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Tinea Corporis Medication

  • Author: Jack L Lesher, Jr, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Nov 17, 2015
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Topical antifungal agents are effective for treating most cases of tinea corporis. Systemic therapy may be indicated for tinea corporis that is extensive, involves immunocompromised patients, or is refractory to topical therapy. For severe infections, systemic therapy can be combined with topical antifungal treatments.

Oral granules of terbinafine (Lamisil) are available in packets containing 125 mg and 187.5 mg and are for use in children with tinea capitis who are aged 4 years and older; these granules can be sprinkled once daily on pudding or mashed potatoes. While approved only for tinea capitis, these oral granules likely are used off label in children with tinea corporis when systemic therapy is needed. The suggested dosing schedule for tinea capitis is 125 mg/d for less than 25 kg body weight, 187.5 mg/d for 25-35 kg body weight, and 250 mg/d for greater than 35 kg body weight.

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Topical allylamines

Naftifine 1% cream or gel (Naftin)

 

Naftifine is a broad-spectrum antifungal agent that appears to interfere with sterol biosynthesis by inhibiting the enzyme squalene 2,3-epoxidase. This inhibition results in decreased amounts of sterols, causing cell death. If no clinical improvement occurs after 4 weeks, reevaluate patient.

Terbinafine topical (Lamisil)

 

Terbinafine topical has fungicidal activity; it is a synthetic allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis of fungi, resulting in a deficiency in ergosterol that causes fungal cell death. Use it until symptoms significantly improve.

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Topical pyridones

Ciclopirox olamine 1% cream (Loprox)

 

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

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Topical benzylamines

Butenafine 1% cream (Mentax)

 

Butenafine inhibits squalene epoxidation, which, in turn, causes blockage of ergosterol biosynthesis (an essential component of fungal cell membranes), causing fungal cell growth to arrest.

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Systemic azoles

Fluconazole (Diflucan)

 

Fluconazole is a synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation, which prevents the conversion of lanosterol to ergosterol, thereby disrupting cellular membranes. It has little affinity for mammalian cytochromes, which is believed to explain its low toxicity. Fluconazole is available as tablet for oral administration, as powder for oral suspension, and as a sterile solution for intravenous use. It has fewer adverse effects and better tissue distribution than older systemic imidazoles.

Itraconazole (Sporanox)

 

Itraconazole has fungistatic activity; it is a synthetic triazole antifungal agent that inhibits fungal cell growth by inhibiting the cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Ketoconazole (Nizoral)

 

Ketoconazole inhibits the synthesis of ergosterol (main sterol of fungal cell membranes), causing cellular components to leak; this results in cell death. It is rarely used because of effective alternative agents and the risk of hepatotoxicity.

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Systemic allylamines

Terbinafine (Lamisil, Daskil)

 

Terbinafine has fungicidal activity; it is a synthetic allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis of fungi, resulting in a deficiency in ergosterol that causes fungal cell death. Use it until symptoms significantly improve.

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Other systemic antifungals

Griseofulvin (Fulvicin)

 

Griseofulvin has fungistatic activity; fungal cell division is impaired by interfering with microtubules. It binds to keratin precursor cells. Keratin is gradually replaced by noninfected tissue, which is highly resistant to fungal invasions.

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Topical azoles

Clotrimazole 1% cream (Mycelex, Lotrimin)

 

Clotrimazole is a nonabsorbable imidazole. It is a broad-spectrum synthetic antifungal agent that inhibits growth of fungus by altering cell membrane permeability, which causes fungal cell death. Therapy is directed at the underlying condition, with the goal of minimizing symptoms and preventing complications.

Ketoconazole topical (Nizoral)

 

Ketoconazole topical is an imidazole, broad-spectrum antifungal agent indicated for topical treatment of tinea corporis. It inhibits the synthesis of ergosterol (main sterol of fungal cell membranes), causing cellular components to leak; the result is cell death.

Miconazole topical (Monistat)

 

Miconazole damages the fungal cell-wall membrane by inhibiting the biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak and resulting in fungal cell death. Lotion is preferred in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.

Oxiconazole 1% cream (Oxistat)

 

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

Sertaconazole 2% cream (Ertaczo)

 

Sertaconazole is a topical imidazole antifungal active against T rubrum, T mentagrophytes, and Epidermophyton floccosum.

Sulconazole 1% cream or solution (Exelderm)

 

Sulconazole is a broad-spectrum antifungal agent that inhibits the synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.

Luliconazole (Luzu)

 

Luliconazole is available as a 1% topical cream administered once daily for 1 week. It is an imidazole antifungal that alters the fungal cell membrane by interacting with 14-alpha demethylase (an enzyme necessary for conversion of lanosterol to ergosterol). It is indicated for tinea corporis.

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Contributor Information and Disclosures
Author

Jack L Lesher, Jr, MD Chief, Professor, Department of Internal Medicine, Section of Dermatology, Medical College of Georgia

Jack L Lesher, Jr, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, Medical Association of Georgia, Society for Investigative Dermatology, Southern Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Rosalie Elenitsas, MD Herman Beerman Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, Pennsylvania Academy of Dermatology

Disclosure: Received royalty from Lippincott Williams Wilkins for textbook editor.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

Additional Contributors

Janet Fairley, MD Professor and Head, Department of Dermatology, University of Iowa, Roy J and Lucille A Carver College of Medicine

Janet Fairley, MD is a member of the following medical societies: American Academy of Dermatology, American Federation for Medical Research, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Mary Elizabeth Rushing Lott, MD and Gwendolyn Zember, MD, to the development and writing of this article.

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Large, erythematous, scaly plaque.
 
 
 
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