Background  Hypertrigliceridaemia is common in patients with HIV, especially those taking protease inhibitors (PIs) or with lipodystrophy.  Although, plasma PI concentrations have been shown to be correlated with virological response there is no clear link between PI concentrations and toxicity, especially long-term side effects, such as lipid metabolism disregulation. Aim  To investigate the relationship between lopinavir (LPV) plasma levels and changes in plasma triglycerides (TG), total cholesterol (TC), and high and low density lipoprotein cholesterol (HDL, LDL) in HIV-infected patients on LPV/ritonavir (r). Patients and methods  Thirty HIV+ patients (Table 1) starting LPV/r + 2 nucleoside reverse transcriptase inhibitors have been enrolled and followed for 12 months.  CD4+ cells, HIV-RNA, glucose, TG, TC, HDL-C and LDL-C plasma concentrations were assessed at baseline (0) and 1, 3, 6 and 12 months after LPV/r initiation.  LPV trough concentrations in plasma (C trough ) were measured by HPLC- MS/MS at 1, 3, 6 and 12 months after LPV/r initiation.  Correlations between LPV C trough and lipid plasma levels were investigated using linear regression and Pearson ’ s correlation. Lopinavir plasma concentrations and lipid elevation patterns in patients on lopinavir/ritonavir-containing regimens. M Boffito 1,2, S Bonora 2, A Sinicco 2, R Raiteri 2, PG Hoggard 1, SH Khoo 1, DJ Back 1, G Di Perri 2 1 University of Liverpool, Liverpool, UK; 2 University of Torino, Torino, Italy CORRESPONDENCE: MARTA BOFFITO Conclusions  A transient increase in TG was observed in this cohort of antiretroviral drug experienced HIV-patients.  However, no correlation between LPV C trough and lipid elevations was observed, suggesting lipid metabolism alterations may not depend on drug plasma concentrations.  Interestingly, our results were not in accordance with other studies performed in different countries, in similar number of patients and with similar follow-up times, which showed a significant relationship between LPV plasma concentrations and hypertriglyceridaemia.  Further studies are warranted to clarify the impact of LPV plasma concentrations on lipid elevation. Figure 2: Linear regression between tryglicerides and LPV C trough Figure 1: Tryglicerides and total cholesterol concentrations over the 12 month follow-up period 10/30 RISK FACTOR (SEX/IVDU) 21/93/2541 (37-64) 30 HCV (+/-) GENDER (F/M) MEDIAN AGE (range) n Table 1: Demographics of the 30 patients enrolled in the study Results  Twenty-four patients reached 12 month follow-up, while 6/30 (20%) had a major increase in TG plasma levels (to  400 mg/dL) during the first 3 months of LPV/r therapy and started lipid regulating treatment (gemfibrozil 600 mg BID, n = 4; fenofibrate 200 mg QD, n = 2). All subjects showed the expected decrease in plasma lipids when treated.  Plasma TG levels showed a transient increase over the 12 month follow-up: they increased during the first 3 months of LPV/r therapy before decreasing at month 6 and 12, without reaching statistical significance (p > 0.05, ANOVA).  No correlation was observed between LPV C trough and TG plasma concentrations, TG increases from baseline, TC, HDL-C and LDL-C. This was confirmed in both group of patients: the 30 enrolled and the 24 who completed the study.  Moreover, comparing the 6 patients who reached a TG level > 400 mg/dL with the 24 who completed the study, no differences were observed in median LPV C trough (6274 vs 6428 ng/mL). Table 2: Tryglicerides and total cholesterol concentrations: comparison between the 30 patients enrolled and the 24 who ended the follow-up period.