Pityriasis lichenoides et varioliformis acuta and Acquired Toxoplasmosis

Rongioletti, Franco; Rivara, Gianpiero; Rebora, Alfredo

doi:10.1159/000248780

Cited by 20 publications

(6 citation statements)

References 6 publications

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“…7 Still another explanation for our findings is that the dominant T-cell clone in PLEVA represents a clonal immunologic response to an unknown antigen or infectious agent. 2,9,[23][24][25] We favor the hypothesis that PLEVA is part of the clonal T-cell cutaneous lymphoproliferative spectrum, such as small plaques parapsoriasis, 26 as previously suggested. 6 The rare occurrence of lymphoma during the course of PLEVA and, in most cases, a spontaneous remission after several months, suggests that a vigorous host immune reaction controls and eventually eliminates the T-cell clone.…”

Section: Commentsupporting

confidence: 74%

T-Cell Clonality in Pityriasis Lichenoides et Varioliformis Acuta

Dereure

Levi²,

Kadin³

2000

Arch Dermatol

136

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Section: Commentsupporting

confidence: 74%

T-Cell Clonality in Pityriasis Lichenoides et Varioliformis Acuta

Dereure

Levi²,

Kadin³

2000

Arch Dermatol

136

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“…67 Empiric treatment with spiramycin resulted in clearing of the cutaneous lesions within a few weeks. In 1997 Nassef and Hammam compared 22 patients clinically and 70 Epstein-Barr virus.…”

Section: Infectious Etiologymentioning

confidence: 99%

Pityriasis lichenoides and its subtypes

Bowers

Warshaw

2006

Journal of the American Academy of Dermatology

200

284

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“…Several dermatoses with a clinical presentation resembling pityriasis lichenoides have been described, including histiocytic medullary reticulosis, 11 acquired toxoplasmosis, 12 eruption during therapy for myelogenous leukemia, 13 exanthem caused by astemizole, 14 group A β‐hemolytic streptococcal infection, 15 early stage of human immunodeficiency virus (HIV) infection, 16 primary parvovirus B19 infection, 17 and secondary syphilis. 18…”

Section: Discussionmentioning

confidence: 99%

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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Pityriasis lichenoides et varioliformis acuta and Acquired Toxoplasmosis

Cited by 20 publications

References 6 publications

T-Cell Clonality in Pityriasis Lichenoides et Varioliformis Acuta

T-Cell Clonality in Pityriasis Lichenoides et Varioliformis Acuta

Pityriasis lichenoides and its subtypes

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

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