The Expanding Class of Non-Nucleoside Reverse Transcriptase Inhibitors for the Treatment of HIV-1 Infection.

alternatives. Because EFV is metabolized by CYP 3A4, other drugs that are inducers or inhibitors of this enzyme may increase or decrease EFV concentrations. Because EFV also induces CYP 3A4, agents that are substrates for this enzyme may have lower concentrations when coadministered with EFV. For example, the concomitant use of the protease inhibitor (PI) atazanavir (Reyataz, ATV, Bristol-Myers Squibb) in treatment-naive patients is not recommended unless it is boosted by ritonavir (RTV, Norvir, Abbott), because ATV’s AUC concentration can decrease significantly when taken with EFV.1,4 Some antifungal agents increase the AUC concentration of EFV, and dosage adjustments are warranted. However, concomitant administration of EFV and voriconazole (Vfend, Pfizer) is contraindicated; voriconazole levels are reduced significantly with standard dosing.1,5 Administration of antimycobacterial agents with EFV may also cause drug interactions. Coadministration with rifampin (Rifadin, Sanofi-aventis) decreases the AUC concentration of EFV, whereas coadmini stration with rifabutin (Mycobutin, Pfizer) decreases the AUC concentration of rifabutin. Thus, it is often recommended that the combination of EFV and rifampin be avoided in favor of combining EFV with a higher-than-normal dose of rifabutin.1,6,7 Some antiepileptic drugs are also affected by EFV. For example, carbamazepine (e.g., Carbatrol, Shire) causes a dual decrease in both EFV and carbamazepine AUC concentrations.1,8 Therefore, it may be advisable to avoid this combination of agents when possible. Additional clinically relevant drug–drug interactions with EFV are presented in Table 1.