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Dermatologic Manifestations of Aspergillosis Medication

  • Author: Annie Chiu, MD; Chief Editor: William D James, MD  more...
 
Updated: Mar 13, 2014
 

Medication Summary

In aspergillosis, high-dose intravenous amphotericin B has traditionally been used to eradicate the underlying organism. However, voriconazole has been approved as a first-line agent in the treatment of invasive aspergillosis and is available in both parenteral and oral formulations. A multicenter, randomized, open-label trial comparing the efficacy of voriconazole to amphotericin B demonstrated better response rates, improved survival, and fewer severe adverse effects in those receiving voriconazole therapy.[15]

Itraconazole, posaconazole, caspofungin, terbinafine, and micafungin have also been reportedly effective in some cases of aspergillosis. The length of treatment varies in the literature, but treatment is likely to be most effective if prolonged. Studies show posaconazole as an alternative treatment for invasive aspergillosis in patients previously resistant to or intolerant of other antifungal therapies.[16] Combination antifungal therapies have also been used in patients with aspergillosis that is associated with a greater degree of treatment resistance.

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Antifungal agents

Class Summary

The mechanism of action may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.

Amphotericin B (Amphocin, Fungizone)

 

Polyene antibiotic produced by a strain of Streptomyces nodosus; can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in fungal cell membrane, causing intracellular components to leak with subsequent fungal cell death.

Itraconazole (Sporanox)

 

Fungistatic activity. Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting CYP-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Voriconazole (VFEND)

 

Used for primary treatment of invasive aspergillosis and salvage treatment for infection with Fusarium species or Scedosporium apiospermum. A triazole antifungal that inhibits fungal CYP450–mediated 14 alpha-lanosterol demethylation, which is essential in fungal ergosterol biosynthesis.

Caspofungin (Cancidas)

 

Used to treat refractory invasive aspergillosis. First of a new class of antifungal drugs (glucan synthesis inhibitors). Inhibits synthesis of beta-(1,3)-D-glucan, an essential component of fungal cell wall.

Micafungin (Mycamine)

 

Member of new class of antifungal agents, echinocandins, that inhibit cell wall synthesis. Inhibits synthesis of 1,3-beta-D-glucan, an essential fungal cell wall component not present in mammalian cells.

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 infections in patients at high risk because of severe immunosuppression.

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Contributor Information and Disclosures
Author

Annie Chiu, MD Cosmetic and General Dermatologist

Annie Chiu, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, Women's Dermatologic Society

Disclosure: Received consulting fee from Temptu for consulting; Received honoraria from Galderma for consulting; Received honoraria from SkinMedica for consulting.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Associate Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Acknowledgements

Alexa F Boer Kimball, MD, MPH Associate Professor of Dermatology, Harvard University School of Medicine; Vice Chair, Department of Dermatology, Massachusetts General Hospital; Director of Clinical Unit for Research Trials in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital

Alexa F Boer Kimball, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Peter Fritsch, MD Chair, Department of Dermatology and Venereology, University of Innsbruck, Austria

Peter Fritsch, MD is a member of the following medical societies: American Dermatological Association, International Society of Pediatric Dermatology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

References
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