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Residual Viremia More Frequent and Higher With
LPV/r Monotherapy Than Triple Therapy
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ICAAC 2016, June 16-20, 2016, Boston
Mark Mascolini
Ultrasensitive assays detected residual viremia more often and at higher levels in people taking lopinavir/ritonavir monotherapy than in those taking the protease inhibitors (PIs) with abacavir/lamivudine, according to a 71-person analysis in the randomized KRETA trial [1]. Viral loads above 50 copies also proved more frequent in the PI monotherapy arm.
The Spanish KRETA study randomized people with lipoatrophy while taking zidovudine, lamivudine, and abacavir to switch to lopinavir/ritonavir monotherapy or to take those PIs plus abacavir/lamivudine [2]. The primary aim was to compare the impact of those regimens on changes in lipodystrophy. KRETA investigators used DXA scans to measure limb fat and body fat at baseline and treatment weeks 48 and 96. Through 96 weeks monotherapy conferred no advantage in limb fat recovery [3].
The residual viremia analysis focused on 71 people who had four or more plasma samples of at least 3 mL at each time point. The investigators used two ultrasensitive assays to measure residual viremia: the ultracentrifugation modified Abbott RealTime assay (UMA) and the tabletop centrifugation assay (TMA). TMA allows handling of highly lipemic samples. Lower limits of detection are 3 copies/mL with UMA and 6 copies/mL with TMA.
The analysis involved 34 people randomized to PI monotherapy and 37 randomized to triple therapy. Age averaged 47 years in both groups, both groups had taken an average of two antiretroviral regimens, and time on last regimen was marginally shorter in the monotherapy group (5.3 versus 6.7 years, P = 0.059). CD4 counts averaged 733 in the monotherapy arm and 820 in the triple-therapy arm (P = 0.263). At baseline the two groups did not differ significantly in body mass index, total body fat, trunk fat, total limb fat, fat-mass ratio, or trunk fat. Change in fat-mass ratio during study treatment did differ significantly between the two arms.
During treatment the ultrasensitive MA assays determined that 9 people in the PI monotherapy arm and 1 in the triple-therapy arm had at least one viral load above 50 copies, a significant difference (26.5% versus 2.7%, P = 0.004). Standard clinical assays recorded at least one viral load above 50 copies in 12 people in the monotherapy arm and 4 in the triple-therapy arm, also a significant difference (35.3% versus 10.8%, P = 0.014). Compared with people on triple therapy, the monotherapy group also had more frequent detectable residual viremia (P = 0.059) and a higher residual viremia level (P = 0.001). Among people who maintained a viral load below 50 copies, residual viremia did not differ significantly between study arms. Residual viremia by MA assay correlated positively with clinical viral load (Pearson correlation 0.914).
Residual viremia did not correlate with any baseline demographic or HIV factor (including age, gender, HCV positivity, CD4 count, duration of HIV diagnosis, or years taking antiretrovirals) or with any fat distribution factor (including total body fat, trunk fat, right or left limb fat, or change in fat-mass ratio during the study).
References
1. McKinnon JE, Bernardino JI, Zhou JY, et al. Correlation of residual viremia on clinical outcomes and lipodystrophy markers in the KRETA study. ICAAC 2016, June 16-20, 2016, Boston. Abstract Sunday-421.
2. ClinicalTrials.gov. Lopinavir/r monotherapy versus abacavir/lamivudine and lopinavir/r for limb fat recovery in persons with lipoatrophy (KRETA). ClinicalTrials.gov identifier NCT00865007. https://clinicaltrials.gov/ct2/show/NCT00865007
3. Bernardino JI, Pulido F, Martinez E, et al. Switching to lopinavir/ritonavir with or without abacavir/lamivudine in lipoatrophic patients treated with zidovudine/abacavir/lamivudine. J Antimicrob Chemother. 2013;68:1373-1381.
http://jac.oxfordjournals.org/content/68/6/1373.long
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