Tinea Corporis Treatment & Management
- Author: Jack L Lesher, Jr, MD; Chief Editor: Dirk M Elston, MD more...
Topical therapy is recommended for a localized infection because dermatophytes rarely invade living tissues. Topical therapy should be applied to the lesion and at least 2 cm beyond this area once or twice a day for at least 2 weeks, depending on which agent is used. Topical azoles and allylamines show high rates of clinical efficacy. These agents inhibit the synthesis of ergosterol, a major fungal cell membrane sterol.
The topical azoles (eg, econazole, ketoconazole, clotrimazole, miconazole, oxiconazole, sulconazole, sertaconazole) inhibit the enzyme lanosterol 14-alpha-demethylase, a cytochrome P-450–dependent enzyme that converts lanosterol to ergosterol. Inhibition of this enzyme results in unstable fungal cell membranes and causes membrane leakage. The weakened dermatophyte is unable to reproduce and is slowly killed by fungistatic action. Sertaconazole nitrate is one of the newest topical azoles. It has fungistatic and anti-inflammatory abilities and is used as a broad-spectrum agent. Some data suggest it is as effective and fungicidal agents. It may have a reservoir effect and therefore is a good choice for noncompliant patients. Lastly, Liebel et al published in vitro data in 2006, reporting this drug has anti-itch properties.
Luliconazole (Luzu) is an imidazole topical cream approved by the FDA in November 2013 for treatment of interdigital tinea pedis, tinea cruris, and tinea corporis. Approval was based on the results of three positive studies that evaluated 679 patients with either tinea pedis or cruris.[22, 23]
Two studies evaluating tinea pedis had a primary endpoint of complete clearance at 4 weeks post-treatment. In the first study, 26% of patients treated with luliconazole were completely cleared compared with only 2% of patients treated with vehicle. In the second study, 14% of patients treated with luliconazole were completely cleared compared with only 3% of patients treated with vehicle.
In the study evaluating tinea cruris, complete clearance was assessed at 3 weeks post-treatment. After 1 week of treatment, 21% of patients treated with luliconazole were completely cleared compared with 4% of patients treated with vehicle.
Allylamines (eg, naftifine, terbinafine) and the related benzylamine butenafine inhibit squalene epoxidase, which converts squalene to ergosterol. Inhibition of this enzyme causes squalene, a substance toxic to fungal cells, to accumulate intracellularly and leads to rapid cell death. Allylamines bind effectively to the stratum corneum because of their lipophilic nature. They also penetrate deeply into hair follicles.
Ciclopirox olamine is a topical fungicidal agent. It causes membrane instability by accumulating inside fungal cells and interfering with amino acid transport across the fungal cell membrane.
A low-to-medium potency topical corticosteroid can be added to the topical antifungal regimen to relieve symptoms. The steroid can provide rapid relief from the inflammatory component of the infection, but the steroid should only be applied for the first few days of treatment. Prolonged use of steroids can lead to persistent and recurrent infections, longer duration of treatment regimens, and adverse effects of skin atrophy, striae, and telangiectasias.
Systemic therapy may be indicated for tinea corporis that includes extensive skin infection, immunosuppression, resistance to topical antifungal therapy, and comorbidities of tinea capitis or tinea unguium. Use of oral agents requires attention to potential drug interactions and monitoring for adverse effects.
The mechanism of action or oral micronized griseofulvin against dermatophytes is disruption of the microtubule mitotic spindle formation in metaphase, causing arrest of fungal cell mitosis. A dose of 10 mg/kg/d for 4 weeks is effective. In addition, griseofulvin induces the cytochrome P-450 enzyme system and can increase the metabolism of CYP-450–dependent drugs. It is the systemic drug of choice for tinea corporis infections in children.
Systemic azoles (eg, fluconazole, itraconazole, ketoconazole) function similar to the topical agents, causing cell membrane destruction.
Oral ketoconazole at 3-4 mg/kg/d may be given. However, this agent carries an associated risk of hepatitis in less than 1 in 10,000 cases and is rarely used orally for dermatophyte infections.
Fluconazole at 50-100 mg/d or 150 mg once weekly for 2-4 weeks is used with good results.
Oral itraconazole in doses of 100 mg/d for 2 weeks shows high efficacy. With an increased dose of 200 mg/d, the treatment duration can be reduced to 1 week. However, the cytochrome P-450 activity of itraconazole allows for potential interactions with other commonly prescribed drugs. When it is appropriate to prescribe the drug, there may be some advantage to giving itraconazole with whole milk to increase absorption.
Based on E-test for susceptibility of T rubrum, voriconazole was the most active and fluconazole was the least active of the azole drugs.
Oral terbinafine may be used at a dosage of 250 mg/d for 2 weeks; the potential exists for cytochrome P-450, specifically CYP-2D6, drug interactions with this agent.
Systemic therapy is needed when the infection involves hair follicles, such as Majocchi granuloma. In this case, topical therapy may serve as adjunct treatment with the oral medication.
The preferred treatment for tinea imbricata is griseofulvin or terbinafine, although some resistance has developed to oral griseofulvin.
Surgical treatment is usually not indicated except for drainage of superficial vesicles, bullae, pustules, or deep abscesses.
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