HEPATOTOXIC LIVER DISEASE FROM ALCOHOL ABUSE: poisoning of the liver due to the intake of large quantities of alcoholic beverages.
The main factors are the amount of alcohol consumed, the nutritional status of the patient and genetic and metabolic traits. There is usually a linear correlation between the severity of alcoholism, depending on the duration of the abuse and the amount consumed, and the development of hepatopathy, although not all those who abuse alcohol develop significant liver damage.
Alcohol is a cause of malnutrition, as it provides calories without essential food constituents, reduces appetite and causes malabsorption through a toxic action on the GI tract and on the pancreas. Malnutrition alone does not cause cirrhosis, but one or more nutritional factors can accelerate the harmful effects of alcohol.
Alcohol is a hepatotoxin whose metabolism creates profound changes in the liver cell. The different individual susceptibility (only 10-15% of alcoholics develop cirrhosis) or the increased susceptibility of women to alcoholic liver disease (even when the values are adjusted for smaller body size) indicate that other factors also come into play. One of these can be represented by the fact that in the gastric mucosa of women there is a reduced amount of alcohol dehydrogenase and, therefore, a slower metabolism. There is also a common tendency for alcoholic hepatopathy to occur in certain families. Thus, genetic factors can also be involved in alcohol metabolism, as shown by the alcohol oxidation deficiency present in some people.
Anatomo-pathological alterations of the liver associated with prolonged alcohol use range from the simple accumulation of neutral fat into hepatocytes, cirrhosis and hepatocellular carcinoma. The widely accepted idea of a sequence of alterations, hepatic steatosis-alcoholic-cirrhosis hepatitis, relate only to criteria of convenience.
Varying ways of consuming alcohol, individual susceptibility to the hepatotoxic effects of alcohol and variability of tissue damage are responsible for extremely divergent clinical situations.
In principle, symptoms may be related to the amount of alcohol consumed and the overall duration of the alcohol abuse. The first symptoms usually appear between the ages of 30 and 40 an_d the most serious problems occur around the age of 40.
Patients with hepatic steatosis are usually asymptomatic. In 33% of cases the liver is enlarged, smooth and sometimes painful. Often routine biochemical investigations are normal, with the exception of frequently elevated g-glutamyl transpeptidase (GGT). Vascular spiders and aspects of hyperestrogenism and hypoandrogenism typical of alcoholism may be evident.
Alcoholic hepatitis may be suspected on a clinical basis, but the diagnosis depends on a biopsy. Histological lesion can be observed at all clinical stages of alcoholic liver disease. Patients with alcoholic liver disease may experience asthenia, fever, jaundice, right upper abdominal quadrant pain, liver murmur, painful hepatomegaly and leukocytosis, as with patients suffering from sepsis, cholecystitis or extrahepatic mechanical obstruction of the biliary tract.
Cirrhosis may also be relatively asymptomatic. It might take on the characteristics of alcoholic hepatitis or could be dominated by complications: portal hypertension with splenomegaly, ascites, hepatorenal syndrome, hepatic encephalopathy or even hepatocellular carcinoma.
With abstinence, non-fibrotic hepatic damage can regress and, in any case, abstaining from alcohol consumption improves the survival chances of patients with alcoholic hepatitis, fibrosis and cirrhosis. The magnitude of alcoholic hepatitis appears to be determined by the degree of associated fibrosis and necrosis of liver cells.
General and nutritional support give good results over time. The use of glutathione may also prove useful.