EASL Clinical Practice Guidelines

Alcoholic cirrhosis

Clinical course

Progressive ALD can lead to alcoholic cirrhosis, which is defined by the occurrence of extensive fibrosis and regenerative nodules. In some patients, alcohol abuse coexists with other known causes of liver disease, such as hepatitis C and B virus infection, as an etiological agent of liver cirrhosis. As with other etiologies, patients with alcoholic cirrhosis are prone to develop clinical decompensations due to portal hypertension and liver failure and are at risk for developing HCC [210]. The clinical course of alcoholic cirrhosis is influenced by the pattern of alcohol intake. Thus, periods of excessive alcohol intake can lead to superimposed ASH and the subsequent clinical exacerbations, while prolonged abstinence can compensate previously complicated cirrhosis.

Population-based studies indicate that only about one third of patients with alcoholic cirrhosis are hospitalized before decompensation [[210], [211]], and in the first year thereafter these patients have an approximate 20% risk of developing ascites, a 6% risk of variceal bleeding, and a 4% risk of hepatic encephalopathy [[211], [212]]. Ascites is typically the first complication [[211], [212]], but other complications such as jaundice, variceal bleeding, and hepatic encephalopathy are also prevalent [[70], [211], [212]]. Importantly, patients with alcoholic cirrhosis are particularly prone to bacterial infections [213]. The incidence of HCC among patients with alcoholic cirrhosis ranges range from 7% to 16% [214] after 5 years to as much as 29% after 10 years. Therefore, screening for HCC should be performed as recommended for any patient with liver cirrhosis. Importantly, patients with alcoholic cirrhosis should be screened for alcohol-induced damage in other organs including the heart (alcoholic myocardiopathy), kidney (IgA-induced nephropathy), nervous system (central and peripheral involvement), and the pancreas (chronic pancreatitis). Importantly, in patients with impaired cognitive function, the existence of alcoholic dementia, withdrawal syndrome, and Wernike's encephalopathy should be ruled out. Patients with alcoholic cirrhosis are often malnourished. A careful clinical and analytical evaluation of the nutritional status is advised and proper nutrition should be ensured. In severe cases, the help of a dietitian is recommended.

Population-based studies following patients from hospital diagnosis of alcoholic cirrhosis have shown 1- and 5-year mortality risks around 30% and 60%, respectively [211]. Among the complications defining decompensated cirrhosis, hepatic encephalopathy is associated with the highest mortality [211]. In most centers, the MELD is used to established prognosis and to list patients for OLT. In the intensive care unit setting, the mortality of patients with alcoholic cirrhosis is better predicted with scoring systems developed for intensive care than with systems developed for liver disease [215].

The persistence of alcohol abuse after diagnosis is the most important factor increasing the risk of complications and death [216]. In these patients, the development of superimposed episodes of ASH carries a bad prognosis. Finally, cigarette smoking has been identified as a predictor of mortality [217], and co-morbid diseases increase the risk of both cirrhosis-related and not cirrhosis-related death [218].


Current clinical management of alcoholic cirrhosis focuses on alcohol abstinence, aggressive nutritional therapy rich in calories and proteins [219], and primary and secondary prophylaxis of cirrhosis complications. The management of clinical decompensations is hampered by poor patient compliance, especially in those who are actively drinking. Alcohol abuse should be treated by addiction specialists and include motivational therapy and anti-craving drugs. In these patients, the use of disulfiram is not recommended due to potential hepatotoxicity. Recent studies suggest that baclofen is useful and safe in patients with advanced liver disease [61].

Several specific therapies have been tested in patients with alcoholic cirrhosis including S-adenosyl-l-methinonine (SAMe), propylthiouracil, colchicine, anabolic–androgenic steroids, and silymarin. These therapies have revealed no consistent beneficial effects on patient outcome.


Suggestions for future studies

  1. Further evaluation of the role of s-adenosyl methionine in alcoholic cirrhosis is needed.