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The Clonal Nature of Pityriasis Lichenoides
Jeffrey M. Weinberg, MD;
Leonard Kristal, MD;
Lillian Chooback, PhD;
Paul J. Honig, MD;
E. Michael Kramer, MD;
Stuart R. Lessin, MD
Arch Dermatol. 2002;138:1063-1067.
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 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.
From the Department of Dermatology, University of Pennsylvania (Drs
Weinberg, Chooback, and Lessin), the Children's Hospital of Philadelphia (Drs
Kristal and Honig), and Thomas Jefferson Medical College (Dr Kramer), Philadelphia,
Pa. Dr Weinberg is now with the Department of Dermatology, St Luke'sRoosevelt
Hospital Center, New York, NY, and Dr Lessin is now with the Fox Chase Cancer
Center, Philadelphia.
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