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Aspergillosis Medication

  • Author: Eloise M Harman, MD; Chief Editor: Ryland P Byrd, Jr, MD  more...
 
Updated: Apr 01, 2015
 

Medication Summary

The treatment of invasive aspergillosis and chronic necrotizing pulmonary aspergillosis (CNPA) requires intravenous antifungal therapy. Voriconazole is usually first-line therapy, sometimes in combination with other agents, such as caspofungin. Another triazole antifungal agent, isavuconazole, is also indicated for invasive aspergillosis. Amphotericin may sometimes be prescribed in treatment failures.

Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction treated with corticosteroids. The addition of oral antifungal therapy with itraconazole may be beneficial in the management of ABPA. Aspergillomas may respond to prolonged oral itraconazole therapy. Intracavitary therapy with amphotericin has also been used in small numbers of patients.

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Antifungal agents

Class Summary

Mechanism of action may involve increasing the permeability of the cell membrane, which, in turn, causes intracellular components to leak.

Amphotericin B (Abelcet, AmBisome, Amphotec)

 

Polyene antibiotic produced by a strain of Streptomyces nodosus. Can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in the fungal cell membrane, causing intracellular components to leak, with subsequent fungal cell death. Newer lipid formulations are as effective as original formulation and have less nephrotoxicity. May be associated with fever, rigors, and nausea (premedication with hydrocortisone and meperidine may be beneficial). Adequate hydration may decrease nephrotoxicity, and patients who can tolerate fluid should be administered pre- and post-hydration.

Itraconazole (Sporanox)

 

Synthetic triazole antifungal agent with greater activity against Aspergillus than fluconazole or ketoconazole. Fungistatic activity. Slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Available in PO formulations (eg, cap, susp) and is useful for prolonged antifungal therapy. IV formulation has recently become available. Because it is insoluble in water, the PO and IV susp are solubilized with hydroxypropyl-beta-cyclodextrin.

Caspofungin (Cancidas)

 

Antifungal with efficacy against A fumigatus,A flavus, and Aspergillus terreus. First of a new class of antifungals called echinocandins. Works on a component of fungal cell walls that is not present in mammalian cells. Indicated for Aspergillus infection in patients who are refractory to or cannot tolerate other therapies. Has not been studied for primary therapy.

Voriconazole (VFEND)

 

Used for primary treatment of invasive aspergillosis and salvage treatment of Fusarium species or Scedosporium apiospermum infections. A triazole antifungal agent that inhibits fungal cytochrome P-450–mediated 14 alpha-lanosterol demethylation, which is essential in fungal ergosterol biosynthesis.

Posaconazole (Noxafil)

 

Triazole antifungal agent. Blocks ergosterol synthesis by inhibiting the enzyme lanosterol 14-alpha-demethylase and sterol precursor accumulation. This action results in cell membrane disruption. Available as oral susp (200 mg/5 mL). Indicated for prophylaxis of invasive Aspergillus and Candida infections in patients at high risk because of severe immunosuppression.

Isavuconazole (Cresemba)

 

Triazole antifungal agent. Isavuconazole is the active moiety of the prodrug isavuconazonium sulfate. It is indicated for invasive aspergillosis and has activity against most strains of the following microorganisms, both in vitro and in clinical infection: Aspergillus flavus, Aspergillus fumigatus, and Aspergillus niger.

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Corticosteroids

Class Summary

Useful in the management of allergic reactions. These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.

Prednisone (Deltasone, Meticorten, Orasone)

 

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

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Contributor Information and Disclosures
Author

Eloise M Harman, MD Staff Physician and MICU Director, Pulmonary Division, Gainesville Veterans Affairs Medical Center

Eloise M Harman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American Medical Womens Association, American Thoracic Society, Phi Beta Kappa, Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Oleh Wasyl Hnatiuk, MD Program Director, National Capital Consortium, Pulmonary and Critical Care, Walter Reed Army Medical Center; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences

Oleh Wasyl Hnatiuk, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

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