Vassilios A Sevastianos and Spyros P Dourakis
Liver disease is responsible for more than 55% of deaths resulting from alcohol abuse, and the prevalence of alcoholic liver disease (ALD) is closely correlated with per capita alcohol consumption. ALD represents a broad range of histological changes ranging from simple steatosis to heavier forms of liver injury, including alcoholic hepatitis (AH), cirrhosis, or the parallel development of hepatocellular carcinoma (HCC). These alterations of the hepatic parenchyma are not necessary to reflect distinct stages of the liver disease progression but rather a continuum relating histological changes that may be observed simultaneously in the same patient.
The fact that only 35% of patients with substantial alcohol abuse develop advanced stages of liver disease suggests that the pathogenesis of ALD involves many other factors 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 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, and the support of the clinical case from the resultant histological, imaging, and laboratory findings.
The beneficial effect of treating AH with corticosteroids occurs in patients with encephalopathy or with poor prognosis, based on the various grading and prognostic systems of gravity, while its harmful effect is evident in patients with milder disease as they manifest an increased risk of infections compared with those not receiving corticosteroids. In patients with alcoholic hepatitis, who cannot take corticosteroids for various reasons and in those with the onset of functional renal failure (hepatorenal syndrome), the use of pentoxifylline is recommended.