While voriconazole has the potential to interact with the ‘statins’ that are CYP3A4 learn more or CYP2C9 substrates, there are no published data describing such an
interaction to date. Similarly, there are no published data describing an interaction between posaconazole and a ‘statin’. Nonetheless, it is reasonable to assume that voriconazole and posaconazole will interact with the statins that are CYP3A4 substrates (lovastatin, simvastatin and atorvastatin). Therefore, if possible, when using voriconazole or posaconazole, the CYP3A4-dependent statins should be used cautiously, if at all. In addition, it is reasonable to assume that voriconazole like fluconazole will interact with fluvastatin, which is a CYP2C9 substrate. Therefore, this combination should be avoided if possible. There are no data examining whether voriconazole or posaconazole R788 cell line interacts with either pravastatin or rosuvastatin. Nonetheless, based upon data with itraconazole, it is likely pravastatin and rosuvastatin can be used with voriconazole or posaconazole. Interactions involving azoles and antiretroviral agents. Patients infected with HIV with low CD4+ counts often require antifungal therapy for the prevention or treatment of opportunistic fungal infections.
The antiretroviral class of agents continues to grow as the treatment of HIV infection continually evolves. The azoles may interact with antiretroviral agents through several mechanisms, and thus, there are many potential interactions between the azoles and certain antiretroviral agents. However, few data from studies of these interactions are available in the literature. Therefore, clinicians should utilise additional resources when combining these drug classes. The drug interaction sections of prescribing information for each agent provide concise listings and summaries of pertinent findings from studies on file with the respective manufacturers of antiretroviral and antifungal agents.
In addition, there are several online resources that are frequently updated and provide information on antiretroviral drug interactions from the literature 3-oxoacyl-(acyl-carrier-protein) reductase and citations of the latest findings presented at scientific symposia. These resources include, but are not limited to the following: http://www.hivinsite.com, http://www.aidsinfo.nih.gov, http://www.drug-interactions.com, http://www.hivmedicationguide.com, http://www.hivpharmacology.com.122 Interactions between the azoles and antiretrovirals that result from the inhibition of CYP-mediated biotransformation can be difficult to predict because certain antiretroviral agents can inhibit and/or induce a given CYP enzyme. In addition, which activity predominates may be dose related. For example, ritonavir is a protease inhibitor that is primarily metabolised by CYP3A4 and somewhat less by CYP2D6.123–126 In addition, ritonavir is a potent CYP3A4 inhibitor that can simultaneously induce CYP3A4.