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Tinea Versicolor

Tinea Versicolor

For 2 years, a slightly pruritic, light brown, scaly rash had been present on a 20-year-old man’s neck. During the past 8 months, the eruption spread to the upper chest and upper arms. The patient reported that the rash changes color with the seasons. Multiple round to oval, hypopigmented, slightly scaly macules were noted on the neck, chest, and upper arms. Tinea versicolor was strongly suspected. Dr Alexander K. C. Leung of Calgary, Alberta, writes that this disease most commonly affects areas of skin that are rich in sebum production, such as the neck, trunk, and upper arms. Lesions arise as multiple small, circular macules that enlarge radially. The eruption varies in color from patient to patient, but each person’s tinea versicolor lesions are a single hue. Hyperpigmented, red to brown lesions erupt in fair-skinned patients, whereas those with dark skin tend to have hypopigmented lesions.1 The characteristic macules are covered with a fine scale and are typically asymptomatic, although some patients complain of mild pruritus. The differential diagnosis of hypopigmented lesions includes pityriasis alba, vitiligo, corticosteroid-induced hypopigmentation, postinflammatory hypopigmentation, and hypopigmented lesions of cutaneous T-cell lymphoma. Hyperpigmented lesions associated with tinea versicolor must be distinguished from seborrheic dermatitis, contact dermatitis, tinea corporis, pityriasis rosea, melasma, secondary syphilis, erythrasma, and nevi. Tinea, or pityriasis, versicolor is a superficial skin infection caused by the dimorphic lipid-dependent yeast, Malassezia furfur, also known as Pityriasis ovale (oval form) and Pityriasis orbiculare (round form). M furfur is a normal commensal on the skin surface. Skin colonization increases with age; 25% of children and almost 100% of adolescents and adults are affected.2 Tinea versicolor occurs when the yeast form of the organism converts to the hyphal form; the impetus for this conversion is not known. Predisposing factors for the outbreak include a warm and humid environment, excessive sweating, skin occlusion, an excess of lipid-containing sebaceous secretions, malnutrition, poor general health, immunosuppression, and a genetic predisposition to the disorder.3,4 The cause of the eruption’s seasonal variations is unknown. The diagnosis is usually based on clinical evidence. If necessary, perform a potassium hydroxide evaluation; examination of scrapings from lesions reveals numerous short, stubby hyphae intermixed with clusters of spores (the so-called spaghetti and meatballs appearance). Wood lamp examination may show yellowish gold fluorescence. Some lesions do not fluoresce. Most patients respond to topical treatment with selenium sulfide (2.5%) lotion; sodium thiosulfate (25%) lotion; or miconazole, clotrimazole, ketoconazole, or terbinafine cream. Oral ketoconazole, fluconazole, itraconazole, or terbinafine may be appropriate for patients with extensive disease, frequent recurrences, or disease that is refractory to topical therapy. Advise patients that hypopigmented areas may not disappear immediately— even after treatment—and that sunlight can accelerate repigmentation. Terbinafine cream was prescribed for this patient. His lesions resolved in 1 month.

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