Obeticholic acid in primary biliary cholangitis: where we stand.

Abstract

PURPOSE OF REVIEW:

This review will summarize the use of obeticholic acid (OCA) in treatment of primary biliary cholangitis (PBC). It seeks to discuss the mechanism of action, evidence for use, appropriate clinical use, and common adverse effects of OCA.

RECENT FINDINGS:

PBC is a chronic, progressive cholestatic liver disease that is a chronic progressive that may lead to end-stage liver disease and need for liver transplantation. Ursodeoxycholic acid (UDCA) has been the mainstay of therapy for PBC for decades. Recent research has led to the discovery that bile acids act as hormones and have many effects, one of which is activating the farnesoid X receptor (FXR). Activation of FXR leads to decreased bile acid synthesis, inflammation, and fibrosis of the liver. OCA is a highly potent FXR agonist.

SUMMARY:

Several clinical trials demonstrated that OCA treatment in PBC led to a significant decrease in serum alkaline phosphatase, a marker for long-term survival. The US FDA-approved OCA in 2016, which led to incorporation of OCA into current guidelines as a second-line treatment for PBC. The most clinically relevant adverse effect of OCA is dose-related pruritus. We review the role of OCA and current guidelines in treatment of PBC.

• Authors: Vignan Manne, Kris V Kowdley
• Journal: Current opinion in gastroenterology (Curr Opin Gastroenterol) Vol. 35 Issue 3 Pg. 191-196 (05 2019) ISSN: 1531-7056 [Electronic] United States
• PMID: 30844895 (Publication Type: Journal Article, Review)

Chemical References

• Cholesterol, HDL
• Receptors, Cytoplasmic and Nuclear
• obeticholic acid
• farnesoid X-activated receptor
• Chenodeoxycholic Acid

Topics

• Chenodeoxycholic Acid (analogs & derivatives, therapeutic use)
• Cholesterol, HDL (blood)
• Dose-Response Relationship, Drug
• Drug Labeling
• Dyslipidemias (blood, chemically induced)
• Humans
• Liver Cirrhosis, Biliary (drug therapy, metabolism)
• Nasopharyngitis (chemically induced)
• Pruritus (chemically induced)
• Receptors, Cytoplasmic and Nuclear (agonists, metabolism)
• Treatment Outcome