Preoperative use of raltegravir-containing regimen as induction therapy: very rapid decline of HIV-1 viral load

Abstract

Known HIV infection and surgery is still a combination that raises dilemmas. Despite safety precautions, occupational blood exposure cannot be completely prevented [1]. To ensure optimal safety for the operating team, we attempt to maximally suppress the viral load before surgery in elective, high-risk surgical interventions (cardiothoracic and orthopedic surgery) [2]. Unfortunately, there are many cases in which surgery is urgent, and there is too little time to achieve complete viral suppression. Faster viral suppression has been observed with newly introduced antiretroviral drugs. Raltegravir is an HIV-1 integrase inhibitor that strongly inhibits viral replication and has been registered recently. As data from phase 2 trials [3,4] and mathematical models [5] have shown very rapid decline in viral load (approximately 2 log10 by week 2), we decided to use raltegravir as a novel addition to the standard regimen to achieve rapid viral suppression before performing surgery. We report two cases in which we applied this strategy in antiretroviral therapy-naive patients who did not have any drug resistance. The first patient is a 46-year-old antiretroviral-naive Hispanic man with an HIV-1 infection since 2004. The patient was admitted with a Streptococcus pneumoniae meningitis and endocarditis, with massive mitral valve and tricuspid valve insufficiency. Despite regular treatment with corticosteroids and high-dose penicillin, a mitral or tricuspid valve replacement, or both, was needed urgently. We started an induction antiretroviral regimen containing tenofovir, emtricitabine and efavirenz combined with raltegravir to maximally suppress the viral load. By day 9, the viral load decreased 3 log10 (from 315 510 to 315 copies/ml). By day 16, the viral load was nearly undetectable (63 copies/ml). Surgery was performed, and the patient recovered speedily. After discharge, raltegravir was discontinued, and tenofovir, emtricitabine and efavirenz were continued as maintenance therapy. The second patient is a 40-year-old antiretroviral-naive white female, with an HIV-1 infection since 2003. She was suffering with progressive dyspnoea caused by a suspected interstitial lung disease. As all diagnostic tests including transbronchial lung biopsy were inconclusive, a surgical lung biopsy was decided for. We treated her with the same regimen as mentioned earlier. By day 14, the viral load had decreased 2.9 log10 (from 418 969 to 499 copies/ml). After surgery, raltegravir was discontinued. Raltegravir was well tolerated in both patients. This is the first report of using raltegravir in this setting. Raltegravir is a very potent inhibitor of HIV replication, with rapid decline of viral load and favourable side-effect profile. We believe it is a valuable addition to antiretroviral therapy in situations in which rapid decline of viral load is desirable. Acknowledgements S.G.P. is the first author. G.E.vdB. reviewed and revised the correspondence. There are no conflicts of interest.