Boosted Atazanavir Research Articles

An observational study in an urban Ugandan clinic comparing virological outcomes of patients switched from first-line antiretroviral regimens to second-line regimens containing ritonavir-boosted atazanavir or ritonavir-boosted lopinavir

BackgroundThe World Health Organisation approved boosted atazanavir as a preferred second line protease inhibitor in 2010. This is as an alternative to the current boosted lopinavir. Atazanavir has a lower genetic barrier than lopinavir. We compared the virological outcomes of patients during the roll out of routine viral load monitoring, who had switched to boosted second- line regimens of either atazanavir or lopinavir.MethodsThis was a cross-sectional study involving adult patients at the Infectious Diseases Institute Kampala, Uganda started on a standard WHO recommended second-line regimen containing either boosted atazanavir or boosted lopinavir between 1 Dec 2014 and 31 July 2015.. Mantel -Haenszel chi square was used to test for the statistical significance of the odds of being suppressed (VL < 400 copies/ml) when on boosted atazanavir compared to boosted lopinavir after stratifying by duration on antiretroviral therapy (ART). Multivariate logistic regression analysis used to determine if the type of boosted protease inhibitor (bPI) was associated with virological outcome.ResultsNinety (90) % on ATV/r and 83% on LPV/r had a VL less than 1000 copies/ml. The odds of being suppressed using the same viral load cut-off while on boosted atazanavir compared to boosted lopinavir was not statistically significant after stratifying for duration on ART (p = 0.09). In a multivariate analysis the type of bPI used was not a predictor of virological outcome (p = 0.60).ConclusionsPatients using the WHO recommended second-line of boosted atazanavir have comparable virological suppression to those on boosted lopinavir.

Boosted- lopinavir versus boosted- atazanavir plus two nucleoside reverse transcriptase inhibitors in second- line antiretroviral therapy in HIV-1 infected patients in Abidjan (Ivory Coast)

Introduction: Atazanavir is a protease inhibitor recently introduce in the therapeutic arsenal for second-line antiretroviral therapy in Ivory Coast. The objective of this study was to compare the efficacy and safety of a second-line treatment with 2 NRTIs + boosted lopinavir (LPV/r) versus 2 NRTIs + boosted atazanavir (ATV/r) in HIV-1 positive patients in Abidjan. Patients and Methods: Retrospective, comparative, single-center study, in 194 HIV-1 positive patients (143 with LPV/r, 51 with ATV/r), failed a first-line treatment, followed in Abidjan on 1 May 2009 to 30 June 2010. The analysis focused on clinical parameters and immuno-virological data. The principal judgement criterion was the proportion of patients with undetectable viral load in both groups after 12 months of HAART. Tolerance was found on the frequency of adverse events grade 3-4 during follow-up. Results: Clinically, improvement of the general condition and regression of opportunistic infections was similar in both groups. The average gain of CD4 after 12 months of follow-up was +357/mm3 in the LPV/r group versus +278 mm3 for ATV/r group (p = 0.012). The percentage of patients with undetectable viral load was similar in both groups (92% vs. 96% ; p = 0.535). The frequency of grade 3-4 adverse events was similar in both groups. Conclusion: HAART with LPV/r is at least as efficient as with ATV/r in second-line treatment, in terms of viral load reduction, with better recovery of CD4. LPV/r is an excellent second-line treatment in resource-limited countries. J Microbiol Infect Dis 2016;6(4): 149-155 Abidjan, Atazanavir, HIV, Lopinavir, Second-line, Sub-Saharan Africa

Choice of antiretroviral drugs for postexposure prophylaxis for adults and adolescents: a systematic review.

The choice of preferred regimens for human immunodeficiency virus postexposure prophylaxis (PEP) has evolved over the last 2 decades as more data have become available regarding the safety and tolerability of newer antiretroviral drugs. We undertook a systematic review to assess the safety and efficacy of antiretroviral options for PEP to inform the World Health Organization guideline revision process. Four databases were searched up to 1 June 2014 for studies reporting outcomes associated with specific PEP regimens. Data on PEP completion and discontinuation due to adverse events was extracted and pooled estimates were obtained using random-effects meta-analyses. Fifteen studies (1830 PEP initiations) provided evaluable information on 2-drug regimens (zidovudine [ZDV]- or tenofovir [TDF]-based regimens), and 10 studies (1755 initiations) provided evaluable information on the third drug, which was usually a protease inhibitor. The overall quality of the evidence was rated as very low. For the 2-drug regimen, PEP completion rates were 78.4% (95% confidence interval [CI], 66.1%-90.7%) for people receiving a TDF-based regimen and 58.8% (95% CI, 47.2%-70.4%) for a ZDV-based regimen; the rate of PEP discontinuation due to an adverse event was lower among people taking TDF-based PEP (0.3%; 95% CI, 0%-1.1%) vs a ZDV-based regimen (3.2%; 95% CI, 1.5%-4.9%). For the 3-drug comparison, PEP completion rates were highest for the TDF-based regimens (TDF+emtricitabine [FTC]+lopinavir/ritonavir [LPV/r], 71.1%; 95% CI, 43.6%-98.6%; TDF+FTC+raltegravir [RAL], 74.7%; 95% CI, 41.4%-100%; TDF+FTC+ boosted darunavir [DRV/r], 93.9%; 95% CI, 90.2%-97.7%) and lowest for ZDV+ lamivudine [3TC]+LPV/r (59.1%; 95% CI, 36.2%-82.0%). Discontinuations due to adverse drug reactions were lowest for TDF+FTC+RAL (1.9%; 95% CI, 0%-3.8%) and highest for ZDV+3TC+boosted atazanavir (21.2%; 95% CI, 13.5%-30.0%). The findings of this review provide evidence supporting the use of coformulated TDF and 3TC/FTC as preferred backbone drugs for PEP. Choice of third drug will depend on setting; for resource-limited settings, LPV/r is a reasonable choice, pending the improved availability of better-tolerated drugs with less potential for drug-drug interactions.

P023: Dyslipidemia and use of lipid-lowering agents in Mexican HIV-positive patients using boosted atazanavir and boosted lopinavir

P023: Dyslipidemia and use of lipid-lowering agents in Mexican HIV-positive patients using boosted atazanavir and boosted lopinavir

Boosted lopinavir- versus boosted atazanavir-containing regimens and immunologic, virologic, and clinical outcomes: a prospective study of HIV-infected individuals in high-income countries.

Current clinical guidelines consider regimens consisting of either ritonavir-boosted atazanavir or ritonavir-boosted lopinavir and a nucleoside reverse transcriptase inhibitor (NRTI) backbone among their recommended and alternative first-line antiretroviral regimens. However, these guidelines are based on limited evidence from randomized clinical trials and clinical experience. We compared these regimens with respect to clinical, immunologic, and virologic outcomes using data from prospective studies of human immunodeficiency virus (HIV)-infected individuals in Europe and the United States in the HIV-CAUSAL Collaboration, 2004-2013. Antiretroviral therapy-naive and AIDS-free individuals were followed from the time they started a lopinavir or an atazanavir regimen. We estimated the 'intention-to-treat' effect for atazanavir vs lopinavir regimens on each of the outcomes. A total of 6668 individuals started a lopinavir regimen (213 deaths, 457 AIDS-defining illnesses or deaths), and 4301 individuals started an atazanavir regimen (83 deaths, 157 AIDS-defining illnesses or deaths). The adjusted intention-to-treat hazard ratios for atazanavir vs lopinavir regimens were 0.70 (95% confidence interval [CI], .53-.91) for death, 0.67 (95% CI, .55-.82) for AIDS-defining illness or death, and 0.91 (95% CI, .84-.99) for virologic failure at 12 months. The mean 12-month increase in CD4 count was 8.15 (95% CI, -.13 to 16.43) cells/µL higher in the atazanavir group. Estimates differed by NRTI backbone. Our estimates are consistent with a lower mortality, a lower incidence of AIDS-defining illness, a greater 12-month increase in CD4 cell count, and a smaller risk of virologic failure at 12 months for atazanavir compared with lopinavir regimens.

Boosted lopinavir vs boosted atazanavir in patients failing a NNRTI first line regimen in an urban clinic in Kampala.

IntroductionIn 2011 Uganda recommended boosted atazanavir (ATV/r) as the preferred PI for second line due to once daily dosing, replacing aluvia (LPV/r) [1, 2]. The evidence was based on the BMS O45 trial, of LPV/r vs ATV/r was performed in a high-income setting, on patients with prior PI use and resistance testing [2, 3]. There are no RCTs or observational studies comparing use of ATV/r with LPV/r in patients failing NNRTI first line antiretroviral therapy in sub-Saharan Africa [3, 4]. The Infectious Diseases Institute (IDI) has a large second line cohort (>1838). This aims to compare clinical, immunologic and virologic response of LPV/r versus ATV/r at IDI.MethodsRetrospective cohort analysis on routinely collected data of patients switched to second line with NRTI backbones TDF/3TC or FTC, AZT/3TC, ABC/3TC from January 2009 to December 2013. Students T-tests and Chi-square tests were used in this analysis.ResultsA total of 1286 (73.5% female) patients were switched to LPV/r 991 (77%) and ATV/r 295 (23%) (p<0.001). NRTI backbones were 760 on TDF/3TC (66.8% LPV/r vs 33.2% on ATV/r), 504 on AZT/3TC (93.3% vs 6.7%), and 22 on ABC/3TC (59% vs 41%). Median (IQR) time on first line for LPV/r was 21 (1–44) months and for ATV/r was 41 months (22–68). Median CD4 (IQR) at switch to LPV/r was 181 cells/uL (66–424) and to ATV/r was 122 (57–238) (p≤0.001). A total of 366 patients had CD4 done at six months after switch and the mean (IQR) CD4 increase was 153 (54–241) for LPV/r versus 116 (52–171) for ATV/r (p=0.232). Additionally, 304 had a CD4 at 12 months and the means were 172 (45–272) for LPV/r vs 179 (60–271) for ATV/r (p=0.426). There was no significant difference in the mean increment by NRTI backbone or by stratifying to viral load (VL) at time of switch to VL <100,000 and ≥100,000. Median (IQR) VL at switch was 61,000 (13,000–2,030,000) LPV/r and 51,000 (14,000_151,000) ATV/r. 269 had a VL done in the first 12 months and 178/250 (71.2%) on LPV/r versus 16/19 (84.2%) on ATV/r were undetectable (p=0.228). 259 (26%) LPV/r versus 33(11%) ATV/r had ≥1 opportunistic infections on second line (p<0.001).ConclusionsThis is an observational study based on our experience at IDI. Like elsewhere in Africa, there is no routine viral load testing, making it difficult to get sensitive analysis of data on ART efficacy within routine clinical practice. Nevertheless, this observational study is reassuring in terms of efficacy of both ATV/r and LPV/r for patients failing first line therapy in our setting.

Intensified ART for Patients with Acute or Recent HIV Infection

Starting antiretroviral therapy (ART) in early HIV infection may result in a smaller viral burden in the latently infected pool. To understand whether intensifying ART in early infection leads to improved virologic and immunologic outcomes, investigators (with partial industry funding) conducted an open-label, randomized trial comparing standard boosted protease inhibitor (PI) therapy (tenofovir/FTC + boosted atazanavir or darunavir) with the same regimen plus raltegravir and maraviroc. Of 40 enrollees, 26 were randomized to five-drug ART and 14 to standard …

Efavirenz Outperforms Boosted Atazanavir among Treatment-Naive HIV-1-Infected Persons in Routine Clinical Care

Effectiveness of antiretroviral therapy (ART) in a routine clinical care may result different from the clinical trials. We assessed the virologic outcomes in treatment-naive persons who received either efavirenz (EFV) or atazanavir/ritonavir (ATV/r) with a backbone of tenofovir/emtricitabine (TDF/FTC) as their combination ART (cART). This was a retrospective cohort study conducted at the Washington University HIV Outpatient Clinic from January 2004 to June 2009. Predictors of virologic suppression (HIV RNA level <400 copies/mL) by week 48 were assessed by multivariate Cox proportional hazards regression models. Of 324 persons, 221(68%) received EFV and 103 (32%) received ATV/r. Persons on EFV had 1.4-fold increased likelihood of virologic suppression (95% confidence interval, 1.0-1.8) when compared to ATV/r after adjustment with primary drug resistance, pre-cART opportunistic infection, HIV RNA levels, and timing to start cART. In routine clinical care settings, EFV had higher likelihood of achieving virologic suppression than ATV/r with backbone of TDF/FTC.

A Randomized Comparative 96-Week Trial of Boosted Atazanavir versus Continued Boosted Protease Inhibitor in HIV-1 Patients with Abdominal Adiposity

Abdominal adiposity in HIV-1 patients initiating antiretroviral therapy may be part of a restoration-to-health phenomenon. Lipoatrophy is associated with long-term thymidine analogue therapy. Individual protease inhibitors (PIs) differ in their effects on lipids and insulin resistance. A randomized open-label multicentre 96-week trial compared changes in fat distribution in patients with suppressed HIV-1 RNA and abdominal adiposity, who either continued on their current twice-daily ritonavir-boosted PI (PI/r) or switched to once-daily boosted atazanavir (ATV/r). Treatment with two nucleoside reverse transcriptase inhibitors was unchanged. Body composition was assessed by dual-energy x-ray absorptiometry (DEXA) and abdominal computerized tomography (CT) scanning. In total, 201 patients were randomized; 131 switched to ATV/r. Viral suppression (<50 copies/ml) was similarly maintained (93% ATV/r versus 89% PI/r). Mean changes from baseline in trunk-to-limb fat ratio were similar; difference estimates 0.03 (95% CI -0.06, 0.12; P=0.48 at week 48) and 0.02 (95% CI -0.10, 0.14; P=0.73 at week 96). More patients in the PI/r arm had a decrease of ≥20% in limb fat from baseline at week 96. Significantly greater reductions in proatherogenic lipids occurred following switch to ATV/r. Both treatment regimens were generally well-tolerated; the incidence of grade 3-4 treatment-related clinical adverse events was 34% among ATV/r recipients versus 4% of PI/r-treated patients. Switching to ATV/r had no demonstrable benefit on abdominal adiposity. Maintenance of efficacy, less limb fat loss and marked reduction in proatherogenic lipids was observed with ATV/r compared with continuing a PI/r regimen.

Optimizing Antiretroviral Product Selection: A Sample Approach to Improving Patient Outcomes, Saving Money, and Scaling-up Health Services in Developing Countries

Over the last decade, increased funding to support HIV treatment programs has enabled millions of new patients in developing countries to access the medications they need. Today, although demand for antiretrovirals continues to grow, the financial crisis has severely constrained funding leaving countries with difficult choices on program prioritization. Product optimization is one solution countries can pursue to continue to improve patient care while also uncovering savings that can be used for further scale up or other health system needs. Program managers can make procurement decisions that actually reduce program costs by considering additional factors beyond World Health Organization guidelines when making procurement decisions. These include in-country product availability, convenience, price, and logistics such as supply chain implications and laboratory testing requirements. Three immediate product selection opportunities in the HIV space include using boosted atazanavir in place of lopinovir for second-line therapy, lamivudine instead of emtricitabine in both first-line and second-line therapy, and tenofovir + lamivudine over abacavir + didanosine in second-line therapy. If these 3 opportunities were broadly implemented in sub-Saharan Africa and India today, approximately $300 million of savings would be realized over the next 5 years, enabling hundreds of thousands of additional patients to be treated. Although the discussion herein is specific to antriretrovirals, the principles of product selection are generalizable to diseases with multiple treatment options and fungible commodity procurement. Identifying and implementing approaches to overcome health system inefficiencies will help sustain and may expand quality care in resource-limited settings.

Population and ultra-deep sequencing for tropism determination are correlated with Trofile ES: genotypic re-analysis of the A4001078 maraviroc study

Background: A4001078 is a study in therapy naive patients of Maraviroc (MVC) plus boosted atazanavir. The Trofile ES (ESTA) was used to determine tropism at Screening. Few re-analyses of genotypic tropism have examined all screened and non-reportable (NR) populations. We aimed to define correlations between methods at screening and evaluate the quantity of X4 using virus in discordant results using ultra-deep sequencing (UDS). Supplement: Abstracts of the Tenth International Congress on Drug Therapy in HIV Infection http://www.biomedcentral.com/content/pdf/1758-2652-13-S4-info.pdf Conference: Tenth International Congress on Drug Therapy in HIV Infection 7-11 November 2010 Glasgow, UK (Published: 8 November 2010) doi:10.1186/1758-2652-13-S4-P128 Cite this article as: Portsmouth et al.: Population and ultra-deep sequencing for tropism determination are correlated with Trofile ES: genotypic re-analysis of the A4001078 maraviroc study. Journal of the International AIDS Society 2010 13(Suppl 4):P128. Full text: PubMed Central: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3112903/

Effects of HIV antiretrovirals on the pharmacokinetics of hormonal contraceptives

Objectives To review available information on pharmacokinetic effects of HIV antiretrovirals on hormonal contraceptives.Methods A PubMed search was conducted from 1964 to 2006 using each antiretroviral generic name and the keywords contraceptive, contraception, ethinyl oestradiol, oestrogen, and progestin. s from the annual Conference on Retroviruses and Opportunistic Infections and International AIDS Society Conferences from 1998–2006 as well as package product inserts were reviewed for completeness.Results Antiretroviral regimens containing protease inhibitors and non-nucleoside reverse transcriptase inhibitors may decrease the area under the curve (AUC) levels of steroids released by hormonal contraceptives. Some antiretroviral-hormonal contraceptive pairs do not decrease steroid hormone levels.Conclusion Pharmacokinetic interactions of antiretrovirals on hormonal contraceptives are specific to the type of antiretroviral and hormonal contraceptive being utilized. HIV-positive women may be counselled to use dual methods of hormonal and barrier contraception to prevent pregnancy with maximal efficacy as well as to reduce possibility of HIV transmission. Oral contraceptives might be administered with non-ritonavir boosted atazanavir or non-ritonavir boosted indinavir without a loss of contraceptive efficacy. Depot medroxyprogesterone acetate may be safe to administer with efavirenz, nevirapine, and nelfinavir. However, further studies are needed to determine the clinical relevance of the interactions between hormonal contraceptives and antiretrovirals and to explore potential dose adjustments to improve contraceptive efficacy.

Atazanavir crystal nephropathy

Atazanavir (Reyataz, Bristol-Myers Squibb Laboratories, New York, New York, USA), an azapeptide inhibitor of HIV protease, is not considered directly nephrotoxic despite recent reports of urinary stones [1–3]. We describe a patient in whom direct nephrotoxic effects of atazanavir appeared to develop. The patient was a 61-year-old white man known to be HIV/hepatitis C coinfected for 20 and 10 years, respectively. He also had a history of renal insufficiency of unknown cause, with a baseline creatinine level of 1.4 mg per decilitre since 2003. At this time, atazanavir 150 mg twice daily was added to his prior treatment, including lamivudine (300 mg/day), didanosine (100 mg/day), and ritonavir (100 mg/day). During the same period, serum creatinine had gradually risen from 1.5 mg/dl to 3.63 mg/dl and the patient had no urinary symptoms. Blood pressure was 120/70 mmHg. Urinalysis revealed 300 mg of protein per deciliter in a 24-h collection, urine pH 7.0, and the urine sediment showed granular casts, epithelial cells and rodlike-shaped crystals (Fig. 1a). There was no hematuria, leukocyturia and culture remained negative. Renal ultrasound revealed normal-sized kidneys without pyelocalyceal distension. A renal biopsy showed unremarkable glomeruli, crystalline precipitation within tubular lumens (Fig. 1b), and interstitium (Fig. 1c) associated with granulomatous reaction. Polarized light microscopy analysis of urine crystals revealed that it was composed of a mixture of 60% atazanavir metabolite and 40% calcium phosphate. Plasma atazanavir concentrations measured 12 h after the last drug intake were 4737 ng/ml (normal 149–219 ng/ml), four-fold higher than the normal range of concentrations reported after boosted atazanavir administration combined with ritonavir (1023 ng/ml) [4].Fig. 1: (a) Rodlike-shaped mildly birefringent urine crystal, measuring 8–20nm and thrusting the white cell. (b) Crystalline precipitation within tubular lumens, and (c) interstitium, with damaged tubules and aggregates of multinucleated giant cells related to the crystal material.Atazanavir was withdrawn and replaced by saquinavir with no renal function improvement. One month later, the patient was treated with oral prednisone 1 mg/kg daily for 4 weeks followed by rapid tapering, resulting in partial recovery of renal function (serum creatinine level improved to 0.90 mg/dl). Only 7% of an atazanavir dose is excreted as unchanged drug in the urine. Furthermore, atazanavir sulphate is slightly soluble in water and its solubility increase with acidity of the urine (pH < 3) [4]. Thus, it is not surprising that intratubular crystal formation might occur and cause renal parenchymal injury. An unusually high atazanavir plasma level, alkaline urine, with pre-existing chronic kidney and liver diseases predisposed our patient to develop this complication. Indeed, the mean AUC (0–∞) was 42% greater in patients with impaired hepatic function than healthy volunteers [4]. One report suggested that atazanavir caused acute interstitial nephritis related to a hypersensitivity-like reaction [5]. However, there have been no previous reports indicating that atazanavir can induce renal failure due to tubular and/or interstitial crystal deposition associated with granulomatous reaction. This case suggests that atazanavir needs to be considered among the possible causes of crystal nephropathy in highly-active antiretroviral therapy-treated HIV-infected patients. It seems reasonable to recommend a short duration steroid therapy if no improvement of the renal function is noted 2 weeks after stopping Atazanavir. This is in order to limit the risk of progression to chronic renal insufficiency.

British HIV Association (BHIVA) guidelines for the treatment of HIV‐infected adults with antiretroviral therapy (2006)

British HIV Association (BHIVA) guidelines for the treatment of HIV‐infected adults with antiretroviral therapy (2006)

Lack of Interaction Between Atazanavir and Proton Pump Inhibitors in HIV-Infected Patients Treated With Ritonavir-Boosted Atazanavir

To the Editor: Conflicting results have been recently published concerning drug interaction between atazanavir (ATV) and antacid treatments, especially proton pump inhibitors (PPIs). In the August 1, 2005 issue of this journal, Khanlou and Farthing1 summarized the results they collected in 10 HIV clinics in Los Angeles, saying that the use of ATV, even boosted with ritonavir (RTV), with PPIs should be avoided. These data require some comments. In this study, the prospective method of plasma collection is not clearly defined. Were the patients interviewed by a physician on the treatment they were really taking? Did the nurse who drew the blood samples ask the patients when they had taken their last dose of ATV and antacid treatment? The median ATV minimum concentrations (Cmins) reported are not in keeping with values observed in recent published studies and in our experience on HIV-infected patients treated with boosted ATV (Table 1).TABLE 1: Median ATV Cmin in Patients Treated With Boosted ATV (300/100 mg/d)Because of its chemical structure, ATV absorption is highly dependent on an appropriate gastric pH. The potential interaction between ATV and PPIs or histamine-2 receptor blockers (H2RBs) is expected to reduce ATV exposure. In the presence of an H2RB, however, the median ATV Cmin reported in this study was 2-fold higher than values observed in the previously reported series (performed in patients without antacid treatment). Such a high ATV Cmin was found in only 1 study on healthy volunteers.2 In presence of PPIs, the median ATV Cmin was found to be strictly comparable to those observed in the previous studies, where a significant reduction should be expected. These results could be explained by too short a time between blood sample collection and drug intake. Assessing the time between ATV intake and blood collection precisely is fundamental in such a study. Only ATV plasma concentrations measured 24 ± 4 hours (Cmin) after the last intake should be taken into account in patients who have received a stable ATV regimen for at least 1 week before blood sampling. Treatments received by the patients included in this study should be detailed. The proportion of patients receiving ATV boosted with RTV may indeed highly influence the Cmin values observed. The results collected in such patients should therefore be distinguished from those collected in patients receiving ATV without RTV. In our prospective cohort of 184 patients, median Cmins measured at 24 ± 4 hours were 499 [26-2205] ng/mL and 99 [12-1159] ng/mL among the 141 patients treated with 300 mg of ATV plus 100 mg of RTV and the 43 patients receiving 400 mg of ATV alone, respectively (P < 0.0001). The combination of ATV with another protease inhibitor or nonnucleoside reverse transcriptase inhibitor may lead to significant drug interactions and should also be noted. During PPI treatment, the time during which the intragastric pH is above 4.0 increases with the acid-suppressive dose, and pH can vary widely during the day in a given individual. Doses of PPIs may affect ATV absorption differently and have to be precisely described. The time interval between ATV and antacid drug administration may also play a role. This is a possible confusion bias if patients did not state the time of their last drug intake accurately. In our cohort, we prospectively compared ATV Cmin in HIV-infected patients receiving ATZ plus RTV, with or without a PPI, to assess this specific drug interaction in clinical practice. Among the first 92 patients enrolled, 13 stated that they were taking a PPI. Among these 13 patients, 10 were using omeprazole (20 mg/d, except for 1 patient who was taking 40 mg/d) and 3 were using rabeprazole (30 mg/d). Median ATV trough concentrations were 551 ng/mL (range: 203-1976 ng/mL) in the patients receiving PPIs and 469 ng/mL (range: 65-1944 ng/mL) in the group without PPIs. Results showed that PPI treatment did not affect ATV Cmin values in our patients.3 A recent case report with pharmacokinetic study showed no interaction between boosted ATV and lansoprazole. Another study showed no clinical or immunovirologic failures in 14 patients treated with ATV and PPIs after a 6-month follow-up.4,5 Our findings are in keeping with these results. Our conclusion is therefore completely different from that of Khanlou and Farthing1 because we observed that PPIs seem to be compatible with boosted ATZ therapy in clinical practice. It is nonetheless recommended to monitor ATV drug concentrations in case of concomitant antacid treatment. Jean-Baptiste Guiard-Schmid, MD* Jean-Marie Poirier, MD† Philippe Bonnard, MD* Jean-Luc Meynard, MD† *Service des Maladies Infectieuses et Tropicales Hôpital Tenon †Service de Pharmacologie Faculté de Médecine St. Antoine and ‡Service des Maladies Infectieuses et Tropicales Hôpital St. Antoine Université Pierre et Marie Curie (Paris VI) Paris, France