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. 2022 Nov 14;11:2022-9-2. doi: 10.7573/dic.2022-9-2

Tinea versicolor: an updated review

Alexander KC Leung 1,✉, Benjamin Barankin 2, Joseph M Lam 3,4, Kin Fon Leong 5, Kam Lun Hon 6,7
PMCID: PMC9677953  PMID: 36452877

Abstract

Background

Tinea versicolor is a common superficial fungal infection of the skin with various clinical manifestations. This review aims to familiarize physicians with the clinical features, diagnosis and management of tinea versicolor.

Methods

A search was conducted in July 2022 in PubMed Clinical Queries using the key terms “tinea versicolor” OR “pityriasis versicolor”. The search strategy included all clinical trials, observational studies and reviews published within the past 10 years.

Results

Tinea versicolor is caused by Malassezia species, notably M. globosa, M. furfur and M. sympodialis. The condition is characterized by scaly hypopigmented or hyperpigmented macules/patches, primarily located on the upper trunk, neck and upper arms. The diagnosis is usually based on characteristic clinical features. If necessary, a potassium hydroxide preparation test can be performed to reveal numerous short, stubby hyphae intermixed with clusters of spores. Most patients with tinea versicolor respond to topical antifungal therapy, which has a better safety profile (fewer adverse events, fewer drug interactions) and lower cost compared to systemic treatment and is therefore the treatment of choice. Oral antifungal therapy is typically reserved for patients with extensive disease, frequent recurrences or disease that is refractory to topical therapy. Advantages of oral antifungal therapy include increased patient compliance, shorter duration of treatment, increased convenience, less time involved with therapy and reduced recurrence rates. On the other hand, oral antifungal therapy is associated with higher cost, greater adverse events and potential drug–drug interactions and is therefore not the first-line treatment for tinea versicolor. Long-term intermittent prophylactic therapy should be considered for patients with frequent recurrence of the disease.

Conclusion

Selection of antifungal agents depends on several factors, including efficacy, safety, local availability, ease of administration, likelihood of compliance and potential drug interactions of the antifungal agent.

Keywords: evoked scale sign, fluconazole, itraconazole, ketoconazole, Malassezia species, pityriasis versicolor, selenium sulfide, terbinafine, zinc pyrithione

Introduction

Tinea versicolor (also known as pityriasis versicolor) is a common superficial fungal infection of the skin. Patients with tinea versicolor typically present with asymptomatic hypopigmented or hyperpigmented, finely scaled, oval or round macules/patches on the trunk and upper arms.1 Patients occasionally report pruritus, particularly when the condition is more extensive. The term ‘versicolor’ refers to the variable colours of the skin lesions that may occur in this disorder. Clinical manifestations of tinea versicolor are myriad, and the differential diagnoses are broad. This review aims to familiarize readers with the various clinical manifestations of tinea versicolor to avoid misdiagnosis, unnecessary investigations and mismanagement of the disease and will also highlight the correct management of this disease.

Methods

A search was conducted in July 2022 in PubMed Clinical Queries using the key terms “tinea versicolor” OR “pityriasis versicolor”. The search strategy included all clinical trials (including open trials, non-randomized controlled trials and randomized controlled trials), observational studies and reviews (including narrative reviews and meta-analyses) published within the past 10 years. Only papers published in the English literature were included in this review. The information retrieved from the search was used in the compilation of this article.

Review

Aetiopathogenesis

Tinea versicolor is caused by dimorphic lipophilic and lipid-dependent yeasts in the genus Malassezia (formerly known as Pityrosporum) species, notably Malassezia globosa (M. globose), M. furfur and M. sympodialis.2–12 Other species that have been implicated include M. restricta, M. obtuse, M. slooffiae, M. pachydermatis and M. japonica.13–16 These yeasts are normal commensals on the skin surface.17,18 Skin colonization increases with age; 25% of children and almost 100% of adults are affected.19 Tinea versicolor occurs when the saprophytic yeast or budding form of the organism converts to the pathogenic hyphal or mycelial form. The fungal infection is localized to the stratum corneum. Predisposing factors for the conversion include a hot and humid environment, hyperhidrosis, application of oily lotion or cream to the skin, wearing of masks, excessive lipid-containing sebaceous secretions, malnutrition, poor general health, use of oral contraceptives, pregnancy, diabetes mellitus, use of topical or systemic corticosteroids, Cushing disease, Helicobacter pylori infection, immunodeficiency and genetic predisposition.20–36 A recent study showed oxidative stress has no role in the pathogenesis of tinea versicolor.29

Hypopigmented lesions (more commonly noted in darker skin tones) seen in tinea versicolor are thought to result from damage to melanocytes and inhibition of tyrosinase by azelaic acid (a dicarboxylic acid) produced by the Malassezia species involved, small melanosomes and accumulation of lipid-like material in the stratum corneum blocking ultraviolet light.37–40 On the other hand, hyperpigmented lesions (more commonly noted in lighter skin tones) may result from a hyperaemic inflammatory response elicited by Malassezia species, more tonofilaments in the granulosum, a thicker stratum corneum and abnormally large melanosomes.8,38,41,42 Keratinase, produced by the Malassezia species, causes loosening of the stratum corneum with subsequent scale formation.43,44

Prevalence

Tinea versicolor occurs worldwide. The prevalence is very high in hot and humid climates.35 In some tropical countries, the prevalence is as high as 50% whereas, in Sweden, the prevalence is as low as 0.5%.17,45,46 Tinea versicolor is most common amongst adolescents and young adults, presumably because of increased sebum production in individuals of these age groups.47–55 Although uncommon, the condition can occur in young children and elderly individuals.47–55 Rarely, tinea versicolor has been reported in infants including neonates.56–60 Tinea versicolor is slightly more common in men than in women presumably due to increased sebaceous activity in men.8,47,54 A positive family history of tinea versicolor is present in approximately 17% of affected individuals.61,62 The incidence of tinea versicolor appears to be the same in all races, though the change in skin pigmentation is more visually apparent in dark-skinned individuals.8

Histopathology

Histological findings include parakeratosis, hyperkeratosis, slight acanthosis and a mild superficial, perivascular infiltrate in the upper dermis.63 Haematoxylin-eosin, methenamine silver or periodic acid–Schiff staining reveal the presence of yeast in a ‘spaghetti and meatballs’ pattern in the stratum corneum.63–65 Hyperpigmented lesions tend to contain more hyphae and spores than hypopigmented lesions.62,65,66 In hypopigmented lesions, the horny layer tends to be slightly hyperkeratotic and there may be a decrease in melanosomes in the stratum spinosum.39,45

Clinical manifestations

Tinea versicolor is characterized by mildly scaly hypopigmented or hyperpigmented macules/patches, most commonly affecting areas of skin that are rich in sebum production such as the trunk (especially the upper part), neck, shoulders and upper arms (Figures 1–3A).19,21,24,67–69 Facial involvement is less common in adults. On the other hand, facial involvement is common in children and may be the only site involved (Figure 3B).19,70 The forehead is the usual site of facial involvement.71–74 Other sites of involvement, such as forearms and thighs, are less common (Figure 4).75 Unusual sites of involvement include the scalp, eyelid, axilla, areola, periareolar area, antecubital fossae, popliteal fossa, pubis, groin, perineum, penile shaft and vulva.75–86

Figure 1.

Figure 1

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Tinea versicolor presenting as multiple hypopigmented macules and patches on the chest (part a) and left shoulder and upper back (part b).

Figure 3.

Figure 3

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Multiple hypopigmented macules and patches on the neck and face of a 5-year-old child (part a) and on the face of a 10-year-old child (part b).

Figure 4.

Figure 4

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Multiple hypopigmented macules and patches on the left forearm.

Typically, lesions arise as multiple, small, oval or round, well-demarcated, round or oval macules.8 Smaller macules may have a powdery appearance because of flaking.87 Over time, the macules enlarge radially and coalesce into patches or very superficial plaques.8 The lesions are covered with a fine scale, which is often difficult to appreciate upon clinical examination. On the other hand, the scale becomes more apparent when the lesion is stretched or scraped (the ‘evoked scale sign’) (Figure 5A,B).1,44,88,89 It should be noted that burned-out or treated lesions usually lack scale.90 In patients with tinea versicolor, when the affected skin is wiped with a piece of wet cloth and scraped, it yields a considerable amount of dirty brown keratin. Tinea versicolor lesions are typically asymptomatic, although some patients complain of mild pruritus,45 which may become worse in hot and humid conditions.

Figure 5.

Figure 5

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Hyperpigmented macules with minimal desquamation on the upper back (part a) and with prominent desquamation on the upper back after the skin lesion was scrapped (the evoked scale sign, part b).

The eruption varies in colour from individual to individual, but each individual usually has lesions of a single hue. Lesions are usually evenly pigmented. In general, hyperpigmented lesions tend to occur in fair-skinned patients whereas hypopigmented lesions tend to occur in dark-skinned individuals.8,91 When hyperpigmented lesions occur in dark-skinned individuals, they are often grey-black, dark brown or black whereas these are often tan, light brown, red or pink in fair-skinned individuals.1,8,40 Lesions may become more apparent following exposure to the sun and are thus more noticeable during the summer months. Mixed hyperpigmented and hypopigmented lesions may be found, especially in the axilla and groin.8,41,91

Several morphological variants have been described. An inverse form of tinea versicolor has been described, especially in patients who are immunocompromised.92 Some authors favour labelling this variant as ‘tinea InVersicolor’.92 In this variant, lesions tend to localize in the flexural areas (axilla, elbow, popliteal fossa and groin) and isolated areas of the extremities (Figure 6).92–94 Atrophying tinea versicolor typically presents with numerous, hypopigmented or erythematous/violaceous, round to oval, scaly lesions with a typically depressed appearance.95–98 Lesions tend to cluster and are generally uniform in size (a few millimetres to several centimetres) on the same patient and may have a wrinkled surface.99 The atrophy is limited to the area affected by tinea versicolor.100 The exact aetiology of the atrophy is not known. It is postulated that the atrophy may result from prolonged use of topical corticosteroids or delayed type IV hypersensitivity to epicutaneous antigens from the Malassezia species.100–104 Folliculocentric tinea versicolor involves the hair follicle and presents with asymptomatic hypopigmented or hyperpigmented macules located exclusively around the follicles105,106; these macules may merge into patches.106 The disorder is typically localized to the chest and back.106,107 A Wood lamp examination reveals folliculocentric fluorescence in hypopigmented areas.107 Papular tinea versicolor presents with multiple, asymptomatic, monomorphic, red-brown papules (2–3 mm), which may or may not show the fine overlying scale.105 They are usually found on the trunk.105 Confetti-like tinea versicolor presents with asymptomatic confetti-like spots with slightly scaly surfaces (Figure 7). The spots are usually bilateral and symmetrically distributed. The formation of scaly, guttate and coalescent hypopigmented patches or plaques is unique in African Americans; this variant is colloquially known as acid skin.108

Figure 6.

Figure 6

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Hyperpigmented macules in the axillary region of a 17-year-old male with tinea InVersicolor.

Figure 7.

Figure 7

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Confetti-like spots on the left arm, left lateral upper chest and armpit of a child with confetti-like tinea versicolor.

Figure 2.

Figure 2

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Multiple erythematous macules and patches on the upper abdomen and chest.

Diagnosis

The diagnosis is usually clinical, based on the characteristic features (multiple hypopigmented or hyperpigmented, centrally coalescing, oval to round, finely scaling macules or patches and the ‘evoked scale sign’).35 However, the varied presentations of tinea versicolor may be confusing to an inexperienced physician. Examination of the lesion with a Wood lamp (filtered ultraviolet light with a peak of 365 nm) may show gold-yellow, yellowish-green or coppery-orange fluorescence, although some lesions do not fluoresce.17,56 The fluorescence may include areas surrounding clinically visible lesions, suggesting that the fungal infection is spreading.17

Dermoscopy is a useful ancillary tool for the diagnosis of tinea versicolor.109–114 Typical dermoscopic findings include alteration in the background pigmentation, a ‘contrast halo’ sign (a ring of hypopigmentation surrounding the primary lesion of increased pigmentary network in a hyperpigmented lesion or a ring of increased pigmentation surrounding the primary lesion of decreased pigmentary network in hypopigmented lesion), fine scale on the involved skin, folliculocentricity and hypopigmentation of the invaded hair follicle.110–114

If necessary, a potassium hydroxide (KOH) preparation test can be performed; examination of scrapings from the border of the lesion soaked with 10–15% KOH reveals numerous short, stubby hyphae intermixed with clusters of spores (the so-called ‘spaghetti and meatballs’ appearance) (Figure 8).51 KOH helps to dissolve the keratin and debris so that the hyphae and spores can be readily visible by microscopy. The border of the lesion contains the highest number of fungi. Because the standard KOH mount does not show a colour contrast, ink blue, Parker blue-black ink, methylene blue, chlorazol black E, Swartz–Lamkin, Swartz–Medrik or Chicago Sky Blue (CSB) 6B staining may be added for better visualization of the causative organism.35,115,116 Thus far, the contrast stain containing 1% CSB 6B has the greatest specificity and sensitivity.115

Figure 8.

Figure 8

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KOH preparation of tinea versicolor showing numerous short, stubby, hyphae intermixed with clusters of spores (the so-called ‘spaghetti and meatballs’ appearance).

Differential diagnosis

The differential diagnoses are broad, especially those with unusual presentations. The differential diagnosis of hypopigmented lesions of tinea versicolor includes pityriasis alba, nevus anemicus, nevus depigmentosus, idiopathic guttate hypomelanosis, eruptive hypomelanosis, progressive macular hypomelanosis, leukoderma punctate, hypomelanosis of Ito, vitiligo, ash-leaf spot in tuberous sclerosis, corticosteroid-induced hypopigmentation, arsenicosis, leprosy, hypopigmented mycosis fungoides and post-inflammatory hypopigmentation.117–124 On the other hand, hyperpigmented lesions of tinea versicolor should be differentiated from tinea corporis, pityriasis rosea, pityriasis rotunda, tinea imbricata, acanthosis nigricans, terra firma-forme dermatosis, café au lait macules, ephelides, solar lentigines, melasma, erythrasma, guttate psoriasis, nummular eczema, seborrheic dermatitis, contact dermatitis, post-inflammatory hyperpigmentation, type 1 (classic adult) pityriasis rubra pilaris, secondary syphilis, confluent and reticulated papillomatosis (also known as Gougerot–Carteaud syndrome), and epidermodysplasia verruciformis (also known as Lewandowsky–Lutz dysplasia).125–138 The distinctive features of many of these conditions help to differentiate them from tinea versicolor.

Complications

Skin discolouration can be cosmetically unsightly and socially embarrassing especially if it occurs in exposed areas of the body. This may have an adverse effect on quality of life. The discolouration of the skin (without overlying scaling) may persist for weeks to months even after completion of successful therapy. The disappearance of the scale is evidence that the hyphal yeast has been eradicated.44 A preliminary study showed that topical application of cycloserine, a transaminase 1 inhibitor, to the hyperpigmented lesions of tinea versicolor twice a day for 5 days resulted in complete clearing of the hyperpigmentation.139 Well-designed, large-scale, multicentre, randomized, placebo-controlled trials are needed to confirm or refute this finding.

Hair thinning and/or hair loss within the tinea versicolor lesions has been reported.140 In a study of 39 patients with tinea versicolor, hair thinning and/or hair loss within the tinea versicolor lesions occurred in 24 (61.5%) patients.140 Hair thinning and/or hair loss occurred most commonly on the forearms, abdomen, neck and, in men, the beard area.

Prognosis

The prognosis is good. Mycological cure is usually achieved soon after antifungal treatment. Tinea versicolor tends to persist for years if left untreated.141–143 The disorder has a high recurrence rate, especially in patients with a positive family history of tinea versicolor.51,63,144,145 Framil et al. followed 102 patients with clinical and laboratory diagnosis of tinea versicolor for one year.145 After appropriate treatment, 33 (33.35%) patients did not have any relapsing episodes, 54 (52.94%) patients had one to four relapsing episodes and 15 (14.7%) patients had more than four relapsing episodes.145 Patients with a positive family history of tinea versicolor also have a longer duration of the disease.51 Relapse rates as high as 80% following treatment have been reported.146

Management

Most patients with tinea versicolor respond to topical antifungal therapy (Box 1). Additionally, topical antifungal therapy has a better safety profile (fewer adverse events, fewer drug interactions) and lower cost compared to systemic treatment and is therefore the treatment of choice. Oral antifungal therapy is typically reserved for patients with extensive disease, frequent recurrences or disease that is refractory to topical therapy (Box 1). For resistant or stubborn cases, combining oral and topical therapies may be considered. Alternative and complementary therapies are still used in many parts of the world.141,142

Box 1. Treatment options for tinea versicolor.

  1. Topical antifungals

    1. Azoles (for example, ketoconazole, econazole, eberconazole, efinaconazole, bifonazole, luliconazole, clotrimazole, miconazole, sertaconazole, sulconazole, oxiconazole, fenticonazole, tioconazole, fluconazole and dapaconazole)

    2. Terbinafine

    3. Naftifine

    4. Butenafine

    5. Ciclopirox olamine

    6. Non-specific topical antifungal agents (for example, selenium sulfide, zinc pyrithione, propylene glycol, Whitfield ointment, sulfur plus salicylic acid and benzoyl peroxide)

  2. Oral antifungals

    1. Itraconazole

    2. Fluconazole

  3. Laser and photodynamic therapies

  4. Alternative therapies

Topical antifungals

Many topical antifungals have proved to be effective in the treatment of tinea versicolor. Various antifungal preparations are available, including shampoos, foams, gels, lotions and creams and are usually applied once to twice daily.1 Shampoo is preferred when a large percentage of the body surface area is involved. Treatment regimens range from a few days to 4 weeks.1,147 A systematic review of 93 controlled trials (n=8327) showed that most topical antifungal medications used to treat tinea versicolor are effective compared to placebo, with numbers needed to treat of 1–3.147 Additionally, greater cure rates can be achieved with higher concentrations of active ingredients in the topical antifungal medications and longer duration of treatment.147,148 The most common side-effects of topical antifungal agents are skin irritation and contact allergy.35

Azoles

Topical azole drugs (for example, ketoconazole, econazole, eberconazole, efinaconazole, bifonazole, luliconazole, clotrimazole, miconazole, sertaconazole, sulconazole, oxiconazole, fenticonazole, tioconazole, fluconazole and dapaconazole) have become an important treatment class for tinea versicolor.149–165 This group of antifungal agents are fungistatic and works by inhibiting the P-450-dependent enzyme lanosterol 14-α-demethylase, which is involved in the biosynthesis of ergosterol.166,167 Ergosterol is an important structural component of fungal cell membranes.62,166 Impairment of biosynthesis of ergosterol may limit cell function and cell growth.62,166 Randomized clinical trials have supported the efficacy of various topical azole antifungal agents.149–165 Of the topical azole antifungal agents, ketoconazole has been most studied for the treatment of tinea versicolor. In addition to its ability to block the synthesis of ergosterol, ketoconazole also has sebum-lowering effects by inhibiting androgenesis, anti-inflammatory effects by inhibiting 5-lipoxygenase and barrier-restoring effects by inhibiting hyperproliferation of keratinocytes.166,168–170 As ketoconazole is highly lipophilic, it concentrates at sites of tinea versicolor, thereby further increasing its efficacy.166 A 2019 systematic view of 40 randomized controlled trials (n=4566) focusing on the use of topical ketoconazole for the treatment of Malassezia-related conditions, such as tinea versicolor, showed that the efficacy rate of topical ketoconazole for the treatment of tinea versicolor was 71–89%.166 Topical azole drugs have a favourable safety. Adverse events are usually mild and uncommon and include skin dryness, irritation, pruritus, burning sensation and erythema.147 Rarely, allergic contact dermatitis may occur.166

Studies have shown that combination therapies using 2% ketoconazole cream and 1% adapalene gel are more efficacious in the treatment of tinea versicolor than ketoconazole cream alone.171,172 To further improve the efficacy of topical ketoconazole, future drug development should focus on improving topical delivery to allow better permeation of drugs into skin by using nanostructured lipid carriers, nanoparticles, microemulsions, copolymeric micelles, niosomes and microemulsions.156,173–176 In this regard, the development of topical gels containing fluconazole-loaded solid lipid nanoparticles allows fluconazole to be used topically as the product exhibits skin penetration as a result of large particle surface area and film formation, enhancing contact between fluconazole and skin.156 Recently, it has been shown that itraconazole-loaded aspasomal cream has a higher efficacy in the treatment of tinea versicolor than non-formulated itraconazole cream alone.177

Terbinafine

Terbinafine, an allylamine antifungal, works by inhibiting squalene epoxidase, thereby blocking the biosynthesis of ergosterol.87,163,178 The accumulation of squalene accounts for its fungicidal activity whilst ergosterol deficiency accounts for its fungistatic activity.163 The effectiveness of topical terbinafine in the treatment of tinea versicolor has been demonstrated in many double- blind, randomized, placebo-controlled studies.178–181

There are very few good quality studies comparing the efficacy of topical terbinafine with topical azole drugs for the treatment of tinea versicolor. Most trials are underpowered to detect clinically meaningful differences. In an open clinical trial, 60 adults with tinea versicolor were randomized to receive either eberconazole 1% cream or terbinafine 1% cream once daily for 2 weeks.163 At the end of the treatment period, there was a significant improvement in all the clinical parameters in both groups. Clinical cure was present in 80% of patients in the eberconazole group versus 63% of patients in the terbinafine group. Mycological cure was achieved in 100% of patients in the eberconazole group versus 97% of patients in the terbinafine group. No adverse events were noted. No relapse was seen in patients treated with eberconazole but one patient treated with terbinafine had a relapse at the end of 8 weeks. The authors concluded that both terbinafine and eberconazole were efficacious and safe in the treatment of tinea versicolor but better response was observed in patients treated with eberconazole. In another study, 110 patients (≥14 years of age) with a clinical diagnosis of tinea versicolor confirmed by KOH microscopy were randomized to receive either terbinafine 1% cream (n=55) or ketoconazole 2% cream (n=55) twice daily.182 Patients with negative mycological examination either with clearance of skin lesions or presence of mild residual skin lesions were considered cure. Cure rates at the end of the second, fourth and eighth weeks of treatment were 72% and 64.3%, 81.2% and 69%, and 70.8% and 61.9% for the terbinafine group and the ketoconazole groups, respectively. The authors concluded that there were no significant statistical differences between the terbinafine group and the ketoconazole group with regard to the cure and recurrence rates. However, the numbers of patients were higher and the recurrent cases were lower in those treated with topical terbinafine. Chopra et al. randomized 50 patients with tinea versicolor confirmed by KOH microscopy to receive either terbinafine 1% cream (n=25) or ketoconazole 2% cream (n=25) once daily for 2 weeks.183 At the end of treatment, the clinical and mycological cure rate was 96% for patients treated with topical terbinafine and 88% for patients treated with topical ketoconazole; no adverse events were reported. At 3 months of follow-up, the relapse rate was 8.33% in patients treated with topical terbinafine and 13.53% in patients treated with topical ketoconazole.

Naftifine

Naftifine is a synthetic allylamine derivative with broad-spectrum antifungal activity.184 The medication works by blocking the biosynthesis of ergosterol via inhibition of squalene epoxidase, with resulting accumulation of squalene, increase in fungal cell membrane fragility and permeability, and inhibition of fungal cell growth.184 As naftifine is highly lipophilic, it can penetrate efficiently into the epidermis when applied topically.184 Open studies have shown that topical naftifine is safe and efficacious in the treatment of tinea versicolor.185–187 Well-designed, large-scale, randomized, double-blind and placebo-controlled studies are necessary to further elucidate its clinical efficacy and safety.

Butenafine

Butenafine, a synthetic benzylamine antifungal agent with fungicidal activity, has also been used topically for the treatment of tinea versicolor.188 The medication inhibits squalene epoxidation with resultant blockage of ergosterol biosynthesis. Small randomized controlled trials have shown the clinical efficacy of topical butenafine in the treatment of tinea versicolor.189–190 In a randomized, double-blind, parallel-group trial, the rate of mycological cure in patients with tinea versicolor treated with topical butenafine and topical bifonazole was 87.5% and 83.3%, respectively, after 2 weeks of treatment.189 The rate of effective clinical response in patients with tinea versicolor treated with butenafine and bifonazole was 91.7% and 83.3%, respectively. There was no significant statistical difference in terms of mycological cure and effective clinical response between treatment with topical butenafine and topical bifonazole. Well-designed, large-scale, randomized, double-blind and placebo-controlled studies are necessary to determine the safety and efficacy of topical butenafine in treating tinea versicolor.

Ciclopirox olamine

Ciclopirox olamine is a hydroxypyridone with broad-spectrum antifungal activity.62,191 The medication works by inhibiting the transport of essential elements, which is required for the synthesis of the fungal cell membrane.63 Ciclopirox olamine also interferes with the synthesis of DNA, RNA and protein. Ciclopirox olamine has been shown to be safe and effective for the treatment of tinea versicolor in several studies.191–193 The safety and efficacy of topical ciclopirox olamine in the treatment of tinea versicolor need to be substantiated by well-designed, large-scale, randomized, double-blind and placebo-controlled studies.

Non-specific topical antifungal agents

Non-specific topical antifungal agents for the treatment of tinea versicolor include selenium sulfide, zinc pyrithione, propylene glycol, Whitfield ointment, sulfur plus salicylic acid and benzoyl peroxide. These topical agents do not act specifically against Malassezia species. Their mode of action is to remove dead, infected stratum corneum either physically and/or chemically.194

Selenium sulfide, available as a shampoo, lotion and cream in 1–2.5% concentrations, is safe and effective in the treatment of tinea versicolor.147,195–197 Studies have shown that the success rate of selenium sulfide shampoo in the treatment of tinea versicolor is comparable to that of topical bifonazole and econazole.198,199 Advantages of selenium sulfide include over-the-counter availability, low cost and convenient application. Disadvantages include irritation of the skin, unpleasant odour, staining of clothes and bedding, and a high relapse rate.195,196

The efficacy of zinc pyrithione 1% shampoo versus its vehicle in the treatment of tinea versicolor has been shown in an open trial200 as well as in a double-blind controlled trial.201 In the latter, 20 patients with tinea versicolor were treated with either zinc pyrithione 1% shampoo or the shampoo base for 5 minutes per day for 2 weeks.201 At the end of the study, all 20 patients treated with zinc pyrithione 1% shampoo had clearing of the tinea versicolor lesions compared to none of the patients in the shampoo base group.

Propylene glycol is a keratolytic agent. Faergemann et al. treated 20 patients with tinea versicolor with propylene glycol 50% in water daily for 2 weeks.202 At the end of treatment, all 20 patients were cured.

Whitfield ointment consists of 3% salicylic acid and 6% benzoic acid in an emulsifying ointment.153,203 Salicylic acid is keratolytic whereas benzoic acid is fungistatic.17 Whitfield ointment has been shown to be effective in the treatment of tinea versicolor in a limited number of studies.153,203

A combination of sulfur and salicylic acid has been shown to be effective in the treatment of tinea versicolor in a small number of studies.204,205 The combination can be in the form of 2% micropulverized sulfur and 2% salicylic acid in a shampoo base.204,205 The formulation is cosmetically pleasant and safe.204

Benzoyl peroxide has been used with success in the treatment of tinea versicolor.206–208 In three studies, the vehicle for benzoyl peroxide was propylene glycol, which by itself is effective in the treatment of tinea versicolor.206–208 As such, it is not certain whether the beneficial effect is due to benzoyl peroxide or propylene glycol. It is possible that benzoyl peroxide and propylene glycol may have a synergistic effect in the treatment of tinea versicolor.

Oral antifungals

Oral antifungals are usually reserved for treating severe, widespread, recalcitrant or recurrent tinea versicolor.17 Advantages of oral antifungal therapy include increased patient compliance, shorter duration of treatment, increased convenience, less time involved with treatment and reduced recurrence rates.17,209 On the other hand, oral antifungal therapy is associated with higher cost, greater adverse events, and potential drug–drug interactions and is therefore not the first-line treatment of tinea versicolor, especially in children.1 Oral azole antifungals, such as itraconazole and fluconazole, are the preferred systemic agents.210,211 Adverse events associated with the use of oral antifungals include fatigue, malaise, headache, cutaneous eruption, pruritus, dyspepsia, nausea, vomiting, abdominal pain, diarrhoea, hypertension, congestive cardiac failure, thrombocytopenia, hypokalaemia, albuminuria, hypertriglyceridemia and abnormal liver function.147,212,213

Oral itraconazole

Oral itraconazole, a triazole derivative with strong keratophilic and lipophilic properties, is highly effective for the treatment of tinea versicolor143,210,214; the absorption of itraconazole is enhanced by food.17,215 The recommended dose is 200 mg per day for 5–7 days.1,63,141,142 Adverse events are uncommon.216 Rarely, congestive heart failure and hepatotoxicity have been reported.35 Oral itraconazole should therefore be avoided in patients with a history of congestive heart failure or in patients with active hepatic disease.35 As itraconazole inhibits the enzyme cytochrome P450-dependent system, the medication may cause drug–drug interactions. As such, oral itraconazole should not be given to patients who are on astemizole or cisapride for fear of cardiovascular adverse events.35

Oral fluconazole

Oral fluconazole, a triazole antifungal, is also highly effective for the treatment of tinea versicolor through the inhibition of cytochrome P450-dependent ergosterol synthesis.217–219 When administered orally, fluconazole can persist in the stratum corneum for approximately 2 weeks following administration.219 The recommended dose is 300 mg once weekly for 2–4 weeks.1,63,211 Because fluconazole has little affinity for mammalian cytochromes, the antifungal has low toxicity. Serious adverse events are rare.35 As fluconazole inhibits the cytochrome P450- dependent system, the medication should likewise be avoided in patients treated with astemizole or cisapride for fear of cardiovascular adverse events.35

Oral ketoconazole

Oral ketoconazole at a dose of 200 mg daily for 10 days is also effective for the treatment of tinea versicolor.147 The risk of hepatotoxic adverse events associated with oral ketoconazole is about 1 in 500 and therefore outweighs its potential benefits.220,221 Because of the risk of hepatotoxicity, adrenal insufficiency and multiple drug–drug interactions, oral ketoconazole should no longer be prescribed.1,35,87

Oral terbinafine

Oral terbinafine is not effective in the treatment of tinea versicolor.87 Terbinafine is not excreted in sweat and fungicidal levels of terbinafine cannot be achieved in the stratum corneum with oral administration of the medication.87

Oral griseofulvin

Oral griseofulvin is not effective for the treatment of tinea versicolor.17,43

Laser and photodynamic therapies

A limited number of studies reported the successful treatment of tinea versicolor with 308-nm excimer laser, narrow-band ultraviolet (UV)-B phototherapy, 5- aminolevulinic acid photodynamic therapy and methylene blue photodynamic therapy.222–225 Well-designed, large-scale, multicentre, randomized, placebo-controlled trials are needed to confirm or refute these findings.

Alternative therapies

A wide variety of alternative medicines have been shown to have some therapeutic effects on tinea versicolor. In some cultures, alternative therapies are popular for the treatment of tinea versicolor. These include topical application of beeswax and honey,226 essential oils of Cymbopogon citratus,227 quince seed mucilage hydrogel decorated with essential oils of Nigella sativa, Citrus sinensis and Cinnamon verum,228 polyherbal Unani formulation,229 Pentas longiflora leaf extract,230 Acalypha wilkesiana leaf extract,231 Artemisia sieberi shrub extract,182 nitric oxide-liberating cream232 and irradiated human amniotic membrane in combination with tea tree oil.233 None of these treatments have yet been subjected to rigorous studies nor randomized clinical trials.

Prophylactic treatment

The relapse rate is high because Malassezia species are normal commensals on the skin surface.87 Good personal hygiene may limit recurrences to a certain extent. Long-term intermittent prophylactic therapy should be considered for patients with frequent recurrence of the disease who desire treatment, especially during the warmer months of the year.87 Unfortunately, research studies evaluating the efficacy of prophylactic antifungal treatment are scarce. Prophylactic administration of topical ketoconazole 2%, clotrimazole 1% or selenium sulfide 2.5% shampoo applied to the whole body for 10 minutes once a month may lead to decreased relapse rate of tinea versicolor.166 An alternative is to prophylactically administer an oral antifungal agent such as itraconazole, especially if topical antifungal prophylaxis is not successful. Oral itraconazole is easy to administer and less time-consuming and thereby has better compliance.63 The recommended dose of itraconazole for prophylaxis is 200 mg twice a day once per month.1,216

Conclusion

Tinea versicolor is a common superficial fungal infection of the skin caused by Malassezia species. Because the clinical manifestations of tinea versicolor are myriad, clinical acumen is essential to make the correct diagnosis. As tinea versicolor is often a chronic and recurrent disease, repetitive treatment courses are often necessary. A wide range of antifungal agents are effective in the treatment of tinea versicolor. In general, topical antifungal agents are the first-line treatment of tinea versicolor as there are fewer adverse events associated with their use. Oral antifungal agents are usually reserved for severe, widespread, recalcitrant or recurrent disease. Apart from considering the severity and extensiveness of tinea versicolor, patient age, and patient and physician preferences, the selection of antifungal agents depends on a number of factors, including the efficacy, safety, local availability, ease of administration, likelihood of compliance and potential drug interactions of the antifungal agent. In clinical practice, it is often the patient preferences and the physician experience that dictate the selected treatment.

Acknowledgements

None.

Footnotes

Contributions: AKCL is the principal author. BB, JML, KFL and KLH are coauthors who contributed and helped with the drafting of this manuscript. All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, take responsibility for the integrity of the work and have given their approval for this version to be published. All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, take responsibility for the integrity of the work as a whole and have given their approval for this version to be published.

Disclosure and potential conflicts of interest: AKCL and KLH are associate editors of Drugs in Context and confirm that this article has no other conflicts of interest otherwise. This manuscript was sent out for independent peer review. The International Committee of Medical Journal Editors (ICMJE) Potential Conflicts of Interests form for the authors is available for download at: https://www.drugsincontext.com/wp-content/uploads/2022/10/dic.2022-9-2-COI.pdf

Funding declaration: There was no funding associated with the preparation of this article.

Correct attribution: Copyright © 2022 Leung AKC, Barankin B, Lam JM, Leong KF, Hon KL. https://doi.org/10.7573/dic.2022-9-2. Published by Drugs in Context under Creative Commons License Deed CC BY NC ND 4.0.

Provenance: Invited; externally peer reviewed.

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