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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

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PubMed Articles [14316 Associated PubMed Articles listed on BioPortfolio]

Novel Treatment Strategies for Primary Biliary Cholangitis.

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Nor-Ursodeoxycholic Acid as a Novel Therapeutic Approach for Cholestatic and Metabolic Liver Diseases.

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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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