Patients with elevated lipid values at baseline have the greatest risk of developing hypercholesterolaemia and hypertriglyceridaemia after starting lopinavir/ritonavir. Antiretroviral-naive patients coinfected with hepatitis C have a low risk of developing hyperlipidaemia after starting lopinavir/ritonavir.

Today, use of antiretroviral (ARV) therapy in patients with AIDS is associated with longer survival [1]. However, several new complications have been described in the last few years, mainly cardiovascular events. Several abnormalities have been related to cardiovascular complications: endothelial dysfunction, dyslipidemia, insulin resistance, or prothrombotic state. However, none of these entities totally explain cardiovascular complications. The aim of this research was to determine the frequency of SPS associated with ARV therapy. MethodsWe performed a cross-sectional study of patients with AIDS who received ARV for at least 6 months. We studied two groups of patients depending on the use of protease inhibitors. SPS was evaluated with a functional assay according to the recommendations described in the literature [2]. Results are expressed as % of platelet aggregometry. Characteristics of the patients are expressed as median and ranges. We used a X 2 test to determine if there were differences between the groups in terms of frequency of SPS. Summary of resultsWe studied 100 patients with AIDS: four women and 96 men. For the whole group, mean age was 45 yrs (range 22 to 77). Mean time of treatment with ARV drugs was 90 months (range 8 to 177). We found that 73% of the patients had criteria to be considered carriers of SPS. Sixtynine percent of the patients had type 2 SPS (only with epinephrine), 27% had type 1 SPS (with epinephrine and ADP), and only 4% of the patients had type 3 SPS (with ADP). The analysis of results according to the group of study showed that 54.8% of patients with SPS were receiving protease inhibitors (p = 0.239). ConclusionSPS was recently described as a relatively frequent cause of either venous or arterial thrombotic events. To date, no single cause of thrombophilia can explain the growing incidence of vascular events associated to ARV in patients with AIDS. A few years ago, our group informed a large series of venous thromboembolic events in patients with AIDS in which none of the thrombophilic causes described in the general population was found significantly. Therefore, we attempted to investigate other causes of thrombophilia that may be affecting patients with AIDS. We have found that SPS is a very frequent condition in patients with AIDS receiving ARV therapy for at least 6 months. Moreover, we found that protease inhibitors are not associated with the appearance of the syndrome in this population. A controlled study about this association is warranted. Mammen EF: Ten years' experience with the sticky platelet syndrome.

Antiretroviral treatment simplification with darunavir/ritonavir or lopinavir/ritonavir monotherapy maintains sustained HIV viremia suppression in clinical trials. However, data about the efficacy of this strategy in routine clinical practice is still limited, and no direct comparison between darunavir/ritonavir and lopinavir/ritonavir has been performed to date. We retrospectively studied all HIV-1-infected subjects who initiated monotherapy with darunavir/ritonavir or lopinavir/ritonavir while having plasma VL<50 c/mL, and had at least 1 subsequent follow-up visit in our clinic. When two consecutive PI-monotherapy regimens were used, each regimen was considered separately. The primary endpoint was the percentage of patients who maintained virological suppression (HIV-1 VL <50 c/mL) through follow-up. Virological failure was defined as at least two consecutive HIV-1 VL >50 c/mL. We also evaluated other reasons for treatment discontinuation. Analyses were performed considering all regimens (full dataset analysis) either as “on treatment” or as “treatment switch equals failure”. Five hundred and seventy-three PI-monotherapy regimens corresponding to 520 subjects were included, 262 with darunavir/ritonavir and 311 with lopinavir/ritonavir. Medians (IQR) follow-up were 50 (26.3–107.6) and 85.6 (36.9–179.1) weeks for subjects on darunavir/ritonavir and lopinavir/ritonavir, respectively (p<0.001). Overall, 67 (11.7%) subjects experienced virological failure, 23 (8.7%) were on darunavir/ritonavir and 42 (13.5%) were on lopinavir/ritonavir (p=0.796). Two hundred and three (77.5%) patients on darunavir/ritonavir and 154 (49.5%) on lopinavir/ritonavir maintained virological suppression in the “treatment switch equals failure” (p=0.002). Other reasons for treatment discontinuation were gastrointestinal toxicity and dyslipidemia in 7.2% and 5.9% of cases, respectively. Gastrointestinal toxicities and dyslipidemia leading to treatment discontinuation were more frequent in patients on lopinavir/ritonavir (10.6% and 10.3%, respectively) than in patients on darunavir/ritonavir (3.1% and 0.8%, respectively). Monotherapy with darunavir/ritonavir or lopinavir/ritonavir as simplification strategy appears to be effective and safe in subjects with virological suppression in clinical practice. Virological efficacy seems to be similar between regimens. However, rates of discontinuation due to toxicities were higher in subjects on lopinavir/ritonavir than darunavir/ritonavir

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