| Alcoholic liver disease | |
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| Classification and external resources | |
Microscopy of liver showing fatty change, cell necrosis, Mallory bodies |
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| ICD-10 | K70. |
| ICD-9 | 571.1 |
| MedlinePlus | 000281 |
| MeSH | D008108 |
Alcoholic liver disease is the major cause of liver disease in Western countries, (in Asian countries, viral hepatitis is the major cause). It arises from the excessive ingestion of alcohol. Even though millions of individuals drink alcohol on a regular basis, only a few heavy drinkers develop liver damage. The liver damage induced by alcohol is not sudden as it occurs slowly over a period of 10-15 years. [1] How alcohol damages the liver is not completely understood. It is known that alcohol produces toxic chemicals like acetaldehyde which can damage liver cells, but why this occurs in only a few individuals is still in debate. When alcohol damages the liver, the function of the organ is not immediately compromised as the liver has a tremendous capacity to regenerate and even when 75% of the liver is damaged, it continues to function as normal. Thus when alcohol-induced liver damage produces symptoms, there is always significant damage which by now is usually irreversible. When alcohol is consumed for a long time, it eventually results in liver scarring or what is known as cirrhosis or end-stage alcoholic liver disease. [2]
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Generally it is believed that certain genes increase metabolism of alcohol which may increase risk of cirrhosis and even alcohol related cancers. Alcohol-induced liver injury can be worsen by hepatitis. If you have hepatitis B or C and drink, you will most likely develop cirrhosis faster. Alcohol-induced liver disease is also worsened in people who have iron overload. Malnutrition can worsen alcohol-induced liver damage. Most alcoholics tend to eat poorly and often substitute alcohol as a meal. The liver has a great capacity to regenerate, but without proper nutrition, it quickly fails.
Fatty change, or steatosis is the accumulation of fat in liver cells which can be seen as fatty globules under the microscope. Alcoholism causes large fatty globules (macrovesicular steatosis). Small fatty globules have different causes. Other causes of macrovesicular steatosis include diabetes, obesity and starvation. Alcoholic fatty change is probably dose-related.[citation needed] The mechanism of alcohol induced fatty liver involves an above average NADH:NAD ratio caused by alcohol metabolism by alcohol dehydrogenase and aldehyde dehydrogenase. A higher NADH concentration induces fatty acid synthesis while decreased NAD level causes decreased fatty acid oxidation. Consequently, the higher levels of fatty acid signals the hepatocytes to compound it to glycerol to form triglycerides.
Some people get an acute hepatitis or inflammatory reaction to the cells affected by fatty change. This is not directly related to the dose of alcohol. Some people seem more prone to this reaction than others. This is called alcoholic steatonecrosis and the inflammation probably predisposes to liver fibrosis.
Cirrhosis is a late stage of liver disease marked by fibrosis and altered liver architecture. It is often progressive and may eventually lead to liver failure. Late complications of cirrhosis or liver failure include portal hypertension, coagulation disorders, ascites and other complications, including hepatic encephalopathy and the hepatorenal syndrome.
Cirrhosis also has number of causes besides alcohol abuse, such as viral hepatitis and non-alcoholic toxins. The late stages of cirrhosis may look similar regardless of cause. This phenomenon is termed a "final common pathway" for the disease.
Fatty change and alcoholic hepatitis are probably reversible. The later stages of fibrosis and cirrhosis tend to be irreversible but can usually be quite well managed for long periods of time.
There are many tests to asses alcoholic liver damage. Besides blood examination, doctors utilize ultrasound and a CT scan to assess liver damage. In some cases a liver biopsy is performed. This minor procedure is done under local anesthesia and involves placing a small needle in the liver and obtaining a piece of tissue. The tissue is then sent to the laboratory to be examined under a microscope.
The first treatment of alcohol-induced liver disease is cessation of alcohol consumption. This is the only way to reverse liver damage or prevent liver injury from worsening. Without treatment, most patients with alcoholic-induced liver damage will develop liver cirrhosis. Other treatment for alcohol hepatitis include:
Doctors recommend a high-calorie rich diet to help the liver in its regeneration process. Dietary fat must be reduced because fat interferes with alcohol metabolism. The diet is usually supplemented with vitamins, minerals, calcium and iron. To enhance liver recovery, one should also change lifestyle and stop smoking.
Individuals with severe alcoholic hepatitis may benefit from short term course of corticosteroids. Other novel therapies include intravenous drugs like infliximab and etanercept.
It is widely believed that alcohol-induced liver damage occurs via generation of oxidants. Thus alternative health care practitioners routinely recommend natural supplements like milk thistle. Unfortunately, there is no valid clinical data to show that milk thistle truly works.
When all else fails and the liver is severely damaged, the only alternative is a liver transplant. While this is a great option, liver transplant donors are scarce and usually there is a long waiting list in any given hospital. One of the criteria to become eligible for a liver transplant is to discontinue alcohol consumption for a minimum of 6 months. [3]
As the liver scars, the blood vessels become non-compliant and narrow. This leads to increased pressure in blood vessels entering the liver. Over time, this causes a back log of blood (portal hypertension) and is associated with massive bleeding. Enlarged veins also develop to bypass the blockages in the liver. These veins are very fragile and do have a tendency to rupture and bleed (varices). Variceal bleeding can be life threatening and needs emergent treatment. Once the liver is damaged, fluid builds up in the abdomen and legs. The fluid buildup presses on the diaphragm and can make breathing very difficult. [4] As liver damage progresses, the liver is unable to get rid of pigments like bilirubin and both the skin and eyes turn yellow. The dark pigment also causes the urine to appear dark and the stools appear pale. Also with the progression of the disease, the liver can release toxic substances (ammonia) which then lead to brain damage. This results in altered mental status, behavior and personality changes.
| • | Alcoholic liver disease is damage to the liver and its function due to alcohol abuse. | &bull | Alcoholic liver disease usually occurs after years of excessive drinking. | &bull | Other factors that contribute to the development of alcoholic liver disease: | |
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