Ursachol 250mg lupine treatment for primary bile cirrhosis (2 blisters x 10 tablets)

pharmacokinetics

Ursodeoxycholic acid normally accounts for a small percentage of the total bile acids of the human body (about 5%).

After drinking, most of Ursodeoxycholic acid is absorbed in passive diffusion path and incomplete absorption. Immediately after being absorbed, Ursodeoxycholic acid continues the metabolic process in the liver to add about 50% without liver disease. The worse the liver disease, the decreasing the metabolism.

In the liver, ursodeoxycholic acid is associated with glycine or taurine, then excreted into the bile. The conjugate substances of ursodeoxycholic acid are absorbed in the small intestine through active and passive mechanisms. Combined substances can also be separated in the ileum thanks to the intestinal enzymes, to form free ursodeoxycholic acids that can reabsorb and re -combine in the liver. Ursodeoxycholic acid is not absorbed through the colon, where most of the 7-dehydroxylate process is performed to form lithocholic acid. Some ursodeoxycholiec acids are Epimeization to form Chenodiol (CDCA) through intermediate path 7-olo.

Chenodiol continues the 7-dehydroxylate process to form lithocholic acid. These metabolites are less soluble and excreted into the feces. A small amount of lithocholic acid is reabsorbed, combined with glycine or taurin and sulfates in 3 positions in the liver. The complex is formed after the sulfate is excreted into the bile and then eliminates through the feces.

Lithocholic acid, when used for a long time for animals, bile stasis in the liver can be fatal due to liver failure in some species that cannot form sulfate complex. Ursodeoxycholic acid is 7-dehydroxylate than Chenodiol. For the same dose of moles of ursodexolic acid and chenodiol, the concentration in the stable state of lithocholic acid in bile acids is lower after using ursodeoxycholic acid compared to Chenodiol.

In humans, lithocholic acid can be sulfate. Although liver lesions are not related to Ursodeoxycholic acid treatment, reducing the amount of sulfate can be encountered in some individuals. However, the shortage has not been clearly proven and very rare, based on several thousand patients during clinical research years when using ursodeoxycholic acid.

In healthy patients, at least 70% of ursodeoxycholic acid (non -unimaginable) bind to plasma proteins. There is no information on ursodeoxycholic acid that has been associated with plasma proteins in healthy patients or in patients with primary bile cirrhosis. Ursodeoxycholic has not been determined, but a small amount of the drug is mostly distributed in bile and small intestine. Ursodeoxycholic acid is excreted mainly on the feces. When treated, the amount of drug excreted in urine increases, but the rest is less than 1% except in patients with severe cholest liver disease. When long -term use Ursodeoxycholic acid, the drug will mainly become bile and bile acid in plasma. At the dose of 13-15 mg/kg/day for long -term use, Ursodeoxycholic acid forms 30-50% bile and bile acid in plasma.

A central, random, double -blind, placeory study is conducted to evaluate the effectiveness of Ursodeoxycholic acid at 13-15 mg/kg/day, divided into 4 doses in 180 patients with primary bile cirrhosis (PBC). After studying for a double time, all patients entered the active treatment stage.

Definition defeat is defined as death, the end of the main effect of evaluating during the study, needed for liver transplantation, hyperlemen through two periods or cirrhosis, varicose veins, ascites or varicose veins, characterized by more fatigue or itching, inability to tolerate drugs, double the amount of bilirubin in serum blood and stop voluntary treatment. After 2 years of double blind treatment, the rate of failure failure decreases in the therapy group with ursodeoxycholic acid (n = 89) when compared to the placebo group (n = 91). The time failure is also significantly prolonged in the group treated with ursodeoxycholic acid does not take into account the period of tissue proliferation or basic bilirubin concentration (> 1.8 mg/dL).

Using define failure in the treatment of rules of voluntary treatment and serum bilirubin levels doubled, the period of failure is significantly lasting in the group treated with ursodooxycholic acid. When compared to the placebo group, Ursodeoxycholic acid is treated significantly improving the biochemical indicators of the liver in serum when compared to the original index including: total bilirubin, SGOT, alkaline phosphatase and IGM.

A second study conducted in Canada randomly selected 222 primary biliary cirrhosis (PBC) patients using Ursodeoxycholic acid 14 mg/kg/day or placebo, in a double blind study for 2 years. In 2 years, significant differences according to statistics between two treatment groups, with the benefits of ursodeoxycholic acid, proven below: Reduce the proportion of patients taking more drugs by 50% increase bilirubin in serum; Discount on average bilirubin, transaminase and alkaline phosphatase; Reduce the rate of failure in treatment and treatment time.

Definition of failure in treatment includes: stop research for any reason, total bilirubin concentration in serum is greater than or equal to 1.5 mg/dl or increasing the concentration equal to or 2 times greater than the basic concentration and the development of ascites or brain disease.