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Pharmacology: Pharmacodynamics: The mechanism of ursodeoxycholic acid is anticholelithic action is not completely understood, it is known that when administered orally ursodeoxycholic acid is concentrated in bile and decreases biliary cholesterol saturation by inhibiting its intestinal absorption. The reduced cholesterol saturation permits the gradual solubilization of cholesterol from gallstones, resulting in their eventual dissolution.
Ursodeoxycholic acid increases bile flow. In chronic cholestatic liver disease, ursodeoxycholic acid appears to reduce the detergent properties of the bile salts, thus reducing their cytotoxicity. Also, ursodeoxycholic acid may protect liver cells from the damaging activity of toxic bile acids (e.g., lithocholate, deoxycholate, and chenodeoxycholate), which increase in concentration in patients with chronic liver disease.
Pharmacokinetics: Ursodeoxycholic acid is absorbed from the small bowel (about 90% of dose).
Ursodeoxycholic acid is extensively bound to plasma proteins.
Hepatic (first-pass hepatic clearance). Exogenous ursodeoxycholic acid is metabolized in the liver to its taurine and glycine conjugates. The resulting conjugates are secreted into bile.
Time to peak concentration is 1 to 3 hour.
The half life of administered ursodeoxycholic acid is 3.5-5.8 days.
The excretion of ursodeoxycholic acid is primarily fecal; very small amounts are excreted into urine. Small amount of unabsorbed ursodeoxycholic acid passes into the colon where it undergoes bacterial degradation (7-dehydroxylation); resulting lithocholic acid is partly absorbed from the colon but is sulfated in the liver and rapidly eliminated in the feces as the sulfolithocholyl glycine or sulfolithocholyl taurine conjugate.
