Erythroderma presents as generalized skin redness. The features of a 39-year-old man who presented with erythroderma are described. His skin biopsy revealed hyphae in the stratum corneum, which established the diagnosis of tinea corporis. His erythroderma resolved following treatment with an oral antifungal agent. Several conditions can be associated with erythroderma. Common etiologies for erythroderma include medications, neoplasms, and papulosquamous disorders. Superficial dermatophyte-associated erythroderma is rare. However, although erythroderma caused by generalized superficial mycosis is infrequently encountered, tinea corporis should be included in the new-onset or chronic erythroderma. The detection of fungal hyphae in the stratum corneum of a biopsy of the erythrodermic skin can not only establish dermatophyte infection as the underlying cause of the individual's erythroderma but also an alternative cause of erythroderma.
Vitiligo is a depigmentation disorder of the skin that occurs secondary to the destruction of melanocytes by an immune‐mediated process. Vitiligo clinically presents with depigmented macules and patches, most commonly on the face, acral sites, and genitalia. It can be characterized as generalized or localized based on distribution. The localized form can be further divided into segmental (linear, band‐like, or Blaschkoid) and non‐segmental vitiligo. The classical treatment of vitiligo includes topical steroids, pulsed oral steroids in unstable vitiligo, phototherapy, a combination of steroid therapy and phototherapy, surgical grafting, as well as intentional depigmentation therapy in severe cases. However, recent advances in understanding the immune mechanisms implicated in the pathogenesis of vitiligo have led to the use of an FDA‐approved topical Janus kinase (JAK) inhibitors for vitiligo. Despite this novel therapy advancement, we recommend the addition of narrowband ultraviolet B (NB‐UVB) to JAK inhibitors in patients with extensive and progressive lesions, or those not fully responsive to JAK inhibitor monotherapy.
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