Also Known As: Ursodeoxycholic acid , Ursodiol, Ursodeoxycholic acid, Actigall
Primary bile acids are produced by the liver and stored in the gall bladder. When secreted into the intestine, primary bile acids can be metabolized into secondary bile acids by intestinal bacteria. Primary and secondary bile acids help the body digest fats. Ursodeoxycholic acid helps regulate cholesterol by reducing the rate at which the intestine absorbs cholesterol molecules while breaking up micelles containing cholesterol. Because of this property, ursodeoxycholic acid is used to treat (cholesterol) gallstones non-surgically.
While some bile acids are known to be colon tumor promoters (e.g. deoxycholic acid), others such as ursodeoxycholic acid are thought to be chemopreventive, perhaps by inducing cellular differentiation and/or cellular senescence in colon epithelial cells.
Ursodeoxycholic acid has also been shown experimentally to suppress immune response such as immune cell phagocytosis. Prolonged exposure and/or increased quantities of systemic (throughout the body, not just in the digestive system) ursodeoxycholic acid can be toxic.
As a pharmaceutical
Ursodeoxycholic acid goes by the trade names Actigall, Ursosan, Egyurso( Egyphar Egypt), Urso, and Urso Forte. In Italy and Switzerland, it is marketed under the name Deursil. In Mexico it is marketed in capsules of 250 mg under the name Coric by Mexican pharmaceutical Landsteiner Scientific.
The drug reduces cholesterol absorption and is used to dissolve (cholesterol) gallstones in patients who want an alternative to surgery. However, if the patient stops taking it, the gallstones tend to recur if the condition that gave rise to their formation does not change; for this reason, it has not supplanted surgical treatment by cholecystectomy.
A Cochrane review to evaluate if ursodeoxycholic acid has any beneficial effect in primary biliary cirrhosis patients included 16 randomized clinical trials with a total of 1447 patients. The primary outcome measures were mortality and mortality or liver transplantation. Although treatment with ursodeoxycholic acid showed a reduction in liver biochemistry, jaundice, and ascites, it did not decrease mortality or liver transplantation.
In absence of biochemical response to 13-15mg/kg/day ursodeoxycholic acid, its use is associated with a risk of 20% hepatocellular carcinoma in patients with primary biliary cirrhosis in 15 years.
In double the recommended daily dose ursodeoxycholic acid reduces elevated liver enzyme levels in patients with primary sclerosing cholangitis, but its use was associated with an increased risk of serious adverse events (the development of cirrhosis, varices, death or liver transplantation) in patients who received ursodeoxycholic acid compared with those who received placebo). After adjustment for baseline stratification characteristics, the risk was 2.1 times greater for death,transplantation, or minimal listing criteria in patients on ursodeoxycholic acid than for those on placebo (P = 0.038). Serious adverse events, were more common in the ursodeoxycholic acid group than the placebo group (63% versus 37% [P < 0.01])).
Research by the Imperial College London has produced promising results in the treatment of arrhythmia, both in patients who have suffered a heart attack and in foetuses, by using ursodiol to change the electrical properties of myofibroblast cells. Myofibroblasts disrupt the transmission of electrical signals controlling heart rhythm.