Efforts to explain the apparent association between alcoholic liver disease and pigment gallstones have, to date, resulted in conflicting conclusions. While some clinical studies suggest hemolysis as the major pathogenetic factor other human and laboratory investigations describe increases in biliary pigment occurring in the absence of detectable hemolysis. In the present acute experiments various ethanol solutions ranging from 25 to 50% (v/v) were infused into miniswine to determine their effects on free hemoglobin in serum and total and unconjugated bilirubin in bile. Rapid and parallel increases in serum ethanol and serum hemoglobin levels were noted. Gradual and reversible increases in unconjugated and total bilirubin were observed after 1 hr. For unconjugated bilirubin the peak levels ranged from two times baseline levels at 25% (v/v) to 12 times baseline levels at 50%. When maximum values of hemoglobin and unconjugated bilirubin were compared in all experiments a strong positive correlation was confirmed. These findings suggest that the acute intravenous administration of ethanol causes intravascular hemolysis over a wide range of concentrations and results in the secretion of significant levels of bilirubin into bile. The role of this mechanism in pigment cholelithiasis remains to be determined.
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