ALCOHOLIC LIVER DISEASE
Alcoholic Liver Disease is a syndrome of progressive inflammatory liver injury associated with long-term heavy intake of alcohol. The pathogenesis is not completely understood.
Though alcoholic liver disease is most likely to occur in people who drink heavily over many years, the relationship between drinking and alcoholic liver disease is complex. Not all heavy drinkers develop alcoholic liver disease, and the disease can occur in people who drink only moderately.
Patients who are severely affected present with subacute onset of fever, hepatomegaly, leukocytosis, marked impairment of liver function (e.g., jaundice, coagulopathy), and manifestations of portal hypertension (e.g., ascites, hepatic encephalopathy, variceal hemorrhage). However, milder forms of alcoholic liver disease often do not cause any symptoms.
Alcoholic liver disease usually persists and progresses to cirrhosis if heavy alcohol use continues. If alcohol use ceases, alcoholic liver disease resolves slowly over weeks to months, sometimes without permanent sequelae but often with residual cirrhosis. Of all chronic heavy drinkers, only 15–20% develops hepatitis or cirrhosis, which can occur concomitantly or in succession.
Causes
Alcoholic liver disease occurs when the liver is damaged by the excessive consumption of alcohol. How alcohol damages the liver and why it does so only in a minority of heavy drinkers is not clear. It is known that the process of breaking down ethanol; the alcohol in beer, wine and liquor produces highly toxic chemicals, such as acetaldehyde. These chemicals trigger inflammation that destroys liver cells. Over time, web-like scars and small knots of tissue replace healthy liver tissue, interfering with the liver’s ability to function. This irreversible scarring, called cirrhosis, is the final stage of alcoholic liver disease.
Malnutrition: Many people who drink heavily are malnourished, either because they eat poorly or because alcohol and its toxic by-products prevent the body from properly absorbing and breaking down nutrients, especially protein, certain vitamins and fats. In both cases, the lack of nutrients contributes to liver cell damage.
Sex: Women have a higher risk of developing alcoholic liver disease than men do. This disparity may result from differences in the way alcohol is processed by women.
Genetic factors: A number of genetic mutations have been identified that affect the way alcohol is broken down in the body. Having one or more of these mutations may increase the risk of alcoholic liver disease.
Pathophysiology
Some signs and pathological changes in liver histology include:
Alcoholic liver disease is characterized by the inflammation of hepatocytes. Between 10% and 35% of heavy drinkers develop alcoholic liver disease. While development of hepatitis is not directly related to the dose of alcohol, some people seem more prone to this reaction than others. This is called alcoholic steato necrosis and the inflammation appears to predispose to liver fibrosis. Inflammatory cytokines (TNF-alpha, IL6 and IL8) are thought to be essential in the initiation and perpetuation of liver injury by inducing apoptosis and necrosis.
Symptoms
It may not have symptoms in the early stages. Symptoms tend to be worse after a period of heavy drinking. Digestive symptoms include:
• Pain and swelling in the abdomen and tenderness,
• Decreased appetite and weight loss,
• Nausea and vomiting,
• Fatigue,
• Dry mouth and increased thirst,
• Bleeding from enlarged veins in the walls of the lower part of the oesophagus.
Skin problems such as:
• Yellow colour in the skin, mucus membranes, or eyes (jaundice).
• Small, red spider-like veins on the skin.
• Very dark or pale skin.
• Redness on the feet or hands.
• Itching.
Treatment
In most patients with alcoholic liver disease, the illness is mild. Their short-term prognosis is good, and no specific treatment is required. Hospitalization is not always necessary. Alcohol use must be stopped, and care should be taken to ensure good nutrition; providing supplemental vitamins and minerals, including folate and thiamine, is reasonable. Patients who are coagulopathic should receive vitamin K parenterally. Anticipate symptoms of alcohol withdrawal, and manage them appropriately.
Cessation of Alcohol Intake: Cessation of alcohol use is the mainstay of treatment of alcoholic liver disease.
Liver Transplantation: Orthotopic liver transplantation is widely used in patients with end-stage liver disease. Most patients with active alcoholic liver disease are excluded from transplantation because of ongoing alcohol abuse. In most liver transplantation programs, patients must abstain from alcohol for at least 6 months before they can be considered for transplantation, and a thorough psychosocial evaluation must demonstrate that patients have a low likelihood of reverting to alcohol abuse.
Surgical Considerations:
Patients with acute alcoholic liver disease are at high risk of developing hepatic failure following general anesthesia and major surgery. Because postoperative mortality rates are high, surgery should be avoided in the setting of acute alcoholic liver disease unless it is absolutely necessary.
Herbal Agents:
Milk thistle: Herbal agents have also been tried in alcoholic liver disease. Silymarin is the active ingredient in milk thistle, is a member of the flavonoids. The precise mechanism of its hepatoprotective mediation is not known, but it is probably related to its antioxidant properties.