Tinea Versicolor Medication

  • Author: Craig G Burkhart, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Feb 28, 2012
 

Medication Summary

Tinea versicolor responds well to both topical and oral antimycotic therapies. Many patients prefer oral therapy because of its convenience.

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Antifungals

Class Summary

Topical antifungals temporarily eradicate the condition, although treatment may need to be intermittently repeated to prevent recurrence. Oral therapy for tinea versicolor is convenient and effective, but it does not prevent recurrences. A once-monthly (for 6 mo) oral dose of fluconazole is a popular alternative.

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Terbinafine topical (Lamisil)

 

Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing fungal cell death. Use medication until symptoms significantly improve. Duration of treatment should be >1 wk but not >4 wk.

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Clotrimazole topical (Mycelex, Lotrimin-AF)

 

Broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing fungal cell death. Reevaluate diagnosis if no clinical improvement after 4 wk.

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Ketoconazole (Nizoral)

 

Both topical and systemic agent. Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. Achieves excellent skin levels with minimal oral dosing. M furfur is eradicated by the presence of ketoconazole in outer skin layers. Tinea versicolor is extremely rare in small children; thus, do not treat children aged < 10 y with oral ketoconazole for tinea versicolor.

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Ciclopirox (Loprox)

 

Interferes with synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells.

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Butenafine (Mentax)

 

Damages fungal cell membranes causing fungal cell growth to arrest.

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Naftifine (Naftin)

 

Broad-spectrum antifungal agent and synthetic allylamine derivative; may decrease the synthesis of ergosterol, which, in turn, inhibits fungal cell growth. If no clinical improvement after 4 wk, reevaluate the patient.

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Econazole (Spectazole)

 

Effective in cutaneous infections. Interferes with RNA and protein synthesis and metabolism. Disrupts fungal cell wall membrane permeability, causing fungal cell death.

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Oxiconazole (Oxistat)

 

Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out and resulting in fungal cell death.

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Contributor Information and Disclosures
Author

Craig G Burkhart, MD, MPH  Clinical Professor, Department of Medicine, Section of Dermatology, The University of Toledo College of Medicine; Clinical Assistant Professor, Department of Dermatology, Ohio State University College of Medicine

Craig G Burkhart, MD, MPH is a member of the following medical societies: American Academy of Dermatology, Ohio State Medical Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Coauthor(s)

Craig N Burkhart, MD, MSBS  Assistant Professor, Department of Dermatology, University of North Carolina at Chapel Hill

Craig N Burkhart, MD, MSBS is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Kathryn Schwarzenberger, MD  Associate Professor of Medicine, Division of Dermatology, University of Vermont College of Medicine; Consulting Staff, Division of Dermatology, Fletcher Allen Health Care

Kathryn Schwarzenberger, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, American Dermatological Association, Dermatology Foundation, Medical Dermatology Society, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Edward F Chan, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine

Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Lorie Gottwald, MD Chief, Division of Dermatology, Associate Professor, Department of Internal Medicine, Medical College of Ohio at Toledo

Lorie Gottwald, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Medical Association, American Medical Student Association/Foundation, and American Medical Women's Association

Disclosure: Nothing to disclose.

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