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Remission Induction of Primary Biliary Cholangitis-autoimmune Hepatitis Overlap Syndrome

2016-10-19 02:38:21 | BioPortfolio

Summary

Biochemical response of primary biliary cholangitis-autoimmune hepatitis overlap syndrome induced by ursodeoxycholic acid only or combination therapy of immunosuppressive agents

Study Design

Allocation: Randomized, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Parallel Assignment, Masking: Open Label, Primary Purpose: Treatment

Conditions

Hepatitis, Autoimmune

Intervention

Ursodeoxycholic acid combination of immunosuppressive agents, Ursodeoxycholic Acid

Location

West China Hospital
Chengdu
Sichuan
China
610041

Status

Not yet recruiting

Source

West China Hospital

Results (where available)

View Results

Links

Published on BioPortfolio: 2016-10-19T02:38:21-0400

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Efficacy and Safety Study of Ursodeoxycholic Acid to Treat Chronic Hepatitis C

This study is a 24-week multicenter, randomized, double-blind control trial with ursodeoxycholic acid (UDCA) in patients with chronic hepatitis C in Japan. The primary objectives of this s...

Ursodeoxycholic Acid for Rhegmatogenous Retinal Detachment

20 patients presenting a rhegmatogenous retinal detachment with more than 4 days of duration will be prospectively included. A single dose of ursodeoxycholic acid will be administered ora...

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Preventive Effect of Enoxaparin, Pentoxifylline and Ursodeoxycholic Acid to Radiation Induced Liver Toxicity

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PubMed Articles [14230 Associated PubMed Articles listed on BioPortfolio]

Ursodeoxycholic acid prevents ventricular conduction slowing and arrhythmia by restoring T-type calcium current in fetuses during cholestasis.

Increased maternal serum bile acid concentrations in intrahepatic cholestasis of pregnancy (ICP) are associated with fetal cardiac arrhythmias. Ursodeoxycholic acid (UDCA) has been shown to demonstrat...

Novel Treatment Strategies for Primary Biliary Cholangitis.

Despite the presumed immunological pathogenesis of primary biliary cholangitis, no clear or even harmful consequences have resulted from treatments designed to modify the immunological condition. Urso...

Effects of Bezafibrate on Outcome and Pruritus in Primary Biliary Cholangitis With Suboptimal Ursodeoxycholic Acid Response.

Adding fibrates improves liver biochemistries in patients with primary biliary cholangitis (PBC) and suboptimal response to ursodeoxycholic acid (UDCA). As there are no consistent data regarding the c...

Ursodeoxycholic acid inhibits the proliferation of colon cancer cells by regulating oxidative stress and cancer stem-like cell growth.

The regulation of reactive oxygen species (ROS) exists as a therapeutic target for cancer treatments. Previous studies have shown that ursodeoxycholic acid (UDCA) suppresses the proliferation of colon...

Simultaneous Determination of Ursodeoxycholic Acid and Chenodeoxycholic Acid in Pharmaceutical Dosage Form by HPLC-UV Detection.

A reversed-phase HPLC method was developed for the simultaneous determination of ursodeoxycholic acid (UDCA) and the epimeric isomer, chenodeoxycholic acid (CDCA), in their synthetic mixtures and in t...

Medical and Biotech [MESH] Definitions

An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.

Agents that increase uric acid excretion by the kidney (URICOSURIC AGENTS), decrease uric acid production (antihyperuricemics), or alleviate the pain and inflammation of acute attacks of gout.

INFLAMMATION of the LIVER in humans due to infection by VIRUSES. There are several significant types of human viral hepatitis with infection caused by enteric-transmission (HEPATITIS A; HEPATITIS E) or blood transfusion (HEPATITIS B; HEPATITIS C; and HEPATITIS D).

Animal form of fatty acid synthase which is encoded by a single gene and consists of seven catalytic domains and is functional as a homodimer. It is overexpressed in some NEOPLASMS and is a target in humans of some ANTINEOPLASTIC AGENTS and some ANTI-OBESITY AGENTS.

Compounds that interfere with FATTY ACID SYNTHASE resulting in a reduction of FATTY ACIDS. This is a target mechanism in humans of some ANTINEOPLASTIC AGENTS and ANTI-OBESITY AGENTS and of some ANTI-INFECTIVE AGENTS which interfere with CELL WALL and CELL MEMBRANE formation.

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