Primary biliary cirrhosis (PBC) is an autoimmune liver disorder characterized by chronic, progressive cholestatic disease.
Epidemiology
Incidence – 25-27/1,000,000 in U.S.
Age – peak onset 40-50 years
Gender – F>M
Risk Factors
Presence of other autoimmune disorder
Family history of PBC
The relative risk of a family member of a first-degree relative of a PBC patient is 50- to 100-fold higher than the general population (ref. 6)
Pathophysiology
Etiology is unknown
Pathogenesis of PBC is believed to be caused by:
Defect in immune tolerance resulting in the expansion of self-mitochondrial antigen specific for T and B lymphocytes
Inappropriate immune response following environmental or infectious agent: modification of mitochondrial proteins or molecular mimicry
PBC is characterized by T-cell mediated destruction of bile duct epithelial cells resulting in loss of ducts and persistent cholestasis which may result to end-stage liver failure without treatment.
Clinical Presentation
Fatigue, pruritus, unexplained hyperlipidemia
Elevated hepatic enzymes
Associated frequently with other autoimmune disorders such as:
CREST
Sicca syndrome
Autoimmune thyroiditis
IgA deficiency
Chronic autoimmune hepatitis (AIH)
PBC and AIH have many overlapping immunologic features
Some patients may have serologic tests and histologic findings suggestive of AIH in addition to PBC
They may represent a continuum of a single disease entity
Diagnosis
Laboratory testing
PBC is strongly associated with antimitochondrial antibody (AMA), M2 type
However, M2 levels in PBC do not appear correlated with clinical activity or disease progression
Approximately 5-10% of PBC patients are AMA negative
PBC is also associated with anti-sp100 (20-30%) of patients and anti-gp210 (15-27% of patients)
Both antibodies are highly specific for PBC
Monitoring
Anti-gp210 is prognostic in PBC
Failure to see a decline with treatment increases risk of progression to end stage hepatic failure
Treatment
Medical therapy – ursodeoxycholic acid does not reduce the risk for mortality or liver transplantation
Aid in the diagnosis of patients suspected of having PBC, especially for those who are anti-mitochondrial autoantibody negative (detects autoantibody against sp100 and gp210)
Negative likelihood ratio for sp100 and gp 210 is 1.3
Additional Tests Available
Click on number for test-specific information in the ARUP Laboratory Test Directory
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Ishibashi H, Shimoda S, Gershwin ME.The immune response to mitochondrial autoantigens.Semin Liver Dis. 2005;25(3):337-346. (Link to PubMed)
Kaplan MM, Gershwin ME.Primary biliary cirrhosis.N Engl J Med. 2005;353(12):1261-1273. (Link to PubMed)
Nakamura M, Shimizu-Yoshida Y, Takii Y, Komori A, Yokoyama T, Ueki T, Daikoku M, Yano K, Matsumoto T, Migita K, Yatsuhashi H, Ito M, Masaki N, Adachi H, Watanabe Y, Nakamura Y, Saoshiro T, Sodeyama T, Koga M, Shimoda S, Ishibashi H.Antibody titer to gp210-C terminal peptide as a clinical parameter for monitoring primary biliary cirrhosis.J Hepatol. 2005;42(3):386-392. (Link to PubMed)
Parikh-Patel A, Gold E, Mackay IR, Gershwin ME.The geoepidemiology of primary biliary cirrhosis: contrasts and comparisons with the spectrum of autoimmune diseases.Clin Immunol. 1999;91(2):206-218. (Link to PubMed)
Reshetnyak VI.Concept on the pathogenesis and treatment of primary biliary cirrhosis.World J Gastroenterol. 2006;12(45):7250-7262. (Link to PubMed)
Reviewed by
Hill, Harry R., M.D. Group Medical Director, Laboratory of Immunology, ARUP Laboratories, and Executive Director of the ARUP Institute for Clinical and Experimental Pathology; Professor and Division Head, Clinical Pathology, University of Utah
Tebo, Anne E., Ph.D. Assistant Medical Director, Immunology at ARUP Laboratories; Clinical Assistant Professor, Clinical Pathology, University of Utah
Comprehensive Review: September 2007
Last Update: March 2008