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).
