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Aspergillosis 2016

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5 Treatment Antifungal Agents for Aspergillosis Amphotericin B (AmB) Î AmB deoxycholate and its lipid derivatives are appropriate options for initial and salvage therapy of Aspergillus infections when voriconazole cannot be administered. However, AmB deoxycholate should be reserved for use in resource-limited settings in which no alternative agents are available. Lipid formulations of AmB should be considered in settings in which azoles are contraindicated or not tolerated (S-M). Î Aerosolized formulations of AmB may be considered as prophylaxis in patients with prolonged neutropenia (patients receiving induction/re- induction therapy for acute leukemia and allogeneic HSCT recipients following conditioning or during treatment of GVHD) and in lung transplant recipients (W-L). Echinocandins Î Echinocandins are effective in salvage therapy (either alone or in combination) against IA, but the IDSA does not recommend their routine use as monotherapy for the primary treatment of IA (S-M). Triazoles Î Triazoles are preferred agents for treatment and prevention of IA in most patients (S-H). Î For patients receiving triazole-based therapy for IA, prolonged azole prophylaxis, or other therapies for which drug interactions with azoles are anticipated, the IDSA recommends therapeutic drug monitoring (TDM) once the steady state has been reached (S-M). • A moderate amount of data for itraconazole, voriconazole, and posaconazole suspension suggests this approach may be valuable in enhancing therapeutic efficacy, in evaluating therapeutic failures attributable to suboptimal drug exposures, and to minimize toxicities potentially attributable to the azoles (S-M). • Further studies are needed to address whether TDM is helpful or necessary with the extended release or intravenous formulations of posaconazole or for isavuconazole. Î Clinicians should obtain serum trough drug levels for azole antifungal agents (itraconazole, voriconazole, posaconazole, and possibly isavuconazole) and for potentially interacting drugs such as cyclosporine, tacrolimus, and sirolimus (and other CYP450 3A4 substrates such as tyrosine kinase inhibitors) to optimize therapeutic efficacy and to avoid potential toxicities of both groups of agents (S-M).

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