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Proposed therapies in primary biliary cholangitis.
- Source :
-
Expert review of gastroenterology & hepatology [Expert Rev Gastroenterol Hepatol] 2016; Vol. 10 (3), pp. 371-382. Date of Electronic Publication: 2016 Jan 06. - Publication Year :
- 2016
-
Abstract
- Primary biliary cholangitis (PBC), previously known as primary biliary cirrhosis, is a model autoimmune disease with chronic cholestasis characterized by the hallmark of anti-mitochondrial antibodies and treated with ursodeoxycholic acid (UDCA). However, approximately 20-40% of patients incompletely respond to UDCA and have an increased risk of disease progression. Although there have been significant advances in the immunobiology of PBC, these have yet to be translated into newer therapeutic modalities. Current approaches to controlling the immune response include broad immunosuppression with corticosteroids as well as targeted therapies directed against T and B cells. In contrast, ameliorating cholestasis is the focus of other therapies in development, including obeticholic acid. In this article the authors will discuss ongoing clinical trials and, in particular, the rationale for choosing agents that may effectively target the aberrant immune response.
- Subjects :
- Animals
Bile Acids and Salts metabolism
Biliary Tract immunology
Biliary Tract metabolism
Biological Products therapeutic use
Cholagogues and Choleretics adverse effects
Humans
Immunosuppressive Agents adverse effects
Liver Cirrhosis, Biliary diagnosis
Liver Cirrhosis, Biliary immunology
Liver Cirrhosis, Biliary metabolism
Stem Cell Transplantation
Treatment Outcome
Biliary Tract drug effects
Cholagogues and Choleretics therapeutic use
Immunosuppressive Agents therapeutic use
Liver Cirrhosis, Biliary drug therapy
Subjects
Details
- Language :
- English
- ISSN :
- 1747-4132
- Volume :
- 10
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Expert review of gastroenterology & hepatology
- Publication Type :
- Academic Journal
- Accession number :
- 26577047
- Full Text :
- https://doi.org/10.1586/17474124.2016.1121810