Hyaluronic acid levels predict increased risk of non-AIDS death in hepatitis-coinfected persons interrupting antiretroviral therapy in the SMART study

Lars Peters, Jacqueline Neuhaus, Amanda Mocroft, Vincent Soriano, Jur̈gen Rockstroh, Gregory Dore, Massimo Puoti, Ellen Tedaldi, Bonaventura Clotet, Bernd Kupfer, Jens D. Lundgren, Marina B. Klein

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Background: In the SMART study, HIV-viral-hepatitiscoinfected persons were, compared with HIV-monoinfected persons, at higher risk of non-AIDS death if randomized to the antiretroviral therapy (ART) interruption strategy. We hypothesized that a marker of liver fibrosis, hyaluronic acid (HA), would be predictive of development of non-AIDSrelated outcomes in coinfected participants in the SMART study. Methods: All participants positive for HCV RNA or hepatitis B surface antigen (HBsAg) and with stored plasma samples were included (n=675). Plasma samples were tested for HA (normal range 0-75 ng/ml) at baseline and months 6, 12 and 24 during follow-up in the drug conservation (DC; interrupt ART until CD4 + T-cell count &λτ;250) group and the viral suppression (VS; continued use of ART) group. Time to non-AIDS death was investigated using Kaplan-Meier analysis. Results: Overall, 52 (31 in DC and 21 in VS) coinfected participants died during follow-up. Coinfected participants who were randomized to The DC group with baseline HA&γτ;75 ng/ml had a cumulative risk of non-AIDS death of 24.6% after 36 months of follow-up compared with 9.3% for participants randomized to the VS group (P=0.005), while the cumulative risk for coinfected participants with HA&λε;75 ng/ml was 4.1% (DC) and 4.7% (VS; P=0.76). The change in HA from baseline to month 24 was 8.3 ng/ml and 4.7 ng/ml in the DC and VS group (P=0.56), respectively. Conclusions: Interruption of ART was particularly unsafe in HIV-hepatitis-coinfected individuals if plasma HA was increased. HA changed very little during follow-up and was not influenced by differences in CD4 + T-cell count or HIV viral load.

Original languageEnglish (US)
Pages (from-to)667-675
Number of pages9
JournalAntiviral Therapy
Volume16
Issue number5
DOIs
StatePublished - 2011

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