Tinea Pedis Medication

  • Author: Courtney M Robbins, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jan 24, 2012
 

Medication Summary

Tinea pedis can be treated with topical or oral antifungals or a combination of both.[7, 8, 9] Topical agents are used for 1-6 weeks, depending on manufacturers' recommendations. A patient with chronic hyperkeratotic (moccasin) tinea pedis should be instructed to apply medication to the bottoms and sides of his or her feet. For interdigital tinea pedis, even though symptoms may not be present, a patient should apply the topical agent to the interdigital areas and to the soles because of the likelihood of plantar-surface infection.

Recurrence of tinea pedis is often due to a patient's discontinuance of medication after symptoms abate. A simple strategy to increase a patient's compliance is to prescribe a large quantity of topical medicine, which may motivate a patient to continue use until the entire tube is empty.

Moccasin-type tinea pedis is often recalcitrant to topical antifungals alone, owing to the thickness of the scale on the plantar surface. The concomitant use of topical urea or other keratolytics with topical antifungals should improve the response to topical agents. In addition, for moccasin tinea pedis caused by Scytalidium species, Whitfield solution, containing benzoic and salicylic acids, can be beneficial. However, patients with extensive chronic hyperkeratotic tinea pedis or inflammatory/vesicular tinea pedis usually require oral therapy, as do patients with concomitant onychomycosis,[10] diabetes,[11] peripheral vascular disease, or immunocompromising conditions.

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Topical imidazoles

Class Summary

Effective in all forms of tinea pedis but are excellent treatments for interdigital tinea pedis because they are effective against dermatophytes and Candida. Some of these drugs (eg, econazole) also have antibacterial activity.

Clotrimazole 1% (Mycelex, Lotrimin)

 

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

Econazole (Spectazole Topical)

 

Effective in cutaneous infections. May interfere with RNA and protein synthesis and metabolism. Disrupts cell membrane permeability, causing death of fungal cells.

Ketoconazole topical (Nizoral)

 

Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak, resulting in death of fungal cells.

Miconazole topical (Monistat)

 

Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out, resulting in fungal cell death. The 2% lotion is preferred in intertriginous areas. If the 2% cream is used, apply sparingly to avoid maceration effects.

Oxiconazole 1% cream (Oxistat)

 

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

Sertaconazole nitrate cream (Ertaczo)

 

Topical imidazole antifungal active against T rubrum, T mentagrophytes, and E floccosum. Indicated for tinea pedis.

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Topical pyridones

Class Summary

Broad-spectrum agents with antidermatophytic, antibacterial, and anticandidal activity and are therefore useful in all forms of tinea pedis but especially effective in interdigital tinea pedis.

Ciclopirox 1% cream (Loprox)

 

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

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Topical allylamines

Class Summary

Effective in treating all forms of tinea pedis. In vitro, these agents have demonstrated potent activity against dermatophyte fungi, so they are useful in treating patients with refractory tinea pedis (eg, chronic hyperkeratotic). Terbinafine 1% (Lamisil) has been shown to be effective in some patients with interdigital tinea pedis with only 1 wk of treatment. Patients with chronic hyperkeratotic tinea pedis generally require 4 wk of treatment.

Naftifine 1% cream and gel (Naftin)

 

Broad-spectrum antifungal agent and synthetic allylamine derivative; may decrease synthesis, which, in turn, inhibits growth of fungal cells.

Terbinafine topical (Lamisil)

 

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

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Topical benzylamines

Class Summary

Sometimes classified as a subset of allylamines. Useful for treating patients with refractory tinea pedis (eg, chronic hyperkeratotic). Have been shown to be effective in some patients with interdigital tinea pedis with only 1 wk of treatment.[12]

Butenafine (Mentax)

 

Damages fungal cell membranes, arresting growth of fungal cells.

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Oral antimycotics

Class Summary

Should be considered in patients with extensive chronic hyperkeratotic or inflammatory/vesicular tinea pedis. Could also be used for patients with disabling disease, patients in whom topical treatments have failed, patients with diabetes or peripheral vascular disease, and patients with immunocompromising conditions.

Itraconazole (Sporanox)

 

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

Terbinafine (Lamisil, Daskil)

 

Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing death of fungal cells. Use until symptoms significantly improve.

Fluconazole (Diflucan)

 

Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation.

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Dermatological agents

Class Summary

May use to supplement antimycotic agents in certain clinical situations.

Aluminum acetate (Otic Domeboro, Burow's Solution)

 

Drying agent for vesicular tinea pedis. Dissolve aluminum acetate tablets in water to produce a 1:10-40 solution.

Ammonium lactate lotion (Lac Hydrin)

 

Used to decrease scaling in patients with hyperkeratotic soles. Contains lactic acid, an alpha hydroxy acid that has keratolytic action and thus facilitates release of comedones. Causes disadhesion of corneocytes. Available in 12% and 5% strengths. Use 12% lotion.

Urea, topical (Carmol-40, Keralac)

 

Used to decrease scaling in patients with hyperkeratotic soles. Promotes hydration and removal of excess keratin by dissolving the intracellular matrix. Available in 10-40% concentration.

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Contributor Information and Disclosures
Author

Courtney M Robbins, MD  Dermatologist, Associated Dermatologists, Birmingham, AL

Courtney M Robbins, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Boni E Elewski, MD  Professor, Department of Dermatology, University of Alabama at Birmingham

Boni E Elewski, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

Gregory J Raugi, MD, PhD  Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle

Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology

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.

Lester F Libow, MD  Dermatopathologist, South Texas Dermatopathology Laboratory

Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association

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

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.

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