Hepatitis due to both HCV and alcohol abuse can coexist. According to a article , it is common for the two conditions to occur simultaneously.
Excessive alcohol consumption can accelerate and multiply the damage due to HCV, worsening liver cirrhosis. However, even small amounts of alcohol can exacerbate HCV. It may also interfere with HCV treatment by causing the virus to become resistant to medication.
Although both conditions are responsible for liver inflammation, there are differences in the symptoms of HCV and alcoholic hepatitis. They may not realize they have the virus until later if it becomes chronic and causes liver damage. By contrast, alcoholic hepatitis causes the rapid onset of:. It is important to note that HCV is contagious. If a person is unsure if they have contracted the infection, they should take safety precautions to prevent others from coming into contact with their blood.
Learn more about preventing the transmission of HCV. Doctors can diagnose HCV via blood tests. If this test is positive, healthcare professionals will use a second blood test to see if the virus has caused a chronic infection. Diagnosing alcoholic hepatitis can be less certain, as there is no diagnostic test for this condition.
Doctors base a diagnosis on the following:. However, it is also important to stop drinking before treatments begin, as alcohol may reduce the effectiveness of some antivirals. For alcoholic hepatitis, abstinence from alcohol is the highest priority for treatment, involving stopping alcohol consumption entirely. Ceasing drinking is the most effective way to reduce the risk of further liver damage, and if someone can do this early in the disease, it may reverse its effects.
However, once an individual develops cirrhosis, this damage becomes permanent. Most people with alcoholic hepatitis need to stay in the hospital. They then may begin a treatment or support program to help them address addiction. Other measures that may help someone minimize liver damage as a result of alcohol consumption include the below.
People who drink large amounts of alcohol tend to have malnutrition due to a lack of calories or nutrients. Treating malnutrition can reverse some of the effects of alcoholic hepatitis. Some individuals may need a feeding tube, while others may benefit from eating a high-protein diet comprising:.
People with alcohol-related hepatitis may be able to take drugs that lower inflammation, such as steroids. This can reduce the risk of further scarring. However, as steroids can have serious side effects, a doctor may prescribe pentoxifylline Trental if someone cannot tolerate them. If a person with HCV or alcoholic hepatitis does not seek treatment, it can lead to serious complications.
International travelers to countries where hepatitis B is common People with hepatitis C People with chronic liver disease People with HIV People who are in jail or prison All other people seeking protection from hepatitis B virus infection. There is no vaccine available for hepatitis C.
How serious is it? Hepatitis A Hepatitis B Hepatitis C People can be sick for a few weeks to a few months Most recover with no lasting liver damage Although very rare, death can occur. Who should be tested? CDC recommends hepatitis C testing for: All adults aged 18 years and older All pregnant women during each pregnancy People who ever injected drugs and shared needles, syringes, or other drug preparation equipment, including those who injected once or a few times many years ago.
Regular testing is recommended for people who currently inject and share needles, syringes, or other drug preparation equipment. People with HIV People who have ever received maintenance hemodialysis.
Regular testing is recommended for people who currently receive maintenance hemodialysis. ABC Table What causes it? The hepatitis B virus can also be transmitted from: Birth to an infected mother Sex with an infected person Sharing equipment that has been contaminated with blood from an infected person, such as needles, syringes, and even medical equipment, such as glucose monitors Sharing personal items such as toothbrushes or razors Poor infection control has resulted in outbreaks in health care facilities Hepatitis C is spread when blood from a person infected with the Hepatitis C virus — even in microscopic amounts — enters the body of someone who is not infected.
The hepatitis C virus can also be transmitted from: Sharing equipment that has been contaminated with blood from an infected person, such as needles and syringes Receiving a blood transfusion or organ transplant before when widespread screening virtually eliminated hepatitis C from the blood supply Poor infection control has resulted in outbreaks in health care facilities Birth to an infected mother Who should be vaccinated?
International travelers to countries where hepatitis B is common People with hepatitis C People with chronic liver disease People with HIV People who are in jail or prison All other people seeking protection from hepatitis B virus infection There is no vaccine available for hepatitis C.
Symptoms: Many people with hepatitis do not have symptoms and do not know they are infected. Hepatitis A. Hepatitis B. Hepatitis C. Hepatitis D. Hepatitis E. Viral Hepatitis Home.
Links with this icon indicate that you are leaving the CDC website. Linking to a non-federal website does not constitute an endorsement by CDC or any of its employees of the sponsors or the information and products presented on the website. You will be subject to the destination website's privacy policy when you follow the link. The primary prevention approach obviously is to avoid the main sources of infection, such as intravenous drug abuse or transfusion of contaminated blood.
Another prevention approach would be to avoid sexual promiscuity, which promotes acquisition of the disease Alter in ways that have not yet been well defined. In addition to these "classic" risk factors, other factors can significantly increase the rate of infection, its persistence, or the rapid evolution of the disease toward the dismal end-stages. Although some of these factors e. Among these controllable risk factors, none is more important than alcohol consumption.
Researchers first became aware of the major effect of alcoholism on HCV infection when they noted that alcoholism was associated with HCV but not hepatitis B even in people who did not show classic risk factors, such as intravenous drug abuse or blood transfusions Rosman et al.
In addition to promoting the acquisition or persistence of HCV, alcohol subsequently was shown to affect the two major processes that are harbingers of rapid and severe progression of liver disease and of the patient's deterioration, namely inflammation and fibrosis.
In addition to the high incidence of HCV infection in heavy drinkers even in the absence of classic risk factors, other observations suggest that heavy alcohol consumption enhances the ability of the virus to enter and persist in the body.
For example, several studies demonstrated a correlation between the presence of virus in the blood i.
Furthermore, moderation of alcohol consumption was shown to result in a decrease in the number of virus particles in the blood i. Researchers do not yet fully understand the mechanism through which alcohol affects the viral titer. It is well known, however, that alcohol impairs the function of certain components of the body's immune system Ince and Wands An impaired immune function, in turn, may influence the ability of the virus to persist in the body rather than be eliminated by immune cells.
Greater alcohol consumption was associated with higher virus levels in the blood. Another mechanism through which alcohol consumption may favor the progression and exacerbation of HCV infection is oxidative stress.
The term "oxidative stress" refers to the presence of excessive levels of highly reactive molecules called free radicals in the cell or a lack of molecules called antioxidants that can eliminate those free radicals. For more information on oxidative stress, see the sidebar below. Various studies have indicated that through as yet unknown mechanisms, HCV infection itself can lead to oxidative stress Larrea et al.
This virus-induced oxidative stress, in turn, may be exacerbated by the breakdown i. The breakdown of nutrients e. Generally speaking, oxidation reactions are those that add oxygen to or remove hydrogen from a substance or both.
For example, the metabolism of alcohol involves two oxidation reactions. First, one enzyme converts alcohol chemically referred to as ethanol to acetaldehyde by removing hydrogen. Then, a second enzyme converts acetaldehyde to acetate by removing additional hydrogen and adding oxygen. Two major enzyme systems are involved in ethanol metabolism in the liver.
The first one involves the enzyme alcohol dehydrogenase. The second system, which is activated mainly after heavy alcohol consumption, is the microsomal ethanol-oxidizing system MEOS.
Particularly the MEOS, however, sometimes generates not only stable, nontoxic molecules but also highly unstable i.
Many of these molecules contain oxygen and are called oxygen radicals. Common oxygen radicals include superoxide O 2. The presence of excess levels of oxygen radicals is called oxidative stress. If unchecked, oxygen radicals can damage cells by attacking vital cell components, such as the fat and protein constituents of the cell wall and the cell's genetic material. For example, oxidative stress can induce enhanced metabolism of fat molecules i. Some of these molecules, in turn, may contribute to the development of fibrosis.
Because the formation of oxygen radicals is a natural process that occurs during many metabolic processes, cells have developed several protective mechanisms to prevent radical formation or to detoxify radicals.
These mechanisms employ molecules called antioxidants, which are found in foods or generated by the body itself. These compounds have several mechanisms of action. For example, GSH can neutralize oxygen radicals by transferring hydrogen to the reactive molecules, thus creating a more stable chemical structure. Using their internal antioxidants, cells can deal with normal levels of oxygen radical formation.
When oxygen radical formation is greater than normal or antioxidant levels are lower than normal, however, oxidative stress occurs that may contribute to cell death and tissue damage, such as fibrosis of the liver. Chronic alcohol consumption can increase oxidative stress in several ways. For example, alcohol metabolism by the MEOS is associated with the generation of oxygen radicals.
Moreover, animal models demonstrated that chronic alcohol consumption reduces the levels of various antioxidants, including GSH Colell et al. Accordingly, treatment with potent antioxidants or with compounds to enhance the body's ability to generate antioxidants may relieve oxidative stress and counteract the fibrosis-inducing effects of alcohol and other conditions e. Colell, A. Selective glutathione depletion of mitochondria by ethanol sensitizes hepatocytes to tumor necrosis factor.
Nanji A. Apoptosis and necrosis: Two types of cell death in alcoholic liver disease. Alcohol Metabolism and Oxidative Stress. It is well known that heavy alcohol consumption can result in toxic effects on the liver i. This toxicity has been linked to alcohol metabolism in the liver Lieber Alcohol chemically referred to as ethanol is broken down mainly by the enzyme alcohol dehydrogenase ADH , which converts ethanol to acetaldehyde and hydrogen.
Excess hydrogen causes a number of metabolic disorders, including fat accumulation in the liver i. The acetaldehyde, which itself is a toxic substance, subsequently is further metabolized by another enzyme Lieber Acetaldehyde contributes to various toxic and metabolic effects of alcohol, but cannot account for all disorders found in alcoholics. Instead, another metabolic pathway called the microsomal ethanol-oxidizing system MEOS Lieber and DeCarli , which also converts ethanol to acetaldehyde, plays a role in some of alcohol's adverse effects.
The physiologic role of the MEOS is to generate the sugar glucose from various precursors; metabolize certain components of fat molecules i. Chronic alcohol consumption strongly increases the activity of the MEOS, including that of an enzyme called cytochrome P Several variants of cytochrome P exist, including one called CYP2E1 whose activity is markedly enhanced after chronic alcohol consumption.
Figure 3 The beneficial and toxic roles of CYP2E1, an enzyme involved in the breakdown of alcohol in the liver that acts in conjunction with another compound i. CYP2E1 typically helps process compounds that are normally present in the body e. Enhanced CYP2E1 activity, however, also results in the increased generation of harmful byproducts e. In addition to its beneficial physiologic function, the MEOS can have some adverse metabolic effects see figure 3.
For example, CYP2E1 has a high capacity to break down some commonly used drugs e. In addition, the MEOS generates toxic free radicals when it has been induced by alcohol. In patients with HCV infection, these free radicals most likely potentiate the HCV-associated oxidative stress and the resulting liver damage. This hypothesis is supported by the observation that in a clinical study, an antioxidant i.
Elevated blood levels of this enzyme, which normally is found in the tissues, including the liver, indicate acute liver disease. The improvement was only partial, however, and occurred in only one-half of the patients.
Therefore, researchers are currently conducting studies with more potent antioxidants, such as a substance called polyenylphosphatidylcholine PPC , which is discussed in more detail in the section "Treatment of Hepatitis C in Drinkers. HCV infection leads to an inflammatory reaction in the liver. This inflammation is caused both by the attack of the virus on the liver cells and by the body's defense mechanisms that are triggered by that attack.
Alcohol appears to potentiate this inflammatory reaction, because HCV-infected patients who consumed alcohol exhibited greater inflammation than did patients who consumed no alcohol Cromie et al. The exact mechanisms through which alcohol enhances hepatic inflammation remain unclear, however.
Several studies have shown that the rate with which HCV-induced hepatic scarring i. Other researchers detected such an acceleration in fibrosis development only with heavy alcohol consumption i. Wiley and colleagues examined the effect of long-term heavy drinking on the progression of tissue damage and clinical symptoms associated with HCV infection. The study included women who consumed more than 40 grams of alcohol approximately 3 standard drinks daily and men who consumed more than 60 grams of alcohol approximately 4 standard drinks daily for more than 5 years.
The investigators concluded that alcohol intake was an independent risk factor for the progression of HCV infection. Specifically, heavy drinkers had a two- to threefold greater risk of cirrhosis and decompensated liver disease than did control subjects. Finally, Harris and colleagues found that a history of heavy alcohol abuse i.
These findings that alcohol can accelerate liver damage associated with HCV infection are particularly important because HCV-infected patients generally do not become sick or die because of the presence of virus in the blood but because of the complications of the cirrhosis see figure 1. The severity of fibrosis was assessed using the Knodell index, which measures changes in the tissue's structure and chemical composition i.
The data show that greater alcohol consumption was associated with more severe fibrosis i. Alcohol influences the scarring process through several mechanisms. One of these is oxidative stress, which, as described earlier, exacerbates the oxidative stress associated with HCV itself. For example, oxidative stress can induce the excessive breakdown of fat molecules i. Some products of lipid peroxidation induced by oxidative stress have been shown to be toxic and promote fibrosis in the liver Tsukamoto Lipid peroxidation products are detectable in the livers of patients with chronic HCV infection, especially in areas where scar tissue is being formed, suggesting a role for lipid peroxidation in HCV-associated liver fibrosis Paradis et al.
The role of oxidative stress in fibrosis also is supported by findings that the physiologic antioxidant vitamin E is depleted in patients with alcohol-induced cirrhosis Leo et al.
Furthermore, Houglum and colleagues demonstrated that in HCV-infected patients who did not respond to treatment with interferon, vitamin E administration prevented the activation of a type of liver cell called stellate cells, whose activation plays a key role in fibrosis development. However, vitamin E treatment was only partially effective because it did not significantly affect liver function as assessed through the levels of liver enzymes in the blood, HCV virus titers, or the degree of liver inflammation.
Therefore, more potent antioxidative agents are now being investigated with regard to their ability to prevent fibrosis and inflammatory reactions. For more information on this approach, see the section on "Treatment of Hepatitis C in Drinkers.
Hepatocellular carcinoma almost exclusively occurs in patients who already have developed cirrhosis see figure 1.
Because HCV infection and alcohol both enhance the risk of cirrhosis, their combination results in a marked increase in the risk of cirrhosis and, consequently, in accelerated development of hepatocellular carcinoma Tsutsumi et al. In fact, in the study by Tsutsumi and colleagues , which was conducted in Japan, more than 50 percent of alcoholic HCV-infected patients developed hepatocellular carcinoma, a percentage considerably higher than that found in patients with only one or none of those two risk factors.
The number of hepatocellular carcinoma cases in the United States also has increased over the past two decades because the prevalence of HCV infection has increased and with it the number of alcoholics infected with HCV. Moreover, the age-specific incidence of hepatocellular carcinoma has progressively shifted toward younger people because of more rapid disease progression El-Serag and Mason As mentioned earlier, approximately one-third to one-half of HCV-infected patients spontaneously recover from the infection or show only minimal disease progression with persistently normal liver function.
For these patients, standard antiviral treatment which is described in the following paragraph is currently not recommended except as part of clinical trials, because treatment frequently is associated with severe side-effects Shaib et al. Nevertheless, a significant number of HCV-infected patients approximately 50 to 60 percent are at risk for progression to severe and often fatal end-stage liver disease Seeff and therefore should receive therapy to prevent this progression.
The decision to administer antiviral treatment depends to a large extent on the physician's ability to estimate the likelihood that a given patient will progress to more severe disease stages.
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