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7‐11 November 2010, Tenth International Congress on Drug Therapy in HIV Infection, Glasgow, UK

ObjectiveTo analyze self‐reported adherence to antiretroviral regimens containing ritonavir‐boosted protease inhibitors, non‐nucleoside reverse transcriptase inhibitors (NNRTI), raltegravir, and maraviroc.MethodsOverall, 372 consecutive subjects attending a reference center for HIV treatment in Florence, Italy, were enrolled in the study, from December 2010 to January 2012 (mean age 48 years). A self‐report questionnaire was filled in. Patients were defined as "non‐adherent" if reporting one of the following criteria:<90% of pills taken in the last month, ≥1 missed dose in the last week, spontaneous treatment interruptions reported, or refill problems in the last 3 months. Gender, age, CD4, HIV‐RNA, years of therapy, and type of antiretroviral regimen were analyzed with respect to adherence.ResultsAt the time of the questionnaire, 89.8% of patients had <50 copies/mL HIV‐RNA and 14.2% were on their first combined antiretroviral therapy. 57% of patients were prescribed a regimen containing ritonavir boosted protease inhibitors (boosted PI), 41.7% NNRTI, 17.2% raltegravir, and 4.8% maraviroc; 49.5% of the subjects were on bis‐in‐die regimens, while 50.5% were on once‐daily regimens, with 23.1% of these on the single tablet regimen (STR): tenofovir/emtricitabine/efavirenz. The non‐adherence proportion was lower in NNRTI than in boosted‐PI treatments (19.4% vs 30.2%), and even lower in STR patients (17.4%). In multivariable logistic regression, patients with the NNRTI regimen (OR: 0.56, 95% CI: 0.34–0.94) and the STR (OR: 0.45, 95% CI: 0.22–0.92) reported lower non‐adherence. Efavirenz regimens were also associated with lower non‐adherence (OR: 0.42, 95% CI: 0.21–0.83), while atazanavir/ritonavir regimens were associated with higher non‐adherence. No other relation to specific antiretroviral drugs was found. A higher CD4 count, lower HIV‐RNA, and older age were also found to be associated with lower non‐adherence, while a longer time on combined antiretroviral therapy was related to higher non‐adherence.ConclusionIn conclusion, older age, higher CD4 cell counts, lower HIV‐RNA viral loads, and the use of STR are all related to lower non‐adherence. In particular, the use of STR maintains an advantage in improving adherence with respect to other cARTs, even with the availability of new, well‐tolerated antiretroviral drugs and drug classes in recent years.

Purpose of the studySince X4/DM HIV‐1 tropism is associated with poorer prognosis and worse response to treatment, the aim of this study was to assess whether X4/DM HIV‐1 tropism is also related with a higher accumulation of resistance in patients experiencing treatment failure.MethodsHIV protease (PR) and reverse transcriptase (RT) resistance mutations and tropism test results were extracted from a national database. Viral tropism data included enhanced sensitivity Trofile assay (ESTA) and geno2pheno results at 10% false positive rate. Historical resistance mutations (HRM) for PI, NRTI and NNRTI, detected in all genotypic tests performed during patient treatment history, were selected according to IAS‐USA indications.Summary of resultsOverall, 1280 patients were included: males 65%, median age 45 years (IQR: 40–50), median CD4 nadir 116 (IQR: 34–272), median past regimens 7 (IQR: 3–12), median previous NRTI used 5 (IQR: 4–7), median previous NNRTI used 1 (IQR 1–2) and median previous PI used 3 (IQR 1–5). HIV tropism was assessed by ESTA in 271 patients (21.2%) and by geno2pheno in 1009 patients (78.8%). Four hundred and fifteen patients (32.4%) carried X4/DM virus and 321 (25.1%) had ≥1 HRM for each antiretroviral class. The mean number of HRM was higher in patients harboring X4/DM virus than in patients harboring R5 virus (5.1±6.4 vs. 4.3±5.9, p = 0.02 at ANOVA test). X4/DM strains also harbored a higher mean number of PI‐related HRM (1.8±2.8 vs. 1.5±2.6, p = 0.003) and NNRTI‐related HRM (1.2±1.6 vs. 0.9±1.4, p = 0.001), but not of NRTI‐related HRM (2.2±2.6 vs. 2.0±2.6). At logistic regression, patients with HRM for all the 3 classes had a significant higher risk of also harboring X4/DM virus (OR: 1.6, 95% CI: 1.0–2.4, p = 0.04). Moreover, X4/DM virus was found to be associated with previous use of NNRTI‐containing regimens (OR: 1.4, 95% CI: 1.1–1–9, p = 0.03) and lower CD4 nadir (OR: 0.9, 95% CI: 0.9–1.0, p = 0.001, per 50‐CD4 increase). The analysis was adjusted by number of genotypic tests, number of treatment lines, age and HV subtype. Single mutations significantly associated with X4/DM tropism were: for PI, V32I and L76V; for NRTI: M41L, K70R, L74V and T215Y and for NNRTI: E138G and V179T.ConclusionsOur data suggest that X4/DM tropism is associated with accumulation of resistance mutations during treatment history. X4/DM tropism is also confirmed to be a marker of a more compromised clinical and immune‐virological condition.

7‐11 November 2010, Tenth International Congress on Drug Therapy in HIV Infection, Glasgow, UK