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cholestatic liver disease and in cholestasis of pregnancy, but the mechanism of action is not clear. After oral administration, there is an increase in the concentration of ursodeoxycholic acid in bile acids and a reduction in the amount of more hydrophobic and potentially toxic bile acids (cholic and chenodeoxycholic acids). It also increases bile acid output and bile flow. Immunological effects may also contribute with reduced abnormal expression of antigens on hepatocytes and a decline in immunoglobulin and cytokine production.
Following administration, ursodeoxycholic acid is solubilised by other bile acids and absorbed with about 50% taken up by the liver and secreted as conjugates into bile. These conjugates are absorbed from the distal ileum and compete with endogenous bile acids for active transport and undergo enterohepatic circulation. Nonabsorbed ursodeoxycholic acid conjugates are deconjugated by colonic bacteria and excreted in the faeces.
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