Atrophying pityriasis versicolor as an idiosyncratic T cell-mediated response to Malassezia: A case series.

TitleAtrophying pityriasis versicolor as an idiosyncratic T cell-mediated response to Malassezia: A case series.
Publication TypeJournal Article
Year of Publication2017
AuthorsLevy JMichael St, Magro C
JournalJ Am Acad Dermatol
Volume76
Issue4
Pagination730-735
Date Published2017 Apr
ISSN1097-6787
KeywordsAdult, Aged, Antigens, CD, Atrophy, CD8-Positive T-Lymphocytes, Diagnosis, Differential, Female, GATA3 Transcription Factor, Histiocytes, Humans, Immunophenotyping, Lupus Erythematosus, Cutaneous, Malassezia, Male, Middle Aged, Mycosis Fungoides, Receptors, CXCR3, Retrospective Studies, Th1 Cells, Th2 Cells, Tinea Versicolor
Abstract

BACKGROUND: Atrophying pityriasis versicolor (PV), first described in 1971, is a rare variant in which lesions appear atrophic.

OBJECTIVE: We sought to determine the pathophysiology of atrophying PV.

METHODS: A retrospective chart review identified 6 cases of atrophying PV. In all cases, routine light microscopy, an elastic tissue stain, and immunohistochemical assessment for the expression of CD3, CD4, CD8, GATA3 and CXCR3 was performed.

RESULTS: All cases demonstrated hyperkeratosis with intracorneal infiltration by pathogenic hyphal forms as well as epidermal attenuation and papillary dermal elastolysis. A supervening, mild-to-moderate, superficial lymphocytic infiltrate was noted and characterized by a focal CD8 T cell-mediated interface dermatitis along with a mixed T-cell infiltrate composed of GATA3 and CXCR3 T cells.

LIMITATIONS: Small sample size and the loss of some patients to follow-up.

CONCLUSION: Atrophying PV represents the sequelae of a mixed helper T-cell (T1 and T2) idiosyncratic immune response to Malassezia and can present as a protracted dermatosis that may clinically mimic an atypical lymphocytic infiltrate. T1 cytokines can recruit histiocytes, a source of elastases, and upregulate matrix metalloproteinase activity, which may contribute to epidermal atrophy.

DOI10.1016/j.jaad.2016.08.062
Alternate JournalJ Am Acad Dermatol
PubMed ID27816291
Related Faculty: 
Cynthia M. Magro, M.D.

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