Published on 18/03/2015 by admin
Filed under Dermatology
Last modified 18/03/2015
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Aditya K. Gupta, Elizabeth A. Cooper and Fiona C. Simpson
Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports
Pityriasis (tinea) versicolor (PV) has a worldwide distribution, though the prevalence is higher in tropical climates than in temperate ones (30–40% vs 1–4%, respectively). PV is caused by the lipophilic yeast species Malassezia. Malassezia organisms are a normal part of human commensal skin flora, and PV results when they are converted from the yeast phase to a mycelial phase which is able to infect the stratum corneum, producing the characteristic hypo- or hyperpigmented lesions.
Infection is associated with sebaceous gland activity, hence infection is most often seen in adults and post-pubescent adolescents, rarely in prepubescent children. An equal prevalence between the sexes has been noted. Predisposing factors include high temperature and humidity, malnutrition, the use of oral contraceptives, hyperhidrosis, genetic susceptibility, increased plasma cortisol levels, and immunodeficiency.
Initially only two species under the genus name Pityrosporum were described. Genetic research in the 1990s confirmed at least seven species of Malassezia, and more have since been discovered. The most common species contributing to PV lesions are M. globosa (50–60%), M. sympodialis (3–59%), M. furfur, and M. slooffiae (each 1–10%). It is not currently known whether the clinical pattern of infection or antifungal susceptibility vary between the different infecting species.
Topical treatment is the first-line therapy in most cases. Topical azoles formulated as gels, creams, solutions, or shampoos (ketoconazole, fluconazole, bifonazole, clotrimazole, miconazole, etc.) have demonstrated efficacy for PV. The allylamine terbinafine has several topical formulations (solution, cream, gel, or spray) that have been used effectively, as have formulations of the benzylamine butenafine. Topical ciclopirox provides both antifungal and anti-inflammatory activity against Malassezia.
Systemic antifungal therapies may be warranted in severe cases, or cases with widespread body involvement, patients with recurrent disease, or those who are immunocompromised. Patients may also prefer a short-duration oral therapy to frequent application of a topical agent.
Second-line therapy for cases refractive to topical therapy may be treated with oral antifungals. Ketoconazole, itraconazole, and fluconazole show high efficacy in the literature. However, in contrast to topical terbinafine, oral terbinafine is not effective, and nor is griseofulvin.
Treatment does not vary with hyperpigmented versus hypopigmented disease. Although fungal organisms may be eradicated after 2 to 4 weeks of therapy, it may take significantly longer before the skin’s normal pigmentation is restored, particularly with hypopigmented lesions.
Relapse of PV is common owing to endogenous host factors: recurrence rates have been reported as high as 60–90% 2 years after treatment. Both ketoconazole (a single 400 mg dose or 200 mg daily for 3 days once monthly) and itraconazole (a single 400 mg dose once monthly for 6 months) have been used in prophylactic regimens for PV, though ketoconazole is not used because of its potential for hepatotoxicity.
Direct microscopy on KOH specimens
Wood’s light
Malassezia organisms should be identified by skin scrapings for definitive diagnosis, and are easily identified where microscopic examination of skin scrapings reveals fungal hyphae in a typical ‘spaghetti and meatball’ pattern. PV lesions fluoresce yellow/green or gold under Wood’s light; however, the examination is positive in only one-third of all PV cases, most likely when the causative organism is M. furfur.
Treatment of Skin Disease Comprehensive Therapeutic Strategies 4e
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Ketoconazole
Bifonazole
Terbinafine
Clotrimazole
Econazole
Oxiconazole
