Atrophying Tinea Versicolor

A 26-year-old African female, originally from Mali, presented for evaluation of “white spots” on her torso, upper arms, and neck of approximately one year duration. Several months before the onset of the eruption, she had been using a skin-lightening cream, called Perfect White, which contains kojic acid as an active ingredient. After the lesions developed, she stopped using the skin-lightening cream. However, the lesions continued to increase in number with associated pruritus. She denied any systemic symptoms and her only medication was a daily multivitamin.

She was started on topical ketoconazole 2% shampoo three times weekly while her liver function tests were pending. Her tests returned within normal limits and she was started on a 2-week course of oral ketoconazole therapy. She subsequently had marked clinical improvement with a decrease in the number and size of atrophic lesions. She continued maintenance therapy with topical ketoconazole 2% shampoo once weekly.

Discussion
Tinea versicolor (TV) is a superficial cutaneous fungal infection caused by Malassezia, which is a dimorphic and lipophilic organism that resides in the stratum corneum. TV atrophy since 1971 (Table 1). These cases do not appear to have an age or sex predilection. A majority of cases documented atrophic lesions localized to the trunk and upper extremities. Notably, one of the cases reported granulomatous lesions localized to the eyelid, cheek, and nose. On histopathological evaluation, all cases with skin biopsies demonstrated poikilodermatous tissue alterations, which include loss of the epidermal retiform pattern, vascular ectasia, and thinning of dermal collagen bundles. Five of the cases, including ours, had evidence of elastolysis, which is not a requirement for diagnosis. Lastly, only four of the patients had a previous history of topical corticosteroid use.
Crowson and Magro coined the term 'atrophying tinea versicolor,' which should be considered one of the rare variants of TV [1]. Some cases of atrophying TV may be associated with a history of long-term topical corticosteroid use, which our patient did not have [2]. The link between topical steroids and the onset of atrophy may be causal or simply coincidental. Skin atrophy may also occur secondary to delayed-type hypersensitivity reactions, the direct effect of Malassezia on NF-κB signaling, or increased synthesis of pro-inflammatory cytokines, such as IL-1β and TNF-α [1]. Histopathology will reveal the classic short hyphae and spores in the stratum corneum as well as partial atrophy of the epidermis. Many cases have evidence of poikilodermatous tissue alterations [1]. Long-standing lesions may also demonstrate is common with a nationwide prevalence of 2-8%. Although difficult to culture, Malassezia globosa and Malassezia furfur are the two species predominantly isolated when cultured on media enriched with C12-to C14-fatty acids. Available growth mediums include Dixon's medium containing Tween 40 and glycerol-monooleate, and Leeming and Notman medium containing Tween 60, glycerol, and full-fat cow's milk. Patients usually present with numerous oval-to-round macules with fine scale scattered on the neck, trunk, and extremities. Predisposing factors include genetic susceptibility, humid environments, immunosuppression, malnutrition, and Cushing disease.
There have been at least 17 reports of TV associated with skin   [4]. Case 3 reported by Park et al [5]. Case 4 reported by Yang et al [6]. Case 5 reported by Romano et al [7]. Cases 6-17 reported by Crowson and Magro [1]. b Poikilodermatous tissue alterations include loss of epidermal retiform pattern, vascular ectasia, and thinning of dermal collagen bundles.
dermal elastolysis, which may be due to histiocytes releasing elastase. Further studies are warranted to elucidate the precise mechanism of atrophy and to examine if certain species of Malassezia have a greater propensity to develop atrophic lesions.
Understandably, these answers have been evasive due to the paucity of cases reported in the literature.
A possible mechanism of hypopigmentation in TV involves the yeast's production of azelaic acid, which inhibits tyrosinase. Additionally, TNF-α inhibits melanogenesis through the NF-κB pathway by down-regulating tyrosinase promoter activity [3]. Interestingly, kojic acid, used by our patient, is also an antityrosinase depigmenting agent found in skin-lightening cosmetic products used to treat hyperpigmentation and melasma. Theoretically, it is possible that the kojic acid used by our patient further enhanced tyrosinase inhibition. There are no documented reports of tinea versicolor, atrophying or otherwise, following topical application of kojic acid.
Atrophying TV should be added to the differential diagnosis of other atrophying conditions, such as anetoderma, atrophoderma of Pasini and Pierini, morphea, lupus erythematosus, dermatomyositis, parapsoriasis, mycosis fungoides, poikilodermatous T-cell dyscrasias, acrodermatitis chronic atrophicans, sarcoidosis, and cutis laxa. Previous reports document complete resolution of lesions, including atrophy, following courses of oral antifungal therapy. Prophylactic therapy may help reduce high recurrence rates.