to 0.82);
- poorer 2-week adherence (AOR 0.46; 95% CI 0.34 to 0.63);
- reduced virological suppression (AOR 0.76; 95% CI 0.57 to 0.99)

• Concurrent injection drug use exacerbated these negative effects on antiretroviral therapy use, adherence, and virological suppression.

Conclusion

"Hazardous alcohol use alone and combined with injection drug use was associated with decreased antiretroviral therapy uptake, adherence, and viral suppression," the authors concluded. "Interventions targeting alcohol use may improve HIV outcomes in individuals with hazardous alcohol use."

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.

12/12/06

Reference
G Chander, B Lau, R D Moore. Hazardous Alcohol Use: A Risk Factor for Non-Adherence and Lack of Suppression in HIV Infection. Journal of Acquired Immune Deficiency Syndromes 43(4): 411-417, December 1, 2006.

http://www.hivandhepatitis.com/recent/2007/011207_e.html

ALCOHOL AND ITS EFFECTS ON HEPATITIS C

SHOULD YOU DRINK ALCOHOL WITH HEPATITIS C ?

Because of the recent widespread press regarding the benefit of consuming "red wine" and heart disease protection, many hepatitis C individuals have asked if they, too, could drink socially. Most people in the United States who drink socially are used to having a glass of wine with dinner, or, perhaps, a mixed drink at a party. Unfortunately, if you have hepatitis C, any consumption of alcohol can potentially be deadly for your liver. And it does not matter whether alcohol is consumed in a drink, in a non-prescription product, or in cough syrup. If you have hepatitis C, alcohol in any form should be completely and totally avoided.

IS IT JUST THE ALCOHOL?

OR SOMETHING IN THE ALCOHOL?

Regardless of the alcoholic beverage consumed, it is the alcohol, itself, that is the culprit in liver damage. Expensive drinks are just as damaging as cheap ones. A one-shot glass of whiskey has the same alcoholic content as a 4 ounce glass of wine, or a 12 ounce can of beer. So…why is alcohol such an enemy to people with hepatitis C?

As the primary organ of detoxification in the body, the liver breaks down most of the alcohol a person drinks. As the liver breaks down alcohol, certain deadly by-products are formed which can be more toxic to the body than the alcohol itself. One of those products is acetaldehyde. This by-product can actually cause liver scarring without inflammation. In most cases, this happens by the interaction of specialized cells produced in the liver to fight infection. For example, cytokines are produced by liver cells and the immune system in response to infection or cell damage. Alcohol use increases the number of cytokines produced. These cytokines often go on a collision course with another type of specialized liver cells, known as stellate cells.

In a normal liver, stellate cells function as storage depots for vitamin A. If activated by cytokines, stellate cells divide rapidly to increase their numbers. Activated stellate cells lose their vitamin A stores and begin to constrict blood vessels that normally deliver oxygen to liver cells. The result is the production of liver scarring without inflammation. This is the primary pathway taken in alcoholic liver cirrhosis.

Long term use of alcohol also increases the inflammatory process itself, a natural body response to tissue damage or infection. This leads to the overproduction of free radicals, molecules that can destroy healthy liver tissue and interfere with important functions such as energy production. Alcohol also interferes with the body's production of natural defenses against these damaging free radicals (i.e. anti-oxidants). Thus, the combination of free radical production and alcohol can lead to liver damage.

A number of studies have shown that alcohol abuse (over 4 drinks per day) accelerates the progression of liver damage. In a person with hepatitis C, this damage is associated with fibrosis and may double the risk of developing cirrhosis of the liver. Other research has clearly shown that the severity of liver disease and the potential for liver cancer in alcoholics versus non-alcoholics increases in the presence of HCV.

Recent studies on HCV viral replication have indicated that the amount of HCV in the blood rises in proportion to increasing alcohol consumption, and drops when alcohol is avoided. This finding may explain why alcoholics generally have a lower response rate to antiviral therapy than non-alcoholics. Other studies have demonstrated a decreased rate of viral clearance from the body among people who drank alcohol, compared to those who did not drink at all. And this decrease in response rate continues for up to six months after stopping all alcohol intake.

Alcohol has also been implicated in the liver's inability to regenerate and to repair itself, a reduced ability of the immune system to fight off viruses, the stimulation of excessive fibrosis in the liver, and an increased absorption and deposition of iron in the liver.

THE BOTTOM LINE - SHOULD YOU OR SHOULDN'T YOU DRINK?

For those with hepatitis C, there are no studies that show conclusively that there is a safe amount of alcohol to drink. Some studies indicate that there is increased liver damage in people with hepatitis C who have had more than 4 drinks of alcohol per day. Other studies demonstrate liver damage can occur with as little as one drink of alcohol per day. Women appear to be more susceptible than men to the damaging effects of alcohol. Women have a lower body mass than men, and they accumulate a higher concentration of alcohol in their blood after consuming the same number of alcoholic drinks. Women's livers also appear to metabolize alcohol at a faster rate than do men's, and their greater estrogen levels appear to add to the effects of alcohol accumulating in their livers. The bottom line…Since no amount of alcohol has been proven to be safe in persons affected with the HCV virus, it is strongly recommended that people with hepatitis C virus…should not drink ANY alcohol at all.

http://www.nu-liver.com/hepatitis-c.htm