Alcoholic Liver Disease (ALD)



Alcohol consumption in the United Kingdom has risen dramatically over the last 50 years and there has been an associated increase in end stage liver disease (cirrhosis) secondary to alcohol. In western society the most common cause of cirrhosis is secondary to alcohol. Ten percent of hospital admissions are thought to relate in part to alcohol.  One in four deaths among men in Europe aged 15-29 years is now attributed to alcohol. There is clear documented evidence that excess alcohol consumption is responsible for increased morbidity and mortality.  ALD is the number one cause of cirrhosis in the western world.

Studies have shown a threshold level (in men this threshold is 80g/day and women 20g/day) that once exceeded over a long period of time increases the risk of liver damage. There is evidence to support the idea that total alcohol consumption over a lifetime is an important factor.  However, not all persons that exceed this threshold will develop cirrhosis, since less than 20% of men consuming more than 12 cans of beer a day for 10 year become cirrhotic.

Stages of alcoholic liver disease

The three stages of ALD are fatty liver, alcoholic hepatitis and cirrhosis. Importantly if patients with fatty change or hepatitis stop drinking the liver may return to normal in most cases. Fatty liver is due to fat cells accumulating within the liver cells. The excess fat causes inflammation within the liver cells.

Alcoholic hepatitis

Alcoholic hepatitis is a condition of fat and inflammation within the liver. Acute inflammation is located primarily in the liver cells. In addition to inflammation and associated cell death. Clinical symptoms in alcoholic hepatitis are varied; some patients may have no symptoms and others extremely ill. Mild symptoms may include anorexia, nausea, vomiting, abdominal pain and distension. More severe symptoms could be decreased consciousness, even coma. 

On examination findings will vary as well, from again mild cases with patients having normal examination, to the other extreme of patients being comatosed. The use of Glasgow alcoholic hepatitis score helps differentiate patients with mild, moderate and severe hepatitis on their admission to hospital, this tool is useful for calculating their prognosis and whether to give them steroids.


Cirrhosis is defined by fibrosis/ scarring in the liver. Patients with cirrhosis can often have normal clinical examinations and no symptoms, due to their disease being stable, however, over time they may gradually deteriorate leading to them developing signs of decompensation. The signs of decompensation include jaundice, ascites and encephalopathy.

Once these features develop they may resolve especially if they occurred as a result of sepsis or recent alcohol binge; though in some patients with end stage cirrhosis they remain in this decompensated state. The Child’s grading of cirrhosis assesses certain parameters and is a well validated tool for assessing mortality of patients with liver disease. The stable compensated patient, who may have stopped drinking, may have no clinical signs.


Management of Fatty liver

Management of patients with fatty liver is centred on assisting them in stopping drinking. It is well documented that patients who stop drinking at an early stage of the disease will return to having a normal liver.  Self help booklets are of some use and a further appointment with their primary care physician a couple of weeks after consultation would be beneficial. The primary care team is ideally suited to provide long term support. In addition other relevant lifestyle advice should be offered.

Management of Alcoholic Hepatitis (AH)

Management of alcoholic hepatitis is dependent on the clinical presentation of the patient. As stated previously some patients will be completely asymptomatic in this cohort it is important that they are advised to stop drinking and appropriate access to the relevant services made available. However in more severe cases admission to hospital is often required.
Other markers for assessing prognosis in alcoholic hepatitis include the Glasgow Alcoholic Hepatitis score, which has been well validated for assessing severity and prognosis.

Treatment of an episode of acute AH is aimed at supporting the various systems and managing the complications of ALD. Steroids have been used in patients with alcoholic hepatitis for many years; however their effect is thought to be limited. The rationale for steroid use is to decrease both the immune response and inflammatory responses. In moderate to severe alcoholic hepatitis there is evidence to support the use of steroids.

Malnutrition is associated with increased mortality in patients with ALD; patients may be deficient in nutrients (zinc, folate) as well a general protein and calories. The severity of liver disease has been associated with the level of malnutrition. Vitamin deficiency is common amongst persons with ALD as well as alcoholics without ALD. The cause of deficiency is related to a variety of factors, including maldigestion and also decreased absorption via the intestine.


Alcoholic liver disease encompasses a wide spectrum of liver disease, in which the first stage is usually fully reversible on cessation of alcohol intake. The outcome in patients with cirrhosis secondary to ALD is still poor especially if patients continue to drink. Advances in medical therapies targeted at managing ALD and its systemic complications are improving, however, the best management would be prevention of development of alcoholic liver disease.

To achieve this public awareness to the problem of ALD needs to be improved. More structured support to alcoholics and people who abuse alcohol. If patients wish to continue drinking then it is important they maintain adequate nutritional status. Unfortunately, alcohol induced cirrhosis has increased over the last fifty years.