Аңдатпа
In virologically suppressed patients, unboosted atazanavir (ATV) 400 mg has demonstrated noninferiority with respect to ritonavir-boosted atazanavir 300 mg (ATV/RTV) as maintenance therapy in combination with backbone, on the basis of three randomized clinical trials.1 One pilot study2 and two open-label clinical trials3, 4 demonstrated the noninferiority of the switch from triple therapy including ATV/RTV to dual therapy with lamivudine (3TC) and ATV/RTV. This regimen containing fewer drugs produced a reduction in bone and renal toxicity while maintaining viral suppression. Considering the toxicity of RTV, and as ATV is the only once-daily protease inhibitor that can be used without a booster, we asked ourselves whether dual therapy with unboosted ATV and 3TC could combine the advantages of simplified therapy with the reduced toxicity of a booster-free regimen. We report our clinical experience in 20 HIV-1-infected patients followed at the Outpatient Clinic of the Infectious Diseases Unit of the University of Verona and switched to a dual regimen containing 3TC and ATV (with or without RTV). All the patients were enrolled in the month of June 2016. Group 1 was composed of 10 treatment-experienced HIV-infected patients switching from triple therapy containing unboosted ATV to dual therapy containing unboosted ATV + 3TC. Group 2 was made up of another 10 treatment-experienced patients switching from triple therapy containing ATV/RTV to dual therapy with ATV/RTV + 3TC. All patients provided informed consent. Each group consisted of eight men and two women. The mean age was 50.1 years in group 1 and 40.3 years in group 2. The mean time since HIV diagnosis was 11.5 and 6.4 years (P = 0.12), respectively. All these patients had undetectable plasma HIV RNA (< 20 HIV-1 RNA copies/mL) for at least 6 months before deintensification, with a mean duration of viral suppression of 83.1 and 18.3 months, respectively (ranges 61−129 and 6−29 months, respectively). No patients had prior virological failure or resistance mutations at the baseline genotypic test. In group 1, the therapy before the switch was tenofovir disoproxil fumarate/emtricitabine (TDF/FTC) + unboosted ATV in one patient and abacavir (ABC)/3TC + unboosted ATV in nine patients, whereas in group 2 five patients were on TDF/FTC + ATV/RTV and five on ABC/3TC + ATV/RTV. Eighteen patients were monoinfected and one in each group was hepatitis C virus (HCV) coinfected. At baseline, compared with group 2, group 1 showed a lower mean bilirubin concentration, a lower mean lipid concentration, and a similar mean creatinine concentration (Table 1). After 6 months, no virological failure was noted and no significant difference found in CD4 cell count between the groups. Plasma HIV RNA continued to be undetectable (either <20 copies/ml or not detectable) in all patients. No changes were detected in lipid profile, bilirubin or renal function (Table 1) in either group between baseline and up to 6 months. Considering the increasing number of nonantiretroviral drugs used to treat comorbidities in aging HIV-infected patients, another advantage of a booster-free regimen is reduced drug−drug interactions. If randomized clinical trials confirm our data, even in a small cohort, this dual treatment with unboosted ATV plus 3TC could be a viable and cost-effective maintenance regimen in virologically suppressed HIV-1-infected patients. Conflicts of interest and funding: The authors have no conflicts of interest to declare. No funding was received for this study.