Tinea Cruris Medication

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

Medication Summary

To achieve the best results, particularly with follicular or extensive tinea cruris, the authors often recommend a combination of topical and systemic therapy.[9]

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Antifungal agents

Class Summary

The 2 classes of antifungal medications used most commonly to treat tinea cruris are the azoles and the allylamines. Azoles inhibit the enzyme lanosterol 14-alpha-demethylase, an enzyme that converts lanosterol to ergosterol, which is an important component of the fungal cell wall. Membrane damage results in permeability problems and renders the fungus unable to reproduce. Allylamines inhibit squalene epoxidase, which is an enzyme that converts squalene to ergosterol, resulting in the accumulation of toxic levels of squalene in the cell and in cell death. Examples of both classes of antifungal agents are available for topical and systemic administration.

Studies have found terbinafine to be effective and well tolerated in children.[10] Terbinafine 1% emulsion gel was found to be more effective than ketoconazole 2% cream in the treatment of tinea cruris.[11]

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Terbinafine (Lamisil)

 

Synthetic allylamine derivative, which inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi that results in a deficiency of ergosterol, causing fungal cell death. Widely studied and effective topical or oral antifungal. Topical form available without prescription. Some clinicians reserve this drug for more widespread/resistant infections because of its broad coverage and increased cost. Studies have found this medication to be effective and well tolerated in children.

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Butenafine (Mentax)

 

Potent antifungal related to the allylamines. Damages fungal cell membranes causing fungal cell growth to arrest.

Available in 1% cream only.

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Clotrimazole topical (Lotrimin, Mycelex)

 

Often, first-line drug used in the treatment of tinea cruris. 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.

Available without a prescription. 1% cream, solution/spray, and lotion available.

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Miconazole (Micatin, Monistat-Derm)

 

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

Available without a prescription, and 2% cream, solution/spray, lotion, and powder forms available. Lotion is preferred in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.

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Ketoconazole topical (Nizoral)

 

2% cream. Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death.

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Econazole (Spectazole)

 

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

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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

Available in 1% cream or solution.

If no clinical improvement after 4 wk, reevaluate patient.

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Oxiconazole (Oxistat)

 

Broad-spectrum antifungal agent. Inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death.

1% cream or lotion.

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Tolnaftate (Tinactin)

 

Nonprescription medication used in the treatment of tinea cruris. Available in 1% cream, solution/spray, and powder.

Haloprogin (Halotex)

 

Agent for use in the treatment of tinea cruris. Prescription only. Available in 1% cream and solution/spray.

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Ciclopirox (Loprox)

 

Synthetic broad-spectrum antifungal agent. Interferes with synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells. Prescription only. Available in 1% cream and lotion.

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Itraconazole (Sporanox)

 

Fungistatic activity. Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P450-dependent synthesis of ergosterol, a vital component of fungal cell membranes. Widely used and well-studied oral antifungal that can be used in the treatment of tinea cruris. Studies have shown that it is tolerated better than griseofulvin. Best results are noted 2-3 wk after the end of treatment.

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Sulconazole (Exelderm)

 

Broad-spectrum antifungal agent. Inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death.

1% cream or solution.

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Griseofulvin (Fulvicin-U/F, Grifulvin-V)

 

Fungistatic activity. Fungal cell division is impaired by interfering with microtubule. Binds to keratin precursor cells. Keratin gradually is replaced by noninfected tissue, which is highly resistant to fungal invasions.

Less effective than itraconazole in treatment of tinea cruris.

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Contributor Information and Disclosures
Author

Michael Wiederkehr, MD  Consulting Staff, Livingston Dermatology Associates; Consulting Staff, Comprehensive Dermatology and Laser Center

Michael Wiederkehr, MD is a member of the following medical societies: Alpha Omega Alpha and American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

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.

Richard P Vinson, MD  Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, 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.

Glen H Crawford, MD  Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital

Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons

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.

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Tinea cruris.
Tinea cruris.
Tinea cruris.
Tinea cruris (hematoxylin and eosin stain).
Tinea cruris (periodic acid-Schiff stain, magnification X 20).
Tinea cruris (Gomori methenamine-silver stain, magnification X 20).
 
 
 
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