Approach

PV is easily treated with both topical and, in some cases, systemic medications. Spontaneous resolution of PV is uncommon and the disease will persist for years if left untreated.[14] After only 2 weeks of antifungal therapy, microscopic fragmentation of Malassezia fungal forms is seen.[7] However, even after successful treatment, patients and clinicians must remember that the pigmentary abnormalities associated with PV may take up to 6 weeks to resolve and that this is not a sign of treatment failure.[35] Hypopigmented lesions, in particular, can take longer to resolve.[20] Because of this, treatment efficacy is often assessed by a negative KOH preparation rather than resolution of dyschromia. In addition, because the conversion of Malassezia yeasts to the pathologic mycelial form is thought to be due, in many cases, to endogenous host factors, recurrence is common in up to 60% of patients in the first year after treatment and up to 80% after 2 years.[7][36] Because of this, clinicians should consider prophylactic treatment for patients who tend to have repeated episodes of disease.[7]

Topical treatments

The preferred first-line treatment for all patients, especially children and pregnant women, is topical therapy.[37] Many topical therapies are available that for the most part are equally effective. The selection of a topical agent should ultimately be based on patient preference. When using any topical therapy, advise the patient to treat the whole neck, trunk, arms, and legs down to the knees, even if only small areas are involved.[25]

Nonspecific topical therapies are older and relatively inexpensive. These agents include zinc pyrithione, propylene glycol, and selenium sulfide. Specific topical therapies are newer agents and include azole antifungals such as ketoconazole, clotrimazole, and miconazole.[25][38] Terbinafine and ciclopirox are also effective.[25] Topical retinoids (e.g., tretinoin, adapalene) may also be used.[39][40] There is no benefit of one specific topical therapy over another, other than appropriate selection of a base (i.e., for hair-bearing skin, lotions, shampoos, and solutions are better than cream-based products).

Pyrithione zinc and propylene glycol have not been adequately tested in pregnant women. However, no teratogenicity or embryotoxicity has been observed in the offspring of laboratory animals treated with pyrithione zinc, and there have been no documented problems in humans.[41][42] Therefore, these agents are the preferred first-line treatments in pregnant women. There is inadequate data to support the use of topical terbinafine or ciclopirox in pregnant women; however, no teratogenicity or embryotoxicity has been observed in animal studies with either drug and they may be used second line. Topical selenium sulfide and the topical azole antifungals are generally not recommended in pregnancy; however, some clinicians still use selenium sulfide topically during pregnancy. Topical retinoids are contraindicated in pregnant women.

Systemic treatments

Systemic therapy is primarily indicated for extensive lesions, for lesions resistant to prior topical therapy, if the patient is immunocompromised, if the patient has difficulty complying with topical therapies, and for patients with frequent relapse. In the treatment of PV, systemic agents are used for only a short time, limiting the risk of adverse effects.[25] The advantage of oral therapy is increased patient compliance, as these agents are more convenient and less time consuming than topical agents.[14] Oral azole antifungals (e.g., ketoconazole, fluconazole, itraconazole) are the preferred drugs.[7][13][14][20][43][44] While studies have failed to consistently demonstrate the efficacy of a single dose of itraconazole in the treatment of PV, there is some evidence to suggest that a short course of itraconazole may be as effective as a multi-day course of treatment.[43][45][46] Systemic azole antifungals are best absorbed in an acid environment. Therefore, advise patients to take the medication with a carbonated beverage. In addition, it is common to have patients take the medication 45 minutes before working out to a sweat, and then waiting several hours after sweating before taking a shower to increase delivery of the medication to the site of action in the stratum corneum.

The above-listed agents differ little in efficacy.[7] Rare adverse effects including nausea, vomiting, and hepatitis can occur with all of the azoles, particularly ketoconazole.[29] However, these adverse effects are uncommon given the short course of treatment in PV. Ketoconazole may cause severe liver injury and adrenal insufficiency. In July 2013, the US Food and Drug Administration (FDA) recommended that oral ketoconazole should only be used for life-threatening fungal infections where alternative treatments are not available or tolerated, and when the potential benefits of treatment outweigh the risks. Its use is contraindicated in patients with liver disease. If used, monitor liver and adrenal function before and during treatment.[47] This recommendation does not apply to topical formulations of ketoconazole. Resistance to traditional systemic agents such as itraconazole and fluconazole has been described, which may necessitate higher doses and longer courses of these medications, or primary use of older topical treatments such as selenium sulfide and pyrithione zinc.[48]

Oral terbinafine and griseofulvin are ineffective in treating PV.[7]

Prophylaxis

In patients with recurrent disease, prophylactic treatment may be necessary after a successful treatment course. First-line prophylactic treatment, especially in children, is with selenium sulfide.[1] If topical prophylactic therapy is ineffective, second-line therapies include pulse-dosed oral azole antifungals.[49][50][51]

Adjunctive measures

Especially in patients with hypopigmented PV, the resulting dyschromia can be long lasting, even after successful pathogen eradication. In patients with prominent hypopigmented PV, consider UV phototherapy with UV-B 3 times weekly after complete eradication of the fungus, as demonstrated by a negative potassium hydroxide (KOH) preparation. Repigmentation can be expected within 3 weeks after starting UV therapy.[52]

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