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The clonal nature of pityriasis lichenoides
Jeffrey M Weinberg1, Leonard Kristal, Lillian Chooback
1Department of Dermatology, University of Pennsylvania, Philadelphia, USA. jwein@bway.net
Background:
Pityriasis lichenoides et varioliformis acuta (PLEVA) and pityriasis lichenoides chronica (PLC) are benign lymphocytic infiltrates of the skin that classically present as either a recurrent papulonecrotic eruption (PLEVA) or a persistent, scaling, papular eruption (PLC). Observations of both types of lesions present on individual patients have led to speculation that both entities are related. Previous studies evaluating the DNA of biopsy specimens from patients with PLEVA and PLC revealed clonal T-cell receptor beta gene rearrangements.
Objective:
To analyze and compare the T-cell populations between lesions of PLEVA and PLC.
Design:
Retrospective and prospective analysis of patient tissue samples, classified by histologic analysis. Extracted DNA from 13 skin biopsy specimens with the diagnosis of PLC and 14 skin biopsy specimens with the diagnosis of PLEVA was analyzed by polymerase chain reaction/denaturing gradient gel electrophoresis (PCR/DGGE).
Setting:
Molecular diagnostic laboratory at an academic medical center.
Patients:
Twenty-seven tissue samples were obtained from patients with a histologic diagnosis of PLEVA or PLC. These samples were analyzed by PCR/DGGE.
Main Outcome Measure:
The presence or absence of T-cell receptor gene rearrangements on PCR/DGGE analysis corresponding to a clonal population of T cells.
Results:
Of 14 PLEVA specimens, 8 (57%) demonstrated monoclonal T-cell receptor gene rearrangements; 1 (8%) of 13 PLC specimens showed a gene rearrangement (P =.008, Fisher exact test).
Conclusions:
Our results demonstrate the polyclonal nature of the lymphocytic infiltrate found in almost all of the PLC specimens, which contrasts with the monoclonal nature found in most of the PLEVA specimens. These differences may represent different stages of the clinical evolution of a single entity that results from varying host immune responses to pathogenic factors. Specifically, we propose that PLEVA is a benign clonal T-cell disorder in which the clone arises from a subset of T cells in lesions of PLC. The host immune response to this clone determines the clinical and histologic findings in PLEVA.