Alcoholic Liver Disease from the Clinical Point of View

Abstract

Liver disease is responsible for more than 55% of deaths resulting from alcohol abuse, while the prevalence of alcoholic liver disease (ALD) is closely correlated with per capita alcohol consumption. ALD represents a wide range of histological changes ranging from simple steatosis to heavier forms of liver injury including alcoholic hepatitis, cirrhosis and/or concurrent development of hepatocellular carcinoma. These alterations of the hepatic parenchyma do not necessarily reflect distinct stages of liver disease progression, but rather a continuum relating to histological changes that may be observed simultaneously in the same patient. The fact that only 35% of patients with heavy alcohol abuse develop advanced stages of liver disease, suggests that in the pathogenesis of ALD a number of other factors are involved that include gender, obesity, drinking patterns, dietary factors, non-sex-linked genetic factors and smoking. Also, long-term drinking can affect synergistically with hepatitis B or C and/or the human immunodeficiency virus, the non-alcoholic fatty liver disease and hepatic disorders such as hemochromatosis. The diagnosis of ALD is based on a combination of findings, including the history of significant alcohol consumption, the clinical evidence of the concomitant liver injury supported by the resultant histological, imaging and laboratory findings. A beneficial effect of alcoholic hepatitis treatment with corticosteroids is observed in patients with encephalopathy or with poor prognosis based on the various grading and prognostic systems of gravity, while the harmful effect is prominent in patients with milder disease, as they manifest an increased risk of infections compared with those not receiving corticosteroids. In patients with alcoholic hepatitis that cannot take corticosteroids for various reasons and in those with the onset of functional renal failure (“hepatorenal syndrome”), use of pentoxifylline is recommended.