Atazanavir and Acid-Lowering Therapy: RESULTS part 2
A survey of 10 HIV clinics in Los Angeles identified 50 patients who were being treated with atazanavir and either a PPI or an H2 receptor antagonist. Trough concentrations of atazanavir were available for 34 of the patients (15 receiving a PPI and 19 receiving an H2 receptor antagonist). For the patients receiving a PPI, the mean CD4 count was 267 cells/mm3, and 2 patients (13%) had a viral load of less than 50 copies/mL. For the patients receiving H2 receptor antagonists, the mean CD4 count was 400 cells/mm3, and 3 patients (16%) had a viral load less than 50 copies/mL. The mean trough concentration of the atazanavir among the 15 patients receiving a PPI was lower than that among the 19 patients receiving an H2 receptor antagonist (0.65 versus 1.12 pg/mL; p value not reported). The mean atazanavir concentrations achieved with different dosing regimens were not reported.
Using a chart review, Antoniou and others attempted to determine the clinical impact of acid-lowering therapy on virologic response in antiretroviral-experienced patients receiving atazanavir-containing regimens. Fifteen patients who had been receiving atazanavir for a minimum of 4 weeks concomitantly with a PPI or an H2 receptor antagonist were included, but only 14 of them had adequate documentation for evaluation. Thirteen of the patients were men, and the median age of all patients was 51.5 years (range 38-68 years). Before initiation of an atazanavir-containing regimen, patients in this cohort had received a median of 3 highly active antiretroviral therapy regimens (range 1-8) over a median of 6.5 years (range 1-9 years). Seven of the patients had a baseline viral load of less than 50 copies/mL. Given that some patients had undetectable viral loads at baseline, it is important to note that in each of these patients, the atazanavir was being used to replace another antiretroviral agent in the context of full viral suppression. Four of the patients were receiving tenofovir, which can also reduce atazanavir levels. Eight of the patients were receiving atazanavir 300 mg boosted with ritonavir 100 mg once daily. Ten patients were taking a PPI, including lansoprazole, omeprazole, pantoprazole, or esomeprazole. Three patients were receiving ranitidine. At last follow- up, 12 of the patients had undetectable viral loads; the duration of follow-up ranged from 8 to 76 weeks.
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The effect of concomitant use of atazanavir and PPIs was further explored in a chart review of 301 HIV- positive patients. Patients included in the relevant analysis were older than 18 years of age and were receiving atazanavir, either alone or in combination with ritonavir, and a PPI. Twelve adults, 6 of whom were female, were identified as meeting the inclusion criteria. The median age was 38 years (range 25-60 years). Seven of the patients had previous treatment experience with protease inhibitors, and 4 had a viral load less than 400 copies/mL at baseline. The PPIs used and their dosing regimens varied among the patients. In total, 9 subjects had undetectable viral loads (less than 400 copies/mL), with durations of concurrent therapy ranging from 4 to 23 months.
Furtek and others14 conducted a chart review for patients receiving atazanavir-containing regimens, comparing the virological responses of those taking concomitant PPI therapy and those not receiving PPIs. Of the 76 patients who were receiving atazanavir, as identified by pharmacy records, only 10 were receiving concomitant PPI treatment: 8 patients received rabeprazole 20 mg daily, 1 patient received rabeprazole 40 mg daily, and 1 patient received omeprazole 20 mg daily. There was no difference in virological outcomes between the 2 groups (p = 1.00; 95% CI 0.21-85.97).