Disseminated Epidermolytic Acanthoma with Disseminated Superficial Porokeratosis and Verruca Vulgaris in an Immunosuppressed Patient

Abstract

A 40-year-old man who had received long term immunosuppressive treatment for 14 years following kidney transplantation developed multiple skin lesions on both antecubital fossae, scalp, and both lower extremities. Histopathologic findings from three skin regions revealed characteristic features of epidermolytic hyperkeratosis, verruca vulgaris, and disseminated superficial porokeratosis, respectively. Although immunocompromised individuals may demonstrate verruca vulgaris or porokeratosis, disseminated epidermolytic acanthoma (DEA) has not been reported to be associated with immunosuppressed status. We suggest that immunosuppression may play a role in the pathogenesis of DEA, as shown in our case.

Multiple Spreading Epidermolytic Acanthomas of the Genital and Perigenital Skin

“…These specific keratins are synthesized by suprabasal keratinocytes during the differentiation of epidermis. These mutations could be induced by factors as UV radiation due to intensive sun exposure [6] or during PUVA therapy [7], immunosuppression (1 case of a kidney-transplanted patient with a long-term immunosuppressive treatment [5]) or repeated trauma [3]. In our patient, the repeated local microtrauma due to intense psychogenic pruritus may represent a possible precipitating factor.…”

Psoriasiform Keratosis: A Lesion Mimicking Psoriasis

“…Three of the 10 patients had 2 lesions each. Multiple lesions of other acanthomas such as benign lichenoid keratosis 6,8 and epidermolytic acanthoma [2][3][4]12 have also been reported.…”

Linear epidermolytic acanthoma of vulva: An unusual presentation

“…[6,7] In a majority of the reports, the lesions are solitary, but multiple lesions have also been described, especially in the scrotum [5] and vulva. [6] Disseminated lesions have also been well documented, [3,4] especially in one patient associated with underlying immunosuppression due to kidney transplantation [4] where up to 100 lesions were present. Another clinical variant called multiple spreading type of EAs of genital and perigenital skin has been recently described in a male.…”

“…[11] These keratins are synthesized by suprabasal keratinocytes during the differentiation of the epidermis. These mutations could be induced by numerous factors as UV radiation through intense sun exposure, [3] immunosuppression [4] or repeated trauma. [5,8] Electron microscopy demonstrates that the mechanism of blister formation is cytolysis rather than acantholysis.…”

“…[2] The term EA is applied to discrete epidermal proliferations characterized by EH. EA has been described in different locations, namely eyelid, leg, anus, [2] abdomen, [3] back, [4] forearm, [4] scrotum [5] and the vulval region. [6,7] In a majority of the reports, the lesions are solitary, but multiple lesions have also been described, especially in the scrotum [5] and vulva.…”