What is alcoholic hepatitis

Alcoholic hepatitis is a progressive inflammation of the liver caused by drinking alcohol (ethanol) ¹⁾. The pathogenesis is not completely understood ²⁾. Steatosis (fatty liver) and cirrhosis (scarring of liver) frequently accompany alcoholic hepatitis.

Alcoholic hepatitis is most likely to occur in people who drink heavily over many years. However, the relationship between drinking and alcoholic hepatitis is complex. Not all heavy drinkers develop alcoholic hepatitis, and the disease can occur in people who drink only moderately.

Alcohol abuse is the most common cause of serious liver disease in Western societies. In the United States alone, alcoholic liver disease affects more than 2 million people (i.e, approximately 1% of the population). The true prevalence of alcoholic hepatitis, especially of its milder forms, is unknown, because patients may be asymptomatic and may never seek medical attention.

Globally, the prevalence of alcoholic hepatitis appears to differ widely among different countries. In the Western hemisphere, when liver biopsies were performed in people who drank moderate to heavy amounts of alcohol and were asymptomatic, the prevalence of alcoholic hepatitis was found to be approximately 25-30%.

If you’re diagnosed with alcoholic hepatitis, you must stop drinking alcohol. People who continue to drink alcohol face a high risk of serious liver damage and death.

Alcoholic hepatitis symptoms

The most common sign of alcoholic hepatitis is yellowing of the skin and whites of the eyes (jaundice).

Other signs and symptoms of alcoholic hepatitis include:

• Loss of appetite
• Nausea and vomiting
• Abdominal tenderness
• Fever, which is often low-grade
• Fatigue and weakness
• Weight loss

Just about everyone who has alcoholic hepatitis is malnourished. Drinking large amounts of alcohol suppresses the appetite, and heavy drinkers get most of their calories in the form of alcohol.

Signs and symptoms of severe alcoholic hepatitis include:

• Fluid accumulation in your abdomen (ascites)
• Confusion and behavior changes due to a buildup of toxins normally broken down and eliminated by the liver
• Kidney and liver failure.

When to see a doctor

Alcoholic hepatitis is a serious disease. Up to 30 to 40 percent of people with severe alcoholic hepatitis can die within one month.

See your doctor if:

• You have any signs or symptoms of alcoholic hepatitis
• You feel you can’t control your drinking
• You would like help to cut back on your drinking

Causes of Alcoholic hepatitis

Alcoholic hepatitis develops when the alcohol that you drink damages your liver. Just how alcohol damages the liver — and why it does so only in some heavy drinkers — isn’t clear.

It is known that:

• The body’s process for breaking down alcohol produces highly toxic chemicals
• These chemicals trigger inflammation that destroys liver cells
• Over time, scars replace healthy liver tissue, interfering with liver function
• This irreversible scarring (cirrhosis) is the final stage of alcoholic liver disease

Other factors that can contribute to alcoholic hepatitis include:

• Other types of hepatitis. If you have hepatitis C and also drink — even moderately — you’re more likely to develop cirrhosis than if you don’t drink.
• Malnutrition. Many people who drink heavily are malnourished, because they eat poorly or because alcohol and its byproducts prevent the body from properly absorbing nutrients. Lack of nutrients contributes to liver cell damage.

Risk factors for Alcoholic hepatitis

The major risk factor for alcoholic hepatitis is the amount of alcohol you consume. The amount of alcohol intake that puts a person at risk of alcoholic hepatitis isn’t known. But most people with the condition have a history of drinking more than 3.4 ounces (100 grams) — equivalent to seven glasses of wine, seven beers or seven shots of spirits — daily for at least 20 years.

Other risk factors include:

• Your sex. Women seem to have a higher risk of developing alcoholic hepatitis possibly because of differences in the way alcohol is processed in women.
• Obesity. Heavy drinkers who are overweight might be likelier to develop alcoholic hepatitis and to progress from that condition to cirrhosis.
• Genetic factors. Studies suggest there may be a genetic component in alcohol-induced liver disease although it’s difficult to separate genetic and environmental factors.
• Race and ethnicity. Although it’s difficult o separate genetic and environmental factors, African-Americans and Hispanics might be at higher risk of alcoholic hepatitis.
• Binge drinking. Consuming five or more drinks at one time might increase your risk of alcoholic hepatitis.

Prevention of alcoholic hepatitis

You might reduce your risk of alcoholic hepatitis if you:

• Drink alcohol in moderation, if at all. For healthy adults, moderate drinking means up to one drink a day for women and up to two drinks a day for men.
• The only certain way to prevent alcoholic hepatitis is to avoid all alcohol.
• Protect yourself from hepatitis C. Hepatitis C is an infectious liver disease caused by a virus. Untreated, it can lead to cirrhosis. If you have hepatitis C and drink alcohol, you’re far more likely to develop cirrhosis than is someone who doesn’t drink. Alcohol consumption may exacerbate injury caused by other pathogenic factors, including hepatitis viruses. Approximately 20% of patients presenting with alcoholic hepatitis have concomitant hepatitis C virus infection ³⁾. Extensive epidemiologic studies suggest that the risk of cirrhosis in patients with chronic hepatitis C infection is greatly exacerbated by heavy alcohol ingestion. Possible mechanisms include the impairment of immune-mediated viral killing or enhanced virus gene expression due to the interaction of alcohol and hepatitis C virus.
• Check before mixing medications and alcohol. Ask your doctor if it’s safe to drink alcohol when taking your prescription medications. Read the warning labels on over-the-counter medications. Don’t drink alcohol when taking medications that warn of complications when combined with alcohol — especially pain relievers such as acetaminophen (Tylenol, others).

Alcoholic hepatitis complications

Complications of alcoholic hepatitis include:

• High blood pressure in the liver. Scar tissue can slow the flow of blood through your liver, causing an increase in pressure in a major blood vessel (portal vein).
• Enlarged veins (varices). Blood that can’t flow freely through the portal vein can back up into other blood vessels in the stomach and esophagus. These blood vessels have thin walls and are likely to bleed if filled with too much blood. Heavy bleeding in the upper stomach or esophagus is life-threatening and requires immediate medical care.
• Ascites. Fluid that accumulates in the abdomen might become infected and require treatment with antibiotics. Ascites aren’t life-threatening but are usually a sign of advanced alcoholic hepatitis or cirrhosis.
• Jaundice. A damaged liver can’t remove the residue of old red blood cells (bilirubin) from your blood. Bilirubin builds up and is deposited in your skin and the whites of your eyes, causing a yellow color.
• Confusion, drowsiness and slurred speech (hepatic encephalopathy). A damaged liver has trouble removing toxins from your body. The buildup of toxins can damage your brain. Severe hepatic encephalopathy can result in coma.
• Cirrhosis. This irreversible scarring of the liver frequently leads to liver failure.
• Kidney failure. A damaged liver can affect blood flow to the kidneys, resulting in damage to those organs.

Diagnosis of alcoholic hepatitis

Your doctor will conduct a physical examination and ask about your history of alcohol consumption. It is important to be honest in describing your drinking habits. Your doctor might ask to interview family members about your drinking.

To test for liver disease, your doctor might recommend:

• Liver function tests
• Blood tests
• An ultrasound, CT or MRI scan of the liver
• A liver biopsy, if other tests and imaging don’t provide a clear diagnosis or if you are at risk of other causes of hepatitis

Alcoholic hepatitis treatment

Treatment for alcoholic hepatitis involves drinking cessation and therapies to ease the signs and symptoms of liver damage.

Drinking cessation

If you’ve been diagnosed with alcoholic hepatitis, you must stop drinking alcohol and never drink alcohol again. It’s the only way of possibly reversing liver damage or preventing the disease from becoming worse. Survival rates for people with alcoholic hepatitis who stop drinking are significantly better than survival rates for people who continue drinking.

If you are dependent on alcohol and want to stop drinking, your doctor can recommend a therapy that’s tailored for your needs. Treatment might include:

• Medications
• Counseling
• Alcoholics Anonymous or other support groups
• Outpatient or residential treatment program

Treatment for malnutrition

Your doctor might recommend a special diet to correct nutritional problems. You might be referred to a dietitian who can suggest ways to increase your consumption of the vitamins and nutrients you lack, including vitamin B1 (thiamine).

If you have trouble eating, your doctor might recommend tube feeding. A tube is passed down your throat or through your side and into your stomach. A special nutrient-rich liquid diet is then passed through the tube.

Medications to reduce liver inflammation

If you have severe alcoholic hepatitis, your doctor might recommend:

• Corticosteroids. These medications have shown some short-term benefit in increasing survival of certain people with severe alcoholic hepatitis. However, corticosteroids have serious side effects and generally aren’t prescribed if you have failing kidneys, gastrointestinal bleeding or an infection.
• Pentoxifylline. Your doctor might recommend this anti-inflammatory medication if you have severe alcoholic hepatitis and can’t take corticosteroids. The overall benefit of pentoxifylline for alcoholic hepatitis isn’t clear. Studies indicate that pentoxifylline might not be effective for people with mild alcoholic hepatitis or for people who haven’t responded to steroid treatment.

Liver transplant

For many people with severe alcoholic hepatitis, a liver transplant is the only hope to avoid death. Survival rates for liver transplant for alcoholic hepatitis are similar to survival rates for transplants associated with other types of liver disease.

However, most transplant centers are reluctant to perform liver transplants on people with alcoholic liver disease because of the fear they will resume drinking after surgery. For transplant to be an option, you would need:

• To find a program that will consider you
• To meet the requirements of the program, including abstaining from alcohol for six months before transplant and agreeing not to resume drinking afterward

Alcoholic hepatitis prognosis

The long-term prognosis of individuals with alcoholic hepatitis depends heavily on whether patients have established cirrhosis and whether they continue to drink. With abstinence, patients with this disease exhibit progressive improvement in liver function over months to years, and the histologic features of active alcoholic hepatitis resolve. If alcohol abuse continues, alcoholic hepatitis invariably persists and progresses to cirrhosis over months to years. In one study, the estimated 5-year survival after hospitalization for severe alcoholic hepatitis was 31.8%. Abstinence was the only independent predictor of long-term survival ⁴⁾.

Mild alcoholic hepatitis is a benign disorder with negligible short-term mortality. However, when alcoholic hepatitis is of sufficient severity to cause hepatic encephalopathy, jaundice, or coagulopathy, mortality can be substantial.

The overall 30-day mortality rate in patients hospitalized with alcoholic hepatitis is approximately 15%; however, in patients with severe liver disease, the rate approaches or exceeds 50%. In those lacking encephalopathy, jaundice, or coagulopathy, the 30-day mortality rate is less than 5%. Overall, the 1-year mortality rate after hospitalization for alcoholic hepatitis is approximately 40%.

In one study, the overall mortality among patients with severe alcoholic hepatitis was 66%. Age, white blood cell (WBC) count, prothrombin time (PT), and female sex were all independent risk factors for the dismal outcome ⁵⁾.

Alcoholic hepatitis score

During the past several decades, various formulas and algorithms have been proposed for predicting the outcome of severe alcoholic hepatitis. The single most reliable indicator of severity is the presence of hepatic encephalopathy.

The American Association for the Study of Liver Diseases guideline recommends using prognostic scoring systems such as the Maddrey discriminant function (MDF) to stratify illness severity and the risk of poor outcome, both initially and over the course of the illness ⁶⁾.

The discriminant function (DF) of Maddrey and coworkers is based on Prothrombin time (PT) – a blood test that measures the time it takes for the liquid portion (plasma) of your blood to clot and bilirubin levels and it is calculated as follows: Discriminant function (DF) = (4.6 × PT prolongation) + total serum bilirubin in mg/dL.

Values greater than 32 indicate severe disease and predict a 30-day mortality rate of approximately 50%, assuming only supportive treatment is given. However, subsequent studies have found the discriminant function (DF) to be an inexact predictor of mortality in patients with alcoholic hepatitis, especially in those who receive glucocorticoids.

Other formulas have been proposed for the assessment of prognosis of alcoholic hepatitis, but none has become popular among clinicians. The Combined Clinical and Laboratory Index of the University of Toronto permits a linear estimate of acute mortality in persons with alcoholic hepatitis. Its major disadvantages are the large number ⁷⁾ of variables that must be scored and the complexity of the calculation itself.

In contrast to the Combined Clinical and Laboratory Index, a much simpler formula for assessing mortality was proposed in a large series of 142 patients with histologically proven alcoholic hepatitis based on PT, serum bilirubin level, and serum albumin level ⁸⁾. According to this study, the mortality rate in patients with a serum bilirubin level greater than 2 mg/dL, a serum albumin level less than 2.5 g/dL, and a PT greater than 5 seconds was 75%. Conversely, patients who did not meet all 3 criteria had a much lower mortality rate (approximately 25%).

Model for end-stage liver disease (MELD) score

Several retrospective studies have shown that the MELD score is useful in predicting 30- and 90-day mortality in patients with alcoholic hepatitis (see the MELD Score calculator). Moreover, the MELD score seems to contain some practical and statistical advantages over Maddrey’s DF in predicting mortality among these patients. In a cohort of 73 patients with alcoholic hepatitis at the Mayo Clinic, the MELD score was the only independent predictor of mortality ⁹⁾. Likewise, in another much larger retrospective study of 202 patients with alcoholic hepatitis, the MELD score was found superior to not only Maddrey’s DF but also to the classical Child-Turcotte-Pugh (CTP) score ¹⁰⁾.

Glasgow alcoholic hepatitis score (GAHS)

The GAHS is one of the most recently described predictors of outcome in patients with alcoholic hepatitis. This scoring system uses 5 different variables, including age, bilirubin level, blood urea nitrogen (BUN) level, PT, and WBC count. The overall accuracy of GAHS, which was validated in 195 patients with alcoholic hepatitis, was 81%, when predicting 28-day outcome ¹¹⁾. In contrast, the modified DF had an overall accuracy of only 50% ¹²⁾.

Asymmetric dimethylarginine (ADMA) score

The ADMA score is the most recently proposed predictor of adverse clinical outcome in patients with severe alcoholic hepatitis. In a small prospective study of 27 patients with alcoholic hepatitis, the ADMA score was a better predictor of outcome than the CTP score, the DF, or the MELD score ¹³⁾.

Other factors that correlate with poor prognosis include older age, impaired renal function, encephalopathy, and a rise in the WBC count in the first 2 weeks of hospitalization.