Purpose: To assess platelet activity in HIV-patients with and without antiretroviral therapy (ART), analysing the influence of the presence or absence of ABC in the regimen. Methods: Observational, pilot study, includ...Purpose: To assess platelet activity in HIV-patients with and without antiretroviral therapy (ART), analysing the influence of the presence or absence of ABC in the regimen. Methods: Observational, pilot study, including 30 asymptomatic HIV-patients: 20 on ART for at least 24 weeks and with undetectable HIV viral load - 10 on ABC, 10 on tenofovir (TDF) - and 10 na?ve patients, and a control group of 10 HIV-negative subjects. No subject was receiving drugs with antiagregant activity. Platelet activity was assessed by measuring time-dependent platelet aggregometry (electrical impedance on fasting whole blood), induced by ADP (1.25, 2.5 μM), collagen (0.5, 1 μg/mL), arachidonic acid (100, 200 μM), and U46619 (receptor agonist of the tromboxano A2) (1.25, 2.5 μM). Statistic program: SPSS, 16.0. Results: Demographic, anthropometric data, and cardiovascular risk factors were similar in all groups, but older age and longer time of HIV infection in the ABC group (50.4 vs 36.1, 34.2 and 42.7 years, respectively;p < 0.05, and 140.3 vs 88.1 and 48.3 months in the two other groups of HIV patients;p < 0.05). Mean CD4 cells count was 564/mm3. Platelet aggregation with exposure to U46619 was higher in the ABC compared with the TDF group (11.1 vs 4.4%;p = 0.007), na?ve patients (11.1 vs 5.7%;p = 0.014), and the HIV-negative group (11.1 vs 6.5%;p = 0.04). These differences remained significant when controlled for age and time of HIV infection. Conclusions: ABC increases platelet aggregability possibly in relation with the receptor of tromboxano. Wider studies are needed to confirm this hypothesis.展开更多
文摘Purpose: To assess platelet activity in HIV-patients with and without antiretroviral therapy (ART), analysing the influence of the presence or absence of ABC in the regimen. Methods: Observational, pilot study, including 30 asymptomatic HIV-patients: 20 on ART for at least 24 weeks and with undetectable HIV viral load - 10 on ABC, 10 on tenofovir (TDF) - and 10 na?ve patients, and a control group of 10 HIV-negative subjects. No subject was receiving drugs with antiagregant activity. Platelet activity was assessed by measuring time-dependent platelet aggregometry (electrical impedance on fasting whole blood), induced by ADP (1.25, 2.5 μM), collagen (0.5, 1 μg/mL), arachidonic acid (100, 200 μM), and U46619 (receptor agonist of the tromboxano A2) (1.25, 2.5 μM). Statistic program: SPSS, 16.0. Results: Demographic, anthropometric data, and cardiovascular risk factors were similar in all groups, but older age and longer time of HIV infection in the ABC group (50.4 vs 36.1, 34.2 and 42.7 years, respectively;p < 0.05, and 140.3 vs 88.1 and 48.3 months in the two other groups of HIV patients;p < 0.05). Mean CD4 cells count was 564/mm3. Platelet aggregation with exposure to U46619 was higher in the ABC compared with the TDF group (11.1 vs 4.4%;p = 0.007), na?ve patients (11.1 vs 5.7%;p = 0.014), and the HIV-negative group (11.1 vs 6.5%;p = 0.04). These differences remained significant when controlled for age and time of HIV infection. Conclusions: ABC increases platelet aggregability possibly in relation with the receptor of tromboxano. Wider studies are needed to confirm this hypothesis.
