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Predictors of the change in bilirubin levels over twelve weeks of treatment with atazanavir

Aoife G Cotter125*, Aisling Brown2, Gerard Sheehan23, John Lambert23, Caroline A Sabin4 and Patrick WG Mallon12

Author Affiliations

1 HIV Molecular Research Group, School of Medicine & Medical Science, University College Dublin, Dublin, Ireland

2 Department of Infectious Diseases, Mater Misericordiae University Hospital, Dublin, Ireland

3 School of Medicine & Medical Science, University College Dublin, Dublin, Ireland

4 Research Department of Infection & Population Health, UCL Medical School, London, UK

5 Clinical Research Centre, Mater Misericordiae University Hospital, Eccles St., Dublin 7, Ireland

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AIDS Research and Therapy 2013, 10:13  doi:10.1186/1742-6405-10-13

Published: 16 May 2013

First paragraph (this article has no abstract)

Atazanavir (ATV) is a protease inhibitor used in the treatment of HIV infection. It is useful in patients on methadone replacement therapy as its once daily dosing facilitates co-administration with methadone and, unlike the non-nucleoside reverse transcriptase inhibitor, efavirenz, it does not accelerate the metabolism of methadone via induction of cytochrome P450 enzymes [1]. ATV is associated with unconjugated hyperbilirubinaemia in 6-40% of patients, overt jaundice in 7-8% and discontinuation in up to 2% [2,3]. The pathophysiology of ATV-hyperbilirubinaemia is analogous to Gilbert’s syndrome; ATV competitively inhibits UDP-glucuronyltransferase (UGT) enzymes leading to reduced glucuronidation of bilirubin and increased levels of unconjugated bilirubin [4,5]. Patients with the UGT1A1*28 genotype are particularly, but not exclusively, vulnerable [6,7]. Our study aimed to determine the clinical predictors of ATV-associated hyperbilirubinaemia in our patient population.

Atazanavir; Unconjugated hyperbilirubinaemia; Bilirubin; Liver; Hepatitis C