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Increased incidence of antiretroviral drug discontinuation among patients with viremic hepatitis C virus coinfection and high hyaluronic acid, a marker of liver fibrosis

Grint, Daniela; Peters, Larsb,c; Rockstroh, Juergen K.d; de Wit, Stephanee; Mitsura, Victor M.f; Knysz, Brygidag; Pedersen, Courth; Kirk, Oleb,c; Lundgren, Jens D.b,c; Mocroft, Amandaafor EuroSIDA in EuroCoord

doi: 10.1097/QAD.0000000000000069
Epidemiology and Social

Background: Most antiretroviral drugs are metabolized by the liver; hepatic disease or liver damage as a result of hepatitis C virus (HCV) could impair this metabolism leading to an increased risk of drug toxicity. This study aimed to determine the risk of antiretroviral drug discontinuation among HCV/HIV coinfected patients.

Methods: EuroSIDA patients taking combination antiretroviral therapy were included. Poisson regression identified factors associated with antiretroviral treatment discontinuation.

Results: A total of 9535 HIV-positive patients with known HCV status were included (6939 HCVAb-negative; 2596 HCVAb-positive at baseline). Viremic HCV infection was associated with a 44% increased risk of antiretroviral drug discontinuation compared with aviremic infection [adjusted incidence rate ratio, aIRR: 1.44 (95% confidence interval, CI 1.22–1.69)]; this relationship was largest among nonnucleoside reverse transcriptase inhibitors [aIRR: 1.59 (95% CI 1.18–2.14)]. In the subset of 935 HIV-positive patients also HCV-positive or HBV-positive with plasma hyaluronic acid measured, hyaluronic acid more than 100 ng/ml was associated with a 37% increased risk of antiretroviral drug discontinuation [aIRR: 1.37 (95% CI 1.08–1.73) vs. hyaluronic acid ≤100 ng/ml] and the effect of HCV viremia became nonsignificant; the largest drug association was seen for protease inhibitors [aIRR: 1.40 (95% CI 1.04–1.89)].

Conclusion: HCV viremia and high levels of hyaluronic acid predict antiretroviral drug discontinuation. Evidence was also found to suggest a link between impaired liver function and protease inhibitor toxicity.

aDepartment of Infection and Population Health, University College London, London, UK

bCopenhagen HIV Programme, University of Copenhagen

cDepartment of Infectious Diseases, Rigshospitalet, Copenhagen, Denmark

dDepartment of Medicine I, University of Bonn, Bonn, Germany

eDepartment of Infectious Diseases, Saint-Pierre Hospital, Brussels, Belgium

fInfectious Diseases Department, Gomel State Medical University, Gomel, Belarus

gDepartment of Infectious Diseases, Medical University, Wroclaw, Poland

hInfectious Diseases Department, Odense University Hospital, Odense, Denmark.

Correspondence to Daniel Grint, HIV Epidemiology & Biostatistics Group, Research Department of Infection and Population Health, UCL, Royal Free Campus, Rowland Hill Street, London NW3 2PF, UK. Tel: +44 20 7794 0500x34684; e-mail: d.grint@ucl.ac.uk

Received 14 June, 2013

Revised 29 August, 2013

Accepted 5 September, 2013

This work was presented in part at the 20th Conference on Retroviruses and Opportunistic Infections (CROI), Atlanta, Georgia, USA in March 2013, abstract number P-158.

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