Tuberculosis Is Not a Risk Factor for Primary Biliary Cirrhosis: A Review of the Literature

Author:

Smyk Daniel S.1,Bogdanos Dimitrios P.123,Pares Albert4,Liaskos Christos2,Billinis Charalambos5,Burroughs Andrew K.6,Rigopoulou Eirini I.3

Affiliation:

1. Institute of Liver Studies, King’s College Hospital and Division of Transplantation Immunology and Mucosal Biology, School of Medicine, King’s College London, London SE5 9RS, UK

2. Cellular Immunotherapy and Molecular Immunodiagnostics, Center for Research and Technology Thessaly, 41222 Larissa, Greece

3. Department of Medicine, University Hospital of Larissa, University of Thessaly School of Medicine, 41110 Larissa, Greece

4. Liver Unit, Hospital Clínic de Barcelona, IDIBAPS, CIBERehd, University of Barcelona, 08036 Barcelona, Spain

5. Faculty of Veterinary Science, University of Thessaly, 43100 Karditsa, Greece

6. The Royal Free Sheila Sherlock Liver Centre, Royal Free Hospital and Department of Surgery, University Collegue London, London NW32QG, UK

Abstract

Primary biliary cirrhosis (PBC) is a progressive cholestatic liver disease characterised serologically by cholestasis and the presence of high-titre antimitochondrial antibodies, and histologically by chronic nonsuppurative cholangitis and granulomata. As PBC is a granulomatous disease andMycobacterium tuberculosisis the most frequent cause of granulomata, a causal relation between tuberculosis and PBC has been suggested. Attempts to find serological evidence of PBC-specific autoantibodies such as AMA have been made and, conversely, granulomatous livers from patients with PBC have been investigated for molecular evidence ofMycobacterium tuberculosis. This paper discusses in detail the reported data in support or against an association betweenMycobacterium tuberculosisinfection and PBC. We discuss the immunological and microbiological data exploring the association of PBC with exposure toMycobacterium tuberculosis. We also discuss the findings of large epidemiologic studies investigating the association of PBC with preexistent or concomitant disorders and the relevance of these findings with tuberculosis. Genome-wide association studies in patients with tuberculosis as well as in patients with PBC provide conclusive hints regarding the assumed association between exposure to this mycobacterium and the induction of PBC. Analysis of these data suggest thatMycobacterium tuberculosisis an unlikely infectious trigger of PBC.

Publisher

Hindawi Limited

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