Skin disorders and Epstein Barr virus primary infection: results of a 31 month survey

Baldari, U

doi:10.1016/0926-9959(94)00087-g

Cited by 2 publications

(1 citation statement)

References 22 publications

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“…erythema nodosum. or GCS (18). The development of these inflammatory dermatoses, especially GCS, may be due to the interaction of EBV and the skin-associated immune system (9,18).…”

Section: Discussionmentioning

confidence: 99%

Gianotti‐Crosti Syndrome Associated with Epstein‐Barr Virus Infection

Hofmann

Schuppe

Adams

et al. 1997

Pediatric Dermatology

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Gianotti-Crosti syndrome (GCS) is a distinct exanthematic, acrolocated eruption of childhood caused by a variety of infectious agents. Historically hepatitis B antigen positive (HBsAG+) papular acrodermatitis of childhood and HBsAg negative (HBsAg-) papulovesicular acrolocated syndrome have been distinguished. Here we characterize the spectrum of associated infectious agents in seven patients with confirmed GCS seen in our departments in the years 1994-1995. Where available, stored frozen serum samples were reanalyzed for antiviral antibodies. The mean age of the two girls and five boys was 22.5 months with a range of 8 to 53 months. None of the patients was HBsAG+. Four patients showed serologic evidence of an acute infection and one patient of a recent Epstein-Barr virus (EBV) infection. In two additional children vaccination preceded the appearance of GCS. In these two patients serologic investigations revealed no evidence of recent infection with most common viruses. Our results underline the role of viral infections other than hepatitis B in the etiology of GCS. EBV infection was the most commonly associated viral disease in our population. We agree with other authors that we should avoid using the terms papular acrodermatitis of childhood and papulovesicular acrolocated syndrome in describing HBsAg+ and HBsAg- forms of GCS.

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“…erythema nodosum. or GCS (18). The development of these inflammatory dermatoses, especially GCS, may be due to the interaction of EBV and the skin-associated immune system (9,18).…”

Section: Discussionmentioning

confidence: 99%

Gianotti‐Crosti Syndrome Associated with Epstein‐Barr Virus Infection

Hofmann

Schuppe

Adams

et al. 1997

Pediatric Dermatology

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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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Skin disorders and Epstein Barr virus primary infection: results of a 31 month survey

Cited by 2 publications

References 22 publications

Gianotti‐Crosti Syndrome Associated with Epstein‐Barr Virus Infection

Gianotti‐Crosti Syndrome Associated with Epstein‐Barr Virus Infection

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

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