Answer: Atrophying tinea versicolor

Discussion

Pityriasis versicolor is a chronic superficial fungal infection that clinically shows red colored, hypo and hyperpigmented lesions involving upper trunk, head, and neck area. ^[1] 'Atrophying tinea versicolor' is an atypical clinical form of pityriasis versicolor proposed by Crowson and Magro. ^[2] According to the reported cases, there are depressed macules involving the trunk and shoulder girdle area. Histologically, in addition to pityrosporum spores and hyphae visible in the cornified layer, skin biopsy of atrophic lesion is accompanied by poikilodermatous alteration, perifollicular elastolysis, and lymphocytic interface dermatitis. ^[2],[3],[4] However, alteration of elastic fibers are not always seen as it is in our case. ^[2]

Atrophying tinea versicolor needs to be distinguished from other diseases with cutaneous atrophic lesion, such as systmemic lupus erythematosus, dermatomyositis, morphea, anetoderma, atrophoderma, cutis laxa, mycosis fungoides, lichen sclerosus, and atrophy due to intralesional steroid therapy. ^[3] Mycological examination is always helpful to exclude other clinical conditions and biopsy can also confirm fungal elements in stratum corneum. Among those clinical conditions, atrophoderma of Pasini and Pierini is clinically similar to that of atrophying tinea versicolor. A diagnostic feature of atrophoderma of Pasini and Pierini is that they show thickened collagen bundle on the histopathologic examination.

Some reports suggested that the atrophic lesion of pityriasis versicolor might be related to the application of topical steroids. These workers have postulated that greater penetration of the drug through the weakened outer two-third of corneal layer affected by pityriasis versicolor may be responsible for the atrophy. ^[5] On the other hand, Crowson and Magro. ^[2] reported that only one patient out of 12 atrophying tinea versicolor patient used topical steroid and therefore it was difficult to say that the atrophic lesion is due to topical steroid. They suggested that the delayed-type hypersensitivity to the epicutaneous antigens derived from the pityrosporum fungi and direct microbial effect upon the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) system could have provoked the atrophic lesion. With small number of reported cases, the cause of atrophying tinea versicolor is still not clear and further evaluation is therefore needed. The prognosis of the disease is relatively good and the mycological recovery and disappearance of atrophic lesion can be achieved with systemic triazolic therapy or combined therapy of systemic triazole and topical imidazole. ^[2],[3],[4] Dermatologists should include atrophying tinea versicolor in the differential diagnosis of the atrophic lesion of skin.