Alcoholic liver disease: Symptoms, treatment, and causes

It’s important to identify the trigger whenever possible in case the condition is reversible. A liver transplant is a challenging procedure, and the rules about who can receive an organ are complex. You’re likely to have ARLD if your AST level is two times higher than your ALT level. According to the National Institute on Alcohol Abuse and Alcoholism, this finding is present in over 80 percent of ARLD patients. The following organizations are good additional resources about alcohol-related liver disease. Research has shown that cirrhosis can be reversed, although this may not occur for all patients.

This can be an outcome of advanced-stage liver disease and often means that a liver transplant is the only option for prolonged survival. A liver transplant is a complicated procedure that depends on a donor’s availability. For example, stopping drinking once diagnosed with fatty liver disease may be able to reverse the condition within 2–6 weeks. There are normally no symptoms, and alcoholic fatty liver disease is often reversible if the individual abstains from alcohol from this point onward. Innate immunity is the first line of antiviral protection in the liver. HCV commandeers this line of defense, and ethanol metabolism potentiates its takeover.

What is Fatty Liver Disease?

Often, by the time doctors detect the damage, it is irreversible. Personal and psychosocial factors are also important because excessive drinking is related to depression and other psychological diseases. Those with cirrhosis often develop kidney problems, intestinal bleeding, fluid in the belly, confusion, liver cancer, and severe infections. Doctors advise those looking into cutting back to choose alcohol-free days, alternate with a non-alcoholic drink when they do consume and exercise instead of going to happy hour.

denial in alcoholism

For more than a decade, alcoholic cirrhosis has been the second leading indication for liver transplantation in the U.S. The applicability of liver transplant for patients with severe alcoholic hepatitis is ethically controversial considering the scarcity of organs for liver transplant and the approximately 20% liver transplant waiting list mortality. Most transplantation centers require 6-months of sobriety prior to be considered for transplantation. This requirement theoretically has a dual advantage of predicting long-term sobriety and allowing recovery of liver function from acute alcoholic hepatitis. This rule proves disadvantageous to those with severe alcoholic hepatitis because 70% to 80% may die within that period.

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A diet high in unsaturated fat increases susceptibility, as does obesity. Alcohol content is estimated to be the beverage volume (in mL) multiplied by its percentage of alcohol. For example, the alcohol content of 45 mL of an 80-proof (40% alcohol) beverage is 18 mL by volume. Although values can vary, the percentage of alcohol averages 2 to 7% for most beers and 10 to 15% for most wines. Thus, a 12-ounce (oz) glass of beer contains between about 5 to 20 g of alcohol, and a 5-oz glass of wine contains between about 12 to 18 g, and a 1 ½-oz shot of hard liquor contains about 14 g. The lower your name is placed on the transplant list, the longer you may need to wait.

Reasons someone might relapse into alcohol misuse after a transplant include a history of mental health conditions, limited access to treatment options, or a lack of social support. You and a doctor can take steps ahead of time to help resolve these issues, which can increase your chance of getting the transplant. Talk to your doctor if you think you have a problem with drinking or are at risk for developing liver disease. They can refer you to programs to help you stop drinking and improve the health of your liver. Alcoholic hepatitis develops when the alcohol you drink damages your liver. Just how alcohol damages the liver — and why it does so only in some heavy drinkers — isn’t clear.

Typical liver vs. liver cirrhosis

These cells express the highest levels of the major ethanol-oxidizing enzymes, alcohol dehydrogenase (ADH), which is located in the cytosol, and cytochrome P450 2E1 (CYP2E1), which resides in the smooth endoplasmic reticulum (ER) (figure 1). Hepatocytes also express very high levels of catalase, an enzyme that inhabits peroxisomes. Catalase normally carries out the detoxification of hydrogen peroxide (H2O2) to water and oxygen. However, when ethanol is present, catalase has an accessory role in ethanol metabolism by using H2O2 to oxidize ethanol to acetaldehyde.

alcoholic liver disease

Patients presenting with severe alcoholic hepatitis may have encephalopathy. Several histopathologic studies have shown that as many as 50% of patients with alcoholic liver disease have increased hepatic iron content compared with healthy controls. This excess deposition of iron may play a significant role in the progression of the alcoholic liver damage.

Ethanol oxidation by catalase is a relatively minor pathway in the liver, but has a larger ethanol-oxidizing function in the brain (Aragon et al. 1992). On further progression, there is marked steatosis, hepatocellular necrosis, and acute inflammation. Eosinophilic fibrillar material (Mallory hyaline or Mallory-Denk bodies) forms in swollen (ballooned) hepatocytes. Severe lobular infiltration of polymorphonuclear leukocytes (neutrophils) is abundantly present in this condition in contrast to most other types of hepatitis where mononuclear cells localize around portal triads. The prevalence of alcoholic liver disease is highest in European countries. Daily consumption of 30 to 50 grams of alcohol for over five years can cause alcoholic liver disease.

Does alcoholic liver affect AST or ALT?

Most patients with alcoholic liver disease will have AST/ALT ratios below 2.0 and many below 1.0, which could conceivably be because some patients could have coexisting alcoholic as well as viral liver disease.

A daily intake of 80 grams of alcohol increases liver-cancer risk 5-fold over that of nondrinkers, whereas heavy alcohol use by HCV-infected individuals increases cancer risk by 100-fold over uninfected heavy drinkers. Excessive alcohol consumption is a global healthcare problem with enormous social, economic, and clinical consequences, accounting for 3.3 million deaths in 2012 (World Health Organization 2014). Excessive drinking over decades damages nearly every organ in the body. However, the liver sustains the earliest and the greatest degree of tissue injury from excessive drinking because it is the primary site of ethanol metabolism (Lieber 2000). After a brief overview of alcohol metabolism in the liver, this article will summarize the mechanisms through which excessive alcohol consumption contributes to the development of various types of alcohol-induced liver damage. It also will review modifiers of alcoholic liver disease (ALD) and discuss currently used treatment approaches for patients with ALD.