[Various biochemical mechanisms of alcoholic liver cirrhosis].

The authors describe the correlations between chronic alcoholism and cirrhosis known not only from clinical observations but also from retrospective assessment of liver biopsy. However, the mechanism of hepatocellular injury by ethanol remains still unclear. It seems that three hypotheses prevail presently: 1) acetaldehyde which is a product of ethanol oxidation in the liver forms with certain biogenic amines alkaloids of the type of salsolinol causing cirrhosis, 2) ethanol or/and acetaldehyde catalyse the development of free radicals which may induce liver damage through lipid peroxides etc, 3) acetaldehyde formed during ethanol oxidation is released into blood or tissue fluids where it binds to albumins with formation of cytotoxic complexes leading to cirrhosis.

Disturbances of fat, carbohydrate, magnesium and protein balance in liver diseases.

40 patients with infectious hepatitis, 25 with chronic aggressive hepatitis, 25 with compensated liver cirrhosis, and 10 with decompensated liver cirrhosis were submitted to examination. The following abnormalities depending upon the stage and severity of hepatic diseases were found: a) disturbances of total lipids, cholesterol, phospholipids, beta-lipoproteids, glycerin, glycerides and neutral fats concentrations; b) marked disorders of glucose tolerance as indicated by the difference between plasma and erythrocyte glucose levels increasing in proportion to the degree of liver damage; c) a fall in plasma and erythrocyte magnesium reflecting the degree of hepatic parenchyma damage; d) a decrease of the albumin/gamma-globulin ratio in proportion to the degree of the impairment of hepatic cells. The presented fat, carbohydrate, magnesium and protein balance indices yield better criterions for the differential diagnostics of hepatic diseases than the routine investigations, and they also make possible objective prognosis.