Tinea Faciei Medication

  • Author: Jacek C Szepietowski, MD, PhD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jan 25, 2012
 

Medication Summary

Topical therapy may be sufficient if follicular papules are not present. The 2 classes of antifungal medication most commonly used to treat tinea faciei in practice are azoles and allylamines. Azoles inhibit lanosterol 14-alpha-demethylase, an enzyme that converts lanosterol to ergosterol, an important component of the fungal cell wall. Membrane damage leads to permeability problems and renders the fungus unable to reproduce. Allylamines inhibit squalene epoxidase, an enzyme that converts squalene to ergosterol; this inhibition also leads to the accumulation of toxic levels of squalene in the cell and to cell death. Several antifungal products from both classes are available for topical and systemic administration.[17]

Re-evaluation of the tinea diagnosis is important if clinical improvement is not observed after 4 weeks of therapy.

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Antifungal agents

Class Summary

With these agents, the mechanism of action may involve an alteration in cell membrane permeability, DNA or RNA synthesis, or intracellular levels of metabolites that are toxic to the fungal cell.

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Butenafine (Mentax)

 

Potent antifungal related to allylamines. Available as a 1% cream.

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Clotrimazole topical (Lotrimin, Mycelex)

 

Broad-spectrum antifungal agent that inhibits yeast and fungal growth by altering cell membrane permeability. Frequently prescribed for patients with tinea faciei. Available without a prescription as 1% cream, solution or spray, and lotion.

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Miconazole (Femizole-7, Micatin, Absorbine)

 

Damages fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased; this effect causes nutrients to leak out. Available as 2% cream, solution or spray, lotion, and powder. Lotion is preferred for use in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.

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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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Oxiconazole (Oxistat)

 

Damages fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased causing nutrients to leak out. Available as a 1% cream or lotion.

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Undecylenic acid & derivatives (Desenex, Cruex, Fungoid AF, Gordochom)

 

Nonprescription agent rarely used in the treatment of tinea faciei. Available in cream or solution or spray.

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Tolnaftate (Absorbine, Aftate, Breeze, Dr. Scholl's Athlete's Foot)

 

Nonprescription medication available in 1% cream, solution or spray, and powder.

Haloprogin (Halotex)

 

Agent for use in the treatment of superficial cutaneous infections. Available in 1% cream and solution or spray.

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Ciclopirox (Loprox)

 

Interferes with synthesis of RNA, DNA, and proteins by inhibiting transport within fungal cells. Available as a 1% cream and lotion for skin.

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Terbinafine (Lamisil, Daskil)

 

Member of allylamine family, fungicidal agents that inhibit ergosterol synthesis by means of squalene epoxidase. Result is a decreased ergosterol level and accumulation of squalene, which is toxic to fungal cells.

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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. Best results are noted 2-3 wk after treatment.

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Fluconazole (Diflucan)

 

Fungistatic activity. Synthetic oral antifungal (ie, broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation. This inhibition prevents the conversion of lanosterol to ergosterol, thereby disrupting cellular membranes.

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Griseofulvin (Fulvicin P/G, Gris-PEG)

 

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

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Contributor Information and Disclosures
Author

Jacek C Szepietowski, MD, PhD  Professor, Vice-Head, Department of Dermatology, Venereology and Allergology, Wroclaw Medical University; Director of the Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Poland

Disclosure: Stiefel GSK Company Salary Employment; Orfagen Consulting fee Consulting; Maruho Consulting fee Consulting; Astellas Consulting fee Consulting; Abbott Consulting fee Consulting; Leo Pharma Consulting fee Consulting

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

Bernice R Krafchik, MBChB, FRCPC  Professor Emeritus, Department of Pediatrics, Section of Dermatology, University of Toronto

Bernice R Krafchik, MBChB, FRCPC is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Royal College of Physicians and Surgeons of Canada, and Society for Pediatric Dermatology

Disclosure: Nothing to disclose.

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

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

Disclosure: Nothing to disclose.

Van Perry, MD  Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio

Van Perry, MD is a member of the following medical societies: American Academy of Dermatology and American Society for Laser Medicine and Surgery

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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Multiple lesions on the face caused by Microsporum canis infection in a patient who also has tinea capitis.
Erythematous scaling lesion on the cheek.
 
 
 
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