Tinea Faciei Medication

Updated: Apr 09, 2021
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
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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. [39]

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


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.

Butenafine (Mentax)

Butenafine is a potent antifungal related to allylamines. It is available as a 1% cream.

Clotrimazole topical (Lotrimin, Mycelex)

Clotrimazole is a broad-spectrum antifungal agent that inhibits yeast and fungal growth by altering cell membrane permeability. It is frequently prescribed for patients with tinea faciei. Clotrimazole is available without a prescription as 1% cream, solution or spray, and lotion.

Miconazole (Femizole-7, Micatin, Absorbine)

Miconazole damages the fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased; this effect causes nutrients to leak out. It is 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.

Econazole topical (Ecoza)

Econazole is effective in cutaneous infections. It interferes with RNA and protein synthesis and metabolism. Econazole disrupts fungal cell wall permeability, causing fungal cell death.

Oxiconazole (Oxistat)

Oxiconazole damages the fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out. It is available as a 1% cream or lotion.

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

Undecylenic acid and derivatives are nonprescription agents rarely used in the treatment of tinea faciei. The formulation is available in cream or solution or spray.

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

Tolnaftate is a nonprescription medication available in 1% cream, solution or spray, and powder.

Ciclopirox (Loprox)

Ciclopirox interferes with the synthesis of RNA, DNA, and proteins by inhibiting transport within fungal cells. It is available as a 1% cream and lotion for skin.

Terbinafine (Lamisil, Daskil)

Terbinafine is a member of the allylamine family, fungicidal agents that inhibit ergosterol synthesis by means of squalene epoxidase. The result is a decreased ergosterol level and an accumulation of squalene, which is toxic to fungal cells.

Itraconazole (Sporanox)

Itraconazole has fungistatic activity. It is a 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 weeks after treatment.

Fluconazole (Diflucan)

Fluconazole has fungistatic activity. It is a 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.

Griseofulvin (Fulvicin P/G, Gris-PEG)

Griseofulvin has fungistatic activity. It interferes with the microtubule annd impairs fungal cell division. Griseofulvin binds to keratin precursor cells. Keratin is gradually replaced with noninfected tissue, which is highly resistant to fungal invasions.