Flexural purpura and Epstein–Barr virus infection

Pozo, Del; Almagro, Manuel; García-Silva, J.; Martínez, Walter; Fonseca, Eduardo

doi:10.1046/j.1365-4362.1998.00398.x

Cited by 3 publications

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“…The presence of purpura in cutaneous lesions induced by EBV infection has been reported as leukocytoclastic vasculitis, 5–6 flexural purpura, 7 petechial mucosal lesions, 8 purpuric exanthems, 9 disseminated purpuric lesions in immunosuppressed patients, 10 and cold‐induced purpura, 1 Our patient developed purpuric lesions in the context of an exanthem clinically similar to acute pityriasis lichenoides.…”

Section: Discussionmentioning

confidence: 52%

Pityriasis lichenoides‐like exanthem and primary infection by Epstein–Barr virus

et al. 2000

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A 43‐year‐old man with a history of recurrent herpes simplex, and without a history of atopy, presented with a sudden appearance of an exanthem 10 days before presenting to the clinic. The exanthem affected the face, flexural areas, hands, and feet. No local symptomatology and no systemic involvement were observed. The exploration revealed a polymorphous exanthem formed by maculopapular lesions, umbilicated vesicles, crusts, and purpuric and necrotic elements, with a pattern of acute pityriasis lichenoides ( Figs 1 and 2). 1 Papular and necrotic lesions localized on the flexion surface of the arm 2 Papular and purpuric elements on the dorsum of the hand The histopathologic examination of a skin biopsy specimen showed a dense lymphohistiocytic infiltrate, with a linear disposition over the entire thickness of the papillary dermis and in the upper part of the reticular dermis. At the dermoepidermal junction, vacuolar alteration of the basal layer was observed, with the presence of mononuclear exocytosis, edema extending to the papillary dermis, and extravasated red cells. Spongiosis, keratinocytic focal necrosis, and parakeratosis were observed in the epidermis ( Fig. 3). 3 Spongiosis, keratinocytic focal necrosis, and parakeratosis are observed in the epidermis. The dermoepidermal junction shows vacuolar alteration of the basal layer and mononuclear exocytosis. In the papillary dermis, a dense lymphohistiocytic infiltrate is present with edema and extravasated red cells Analytical explorations revealed lymphocytosis and slight elevation of transaminases. Serologies to hepatitis A virus, hepatitis B virus, hepatitis C virus, cytomegalovirus, human immunodeficiency virus (HIV) 1 and 2, syphilis, and human parvovirus B19 were negative. The CD4 and CD8 lymphocyte counts were normal. The serology to Epstein–Barr virus (EBV) ( Table 1) was consistent with a primary infection by EBV. Oral acyclovir treatment, 1 g daily for 7 days, was started and the exanthem disappeared in 7 days. Serologic evolution of EBV infection in our patient January 1998 February 1998 April 1998 IgM VCA++–IgG VCA+ (2,63)+ (1,97)+ (2,01)EBNA––+ EBNA, Epstein–Barr nuclear antigen; IgG, immunoglobulin G; IgM, immunoglobulin M; VCA, viral capside antigen.

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