Receptor Tyrosine Kinase Signaling found the largest virological treatment effects at W48

percentage Cyclovirobuxine D of individuals on OBT regimens with GSS of 0, 1, or 2; and use of CCR5 inhibitors. Missing GSS values were considered to be 0. All analyses were performed using STATA 9.0 . Results Our process for identifying eligible studies is summarized in Figure 1. By combining keywords, we identified 1121 titles and abstracts, of which 961 were not eligible. Of the remaining 160 potentially relevant studies, we examined in detail 80 clinical trials and excluded 70 of them because the design of the study was ineligible , because of lack of randomization or data at W48 . Moreover, we excluded one clinical trial that evaluated vicriviroc and met all lusion criteria , because the doses used differed from those used in Phase III clinical trials. We finally retained 10 trials that met our lusion criteria .
Four of these used CCR5 inhibitors Receptor Tyrosine Kinase Signaling and six used other new antiretroviral drugs. One trial was a yet unpublished study presented at a scientific conference in 2010 . The 10 studies luded a total of 6401 patients. Their demographic and clinical characteristics at lusion are summarized in Table 1. The mean age ranged from 41.3 to 46.0 years, 86% of patients were male, and 39.2–91.8% had a history of AIDS defining events . The median baseline CD4 count was 42– 257 cells/mL and the median HIV RNA was 4.55–5.17 log10 copies/mL. The proportion of patients whose OBT regimen GSS was 0 was 0.5–25.7%, 4–42% of patients had a GSS51 and 15.5–38.7% a GSS52. When we excluded the Gathe study , the proportions of patients with GSS50 or GSS51 were 9.1–25.7% and 25.3–42%, respectively.
Determinants ion milling of virological success at W48 We excluded the study of Saag on maraviroc from our evaluation of determinants of virological success, because it assessed the efficacy of maraviroc in non R5 tropic HIV 1 infected patients, and its main outcome was CD4 cell count change at W48. In the nine remaining studies, 41.7% of patients in the treatment groups and 23.6% in the placebo groups had undetectable HIV RNA. Patients in the treatment groups were almost three times more likely to have undetectable HIV RNA at W48 than patients on OBT plus placebo . We found significant heterogeneity among trials with ORs ranging from 1.12 to 22.68. The TMC125 C223 and VICTOR E3 and E4 studies contributed most to this heterogeneity.
In univariate meta regression analysis, we found the largest virological treatment effects at W48 when trials enrolled mostly men and when GSS was 0, 1 and 2 . We did not find associations between virological treatment effects and any other variables,We luded all 10 studies in our analysis of CD4 cell count changes. CD4 count reases in patients in the treatment groups were 9–62 cells/mL larger than in patients in the placebo groups. The pooled difference was 39 cells/mL when we used nonstandardized mean differences and 0.33 cells/mL when we used standardized mean differences. There was significant heterogeneity among trials . In univariate meta regression analysis, we found the largest immunological treatment effects at W48 when mostly men were enrolled in trials and when GSS was 0, 1 and 2 . Lower proportions of patients with undetectable HIV RNA at W48 in the placebo group were also associated with larger immunological treatment effects .

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