Time to AIDS from 1992 to 1999 in HIV-1-Infected Subjects with Known Date of Infection.

To estimate the change in AIDS incubation time during three periods characterized by different availability of antiretroviral treatments, data from the French Hospital Database on HIV of 4702 HIV-1-positive subjects with a documented date of infection were analyzed. Times from seroconversion to AIDS were compared in three periods: period 1 from January 1992 to June 1995 (monotherapy); period 2 from July 1995 to June 1996 (dual therapy); and period 3 from July 1996 to June 1999 (triple therapy). Nonparametric survival analyses were performed to account for staggered entries in the database and during each period. From periods 1 to 3, antiretroviral treatments were initiated earlier after infection, more subjects were treated, and the nature of regimens changed (25.6% of subjects were treated with monotherapy in period 1, 34.6% were treated with dual therapy in period 2, and 53.4% were treated with triple therapy in period 3). Compared with period 1, the relative hazard (RH) of AIDS was 0.31 in period 3 (95% confidence interval [CI]: 0.24-0.39). When comparing period 3 with period 2, the RH of AIDS was 0.36 (CI: 0.29-0.45). Assuming a log normal distribution, the median time to AIDS was estimated as 8.0 years in period 1 (CI: 6.0-10.6), 9.8 years in period 2 (CI: 8.5, 11.2), and 20.0 years in period 3 (CI: 17.1-23.3). This lengthening in time to AIDS from 1992 to 1999 was particularly marked in the period after the introduction of triple therapy, including protease inhibitors

Predictors of medical events and of their competitive interactions in the Cardiac Insufficiency Bisoprolol Study 2 (CIBIS-2).

Predictive factors for medical events and interactions between events were not reported in the Cardiac Insufficiency Bisoprolol Study 2 (CIBIS-2). We examined the interactions among death, permanent treatment withdrawals, nonlethal cardiovascular hospitalizations and their own occurrence in a given patient, the treatment received, and baseline variables during CIBIS-2. METHODS AND RESULTS: A Cox model for censored data was used to analyze the relations among baseline variables, medical events, and their interactions with treatment. We used competitive risk analysis to examine the interactions between successive events in a given patient during follow-up. No baseline variable predicted the reduction of mortality with bisoprolol. Withdrawal from bisoprolol therapy was more frequent in patients whose baseline heart rate was in the lower tertile of the distribution (P =.0002) but otherwise was not different between patients randomized to bisoprolol and to placebo. Event history analysis revealed that bisoprolol reduced mortality (P =.0006) and hospitalizations for nonlethal cardiovascular events (P =.003) in patients in whom treatment was not permanently withdrawn. Analysis of survival curves in patients who permanently discontinued treatment showed that bisoprolol did not reduce mortality compared with placebo in this population (relative risk 1.03, 95% CI 0.67-1.59; P =.88). Recurrent nonlethal events were reduced by bisoprolol. CONCLUSION: In CIBIS-2, medical events were significantly influenced by treatment withdrawal. Patients who derive benefit from bisoprolol therapy are those in whom treatment is not permanently withdrawn

Aids

OBJECTIVES: Epstein-Barr virus (EBV) has been implicated in lymphomagenesis of HIV-related classical Hodgkin lymphoma (HIV-cHL). The utility of EBV molecular and serological biomarkers has scarcely been examined in HIV-cHL in the recent combined antiretroviral therapy (cART) era. DESIGN: We evaluated EBV DNA load and a panel of EBV antibodies in HIV-cHL patients prospectively enrolled in the French ANRS-CO16 Lymphovir cohort between 2008 and 2015. METHODS: Pretreatment whole blood, plasma EBV DNA load and serological profiles were analysed in 63 HIV-infected patients diagnosed with cHL. For the 42 patients with available material, comparisons were performed between values at diagnosis and 6 months after the initiation of chemotherapy. RESULTS: Pretreatment whole blood and plasma EBV DNA loads were positive in 84 and 59% of HIV-cHL patients, respectively. Two-year progression-free survival estimates did not differ between the patients with pretreatment whole blood (n = 53) or plasma (n = 37) EBV DNA(+) and the patients with pretreatment whole blood (n = 10) or plasma (n = 26) EBV DNA(-) (92 vs. 80% or 89 vs. 92%, P = 0.36 and 0.47, respectively). At diagnosis, 47% of patients harboured an EBV reactivation serological profile. Following chemotherapy, whole blood and plasma EBV DNA levels significantly declined from medians of 1570 [interquartile range, 230-3760) and 73 (0-320) copies/ml to 690 (0-1830) and 0 (0-0) copies/ml, respectively (P = 0.02 and P < 0.0001, respectively]. Anti-EBV IgG antibody level significantly dropped at 6-month follow-up (P = 0.004). CONCLUSION: Whole blood and plasma EBV DNA loads do not constitute prognostic markers in HIV-cHL patients in the modern cART era