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Journal ArticleDOI

Ursodeoxycholic acid in cholestatic liver disease: Mechanisms of action and therapeutic use revisited

Gustav Paumgartner, +1 more
- 01 Sep 2002 - 
- Vol. 36, Iss: 3, pp 525-531
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TLDR
Experimental evidence suggests three major mechanisms of action of UDCA, which may improve serum liver chemistries, delay disease progression to severe fibrosis or cirrhosis, and may prolong transplant‐free survival in primary biliary Cirrhosis and primary sclerosing cholangitis.
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This article is published in Hepatology.The article was published on 2002-09-01. It has received 643 citations till now. The article focuses on the topics: Ursodeoxycholic acid & Bile acid.

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Citations
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Journal ArticleDOI

Enterohepatic Bile Salt Transporters in Normal Physiology and Liver Disease

TL;DR: A key regulator of hepatocellular bile salt homeostasis is the bile acid receptor/farnesoid X receptor FXR, which activates transcription of the BSEP and OATP8 genes and of the small heterodimer partner 1 (SHP) as mentioned in this paper.
Journal ArticleDOI

Bile-acid-induced cell injury and protection

TL;DR: The major beneficial effects of treatment with ursodeoxycholic acid are protection against cytotoxicity due to more toxic BAs; the stimulation of hepatobiliary secretion; antioxidant activity, due in part to an enhancement in glutathione levels; and the inhibition of liver cell apoptosis.
Journal ArticleDOI

Herb-drug interactions: a literature review.

TL;DR: An extensive review of the literature identified reported herb-drug interactions with clinical significance, although the underlying mechanisms for the altered drug effects and/or concentrations by concomitant herbal medicines are yet to be determined.
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Intrahepatic cholestasis of pregnancy

TL;DR: The hydrophilic bile acid ursodeoxycholic acid (10–20 mg/kg/d) is today regarded as the first line treatment for intrahepatic cholestasis of pregnancy.
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The nuclear receptor SHP mediates inhibition of hepatic stellate cells by FXR and protects against liver fibrosis

TL;DR: It is established that FXR ligands might represent a novel therapeutic option to treat liver fibrosis and that SHP binds JunD and inhibits DNA binding of adaptor protein (AP)-1 induced by thrombin.
References
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Journal ArticleDOI

A multicenter, controlled trial of ursodiol for the treatment of primary biliary cirrhosis. UDCA-PBC Study Group.

TL;DR: Ursodiol is a safe and effective treatment for primary biliary cirrhosis and follow-up analysis of 95 liver-biopsy specimens showed a significant improvement in the mean histologic score and in all the characteristic histologic features except fibrosis only in the group given ursodiol.
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Combined analysis of randomized controlled trials of ursodeoxycholic acid in primary biliary cirrhosis

TL;DR: Survival free of liver transplantation was significantly improved in the patients treated with UDCA compared with the patients originally assigned to placebo, and long-term UDCA therapy improves survival free of Liver transplantation in patients with moderate or severe disease.
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Toxic bile salts induce rodent hepatocyte apoptosis via direct activation of Fas

TL;DR: Data suggest that GCDC-induced hepatocyte apoptosis involves ligand-independent oligomerization of Fas, recruitment of FADD, activation of caspase 8, and subsequent activation of effector proteases, including downstream caspases and cathepsin B.
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Ursodiol for Primary Sclerosing Cholangitis

TL;DR: Ursodiol (ursodeoxycholic acid) benefits patients with primary biliary cirrhosis, another cholestatic liver disease, and well-documented primary sclerosing cholangitis in a randomized, double-blind study comparing ursodiol with placebo.
Journal ArticleDOI

Ursodeoxycholic acid in the treatment of primary biliary cirrhosis

TL;DR: UDCA was extraordinarily safe and well tolerated, and its use was associated with delayed progression of the disease as defined in this study, however, the lack of effects on symptoms, histology, and the need for liver transplantation or survival indicate that further evaluation is necessary.
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