|Year : 2014 | Volume
| Issue : 1 | Page : 32-35
The enigma of color in tinea versicolor
Divya Gupta, Devinder Mohan Thappa
Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India
|Date of Web Publication||26-Jun-2014|
Devinder Mohan Thappa
Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry 605 006
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Gupta D, Thappa DM. The enigma of color in tinea versicolor. Pigment Int 2014;1:32-5
Tinea versicolor is a common superficial fungal infection of the skin, especially in the hot and humid environment of India. It is caused by the Malassezia species which is a dimorphic, lipophilic fungus. Hence, the sebaceous areas of the body that is, face, neck, upper back, and chest are most frequently affected. There is a variable age distribution of this disease, and a great majority of cases occur during adolescence. The organism is found as part of the normal flora of the skin in 90-100% of subjects. Tinea versicolor results when there is an overgrowth of this commensal fungus due to certain predisposing factors such as heat, moisture, and occlusion of the skin by dressings, clothing, or cosmetics.
The disease can present as hypo- or hyper-pigmented macules, initially folliculocentric, and later coalescing to form geographic lesions with polycyclic margins. In Indians, 75-85% of the lesions are hypopigmented [Figure 1], 5-15% are mixed and the rest of the cases are hyperpigmented [Figure 2].  It is an asymptomatic disorder and alterations of skin pigmentation are often the presenting complaint in tinea versicolor. The color of lesional skin in tinea versicolor varies from brown to pink to white in different individuals. The macules and patches, as implied by the name "versicolor", may be hypo- and hyper-pigmented, leukodermal, erythematous, or dark brown. Sometimes, overlapping lesions produce a striking tri-colored pattern of pigmentation known as "trichrome pityriasis versicolor".  Although mild pruritus can sometimes occur, most patients are distressed by the color alteration rather than other symptoms. However, the exact pathogenesis of hyper- and hypo-pigmentation in tinea versicolor lesions remains an enigma to this day.
Amongst early theories, race and ethnicity were believed to be important factors, and it was believed that hypopigmented macules were more common in dark skinned patients and hyperpigmented lesions in fair skinned individuals.  Aljabre et al.  disproved this theory in their study, which found that there was no correlation between the pigmentary variations of tinea versicolor and the type of skin, sex, and age of the patients. In fact, they observed that some patients had both hypo-and hyper-pigmentation and propounded that there were other factors involved in the production of pigmentary changes in tinea versicolor. In their study, they also refuted the suggestions that early lesions of tinea versicolor are light brown or hypopigmented, which eventually evolve into hyperpigmented macules.  They suggested that the pigmentary differences in tinea versicolor were related to different strains of Malassezia; however, this view could not be proven.
Another early theory related to the prevention of tanning of the infected areas by fungal scales or a thinning of the stratum corneum with subsequent loss of melanin granules and degenerative cellular changes within the melanocytes.  The damaged melanocyte theory was used to explain why repigmentation may take months or years to occur after resolution of infection.
However, the etiology of hypopigmentation is more complex than can be explained by the sun-screening effect of infected scales in the stratum corneum. Moreover, depigmented skin lesions of this infection have also been described over the sun protected genital region.  Charles et al.  found smaller melanosomes and melanosome granules in lesional hypopigmented skin as compared to adjacent uninvolved skin. The dendrites of melanocytes had marked "melanin loading" with melanosomes when compared with dendrites in the normal skin, indicating decreased melanin uptake by the keratinocytes in the affected area. It appears then, that the presence of the fungus in the skin initiates the production of abnormal melanosome granules and possibly the faulty transfer of these granules to the keratinocytes. The mechanism for this is unknown. In addition, formation of melanosome complexes followed by their subsequent destruction within lysosomes may also contribute to the decreased pigment within the epidermis noted in involved skin. 
Borgers et al.  found lipid laden spheres by electron microscopy both intra and extra-cellularly within the stratum corneum, which were confirmed by lipid specific stains like Oil Red O and Sudan Black B. Significantly, this lipid material persisted in the skin layer even 4 weeks after treatment with itraconazole. The authors postulated that the hypochromic reaction was related to filtering of ultraviolet light by this "lipid screen". Persistence of the lipidic material for a few weeks after treatment is consistent with the observation that hypopigmentation persists for 3-4 weeks after the disappearance of viable fungi from the skin. 
Other theories of hypopigmentation include damage to melanocytes and inhibition of tyrosinase by dicarboxylic acid, especially azelaic acid, produced by Malassezia furfur. These changes are most likely due to the cytotoxic effect of dicarboxylic acids (azelaic acid, oleic acid, and vaccinic acid) on melanocytes and melanogenesis. There may be two possible theories that explain this effect of dicarboxylic acids. The first is that they may interfere with mitochondrial enzymes (based on vacuolization and degeneration in the mitrochondria). The second is that they may be closely related to the pathway of melanin synthesis, leading to the formation of fewer and smaller melanosomes and partial degeneration of melanocytes. , It has also been suggested that the lipoperoxidation process induced by Malassezia may account for the clinical hypopigmented appearance of the skin patches. 
Hyperpigmentation, on the other hand, has been explained by abnormally large melanosomes,  a thick stratum corneum,  and a hyperemic inflammatory response. , Galadari et al.  found a definite increase in the thickness of the keratin layer. Malassezia spores and hyphae were more numerous in hyperpigmented lesions as compared with hypopigmented ones. The superficial perivascular lymphocytic inflammatory cell infiltrate was more pronounced in the hyperpigmented areas. Hypopigmented lesions showed only a low grade inflammatory cell infiltrate. The inflammatory responses have been reported to act as a stimulus to the melanocytes resulting in production of more pigment. , In several specimens of hypopigmented and hyperpigmented lesions, degenerated keratinocytes were found to be scattered within the stratum malpighii, though their contribution to the pigmentary disturbance was deemed unlikely.  The number of melanosomes were approximately the same in hyperpigmented lesions of tinea versicolor and the normal skin areas.  The granular layer of the involved skin had more tonofilaments, which also contributed to the dark color. 
In a recent study, the ratio between keratinocytes and Malassezia was shown to be important, with the latter inhibiting the growth rate of keratinocytes. Cytokines like interlukin (IL)-1α, IL-6, tumor necrosis factor-α and endothelin-1 were increased and were deemed to play a role in hyperpigmentation.  The various theories of hypo- and hyper-pigmentation are summarized in [Table 1] and [Table 2]. The histopathological differences are summarized in [Table 3].
|Table 3: Histopathological differences between hypo- and hyper-pigmented TV |
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Regarding the epidemiology of tinea versicolor, there is no difference in the prevalence of this organism in dark and light skins. It may also be possible that hypopigmented lesions in light skinned individuals are less noticeable as compared to hyperpigmented lesions (and vice versa) and thus escape attention.  In a study by Park et al., higher humidity, increased sebum excretion rate and increased transepidermal water loss were seen in both hyper- and hypo-pigmented pityriasis versicolor skin lesions by multiprobe adapter 5-a noninvasive physiological parameter of the skin. However, there was no significant difference in the type of Malassezia species between hyper- and hypo-pigmented skin lesions. 
The differential diagnosis of tinea versicolor includes pityriasis rosea, pityriasis alba, seborrheic dermatitis, and vitiligo. There are a number of therapeutic options for treating tinea versicolor. The antifungals used can be divided into topical and oral medications. Topical medications must be applied over entire trunk (from neck to waist) as lesions may be widespread and sometimes clinically unapparent. Systemic medication is preferred in patients with severe disease, frequent relapses, or in whom topical agents have failed. The yeast is part of the normal flora, and sometimes resides deep in the hair follicles. This may contribute to the high recurrence rate. Other reasons for recurrence include endogenous or exogenous predisposing factors that are still present after treatment. Therefore, it may be considered a chronic disease with prophylaxis being an integral part of the overall treatment.  In dark skinned patients, postinflammatory hypopigmentation tends to persist for a longer time, and aggressive and early treatment of the tinea versicolor lesions is desirable.  The various treatment modalities for tinea versicolor are summarized in [Table 4].
| Conclusion|| |
Tinea versicolor is a common disease encountered by dermatologists, which produces pigmentary changes in skin through hitherto unknown mechanisms. It may, on the strength of current evidence, be tempting to think that the variation in appearance of these lesions may be due to differences in ultrastructural composition already present in healthy dark or light skin.
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[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4]