Tinea versicolor (pityriasis versicolor)

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Tinea versicolor (pityriasis versicolor)

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

image

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.

Management Strategy

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.

First-line therapy

Topical antifungal agents  
image Ketoconazole A
image Bifonazole A
image Terbinafine A
image Clotrimazole A
image Econazole A
image Oxiconazole A
image Butenafine A
image Ciclopirox A
image Fluconazole shampoo A
image Selenium sulfide 2.5% B
image Tioconazole B
image Zinc pyrithione shampoo B

Second-line therapy

Oral antifungal agents  
image Itraconazole A
image Ketoconazole A
image Fluconazole A
Oral prophylaxis  
image Itraconazole A

Third-line therapy

image Pramiconazole (oral triazole) A
image Adapalene A
image Naftifine (topical allylamine) B
image Isotretinoin E

A double-blind, randomized, placebo-controlled, dose-finding study of oral pramiconazole in the treatment of pityriasis versicolor.

Faergemann J, Todd G, Pather S, Vawda ZFA, Gillies JD, Walford T, et al. J Am Acad Dermatol 2009; 61: 971–6.

Participants were randomized into six pramiconazole treatment groups: (1) 100 mg taken once; (2) 200 mg taken once; (3) 200 mg taken once daily for 2 days; (4) 200 mg taken once daily for 3 days; (5) 400 mg taken once; (6) placebo taken once daily for 3 days. The primary efficacy outcome was effective treatment (negative KOH microscopy and resolution of erythema, desquamation, and pruritus or minimal residuals for participants with severe baseline scores). At day 28, the highest proportion of participants with an effective cure received 200 mg daily for 2 days, 84.0% (95% CI: 69.6 to 98.4) and 200 mg daily for 3 days, 84.6% (95% CI: 70.7 to 98.5).

Pramiconazole is not currently approved or marketed. As more data accumulates, the level of evidence may alter.

[/level-membership-for-dermatology-category][not-level-membership-for-dermatology-category]

Tinea versicolor (pityriasis versicolor)

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

image

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.

Management Strategy

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.

First-line therapy

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Topical antifungal agents  
image Ketoconazole A
image Bifonazole A
image Terbinafine A
image Clotrimazole A
image Econazole A
image Oxiconazole A