Alcoholic fatty liver (alcoholic hepatosteatosis)

Lipids that accumulate in alcoholic fatty liver may come from many sources: diet, adipose tissue, hepatic synthesis of novo from glucide. Predominant source depends on the chronic or acute consumption of alcohol, lipid content in diet. In alcoholics, the majority of the lipids in the liver are derived from diet and from oxidation of fatty acids. Accumulation of lipids during the chronic consumption of alcohol does not continue forever, modification of the redox state of the whole liver will slow down during the chronic consume of the alcohol.

Morphopathologicallys teatosis represents the presence of the lipid in more than 5% of hepatocyte. Macroscopically, the liver is enlarged, firm with a yellowish color. Microscopically it can be observed an increase in fat deposits, later intrahepatic cholestasis, migh appear.
Clinically an asymptomatic hepatomegaly is observed and sometimes stigmas of chronic liver disease like contraction of Dupuytren, testicular atrophy, palmar erithrosis, sidernavy, and gynecomastia. Later, fatigue, cachexia, fever, anorexia, nausea, vomiting, jaundice, painful hepatomegaly, splenomegaly and ascites might appear. Majority of this is associated with alcoholic hepatitis.
Positive diagnosis is done by histological examination and imagistic evidence by doing an ultrasound examination. A particular form is the focal steatosis, which makes it difficult to differentiate with a tumoral formation.
Complications that might appear in patients with alcoholic steatosis are sudden death through fatty embolida, alcoholic cessation syndrome or hypoglicemia.
Treatment consits in stopping of alcohol consumption, correction of malnutrition and drugs so called hepatoprotectors (slimarine and mainly vitamin B complex) with disputable efficiency.