Pityriasis Lichenoides Workup

Updated: Sep 11, 2020
  • Author: Jeffrey P Callen, MD; Chief Editor: Dirk M Elston, MD  more...
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Laboratory Studies

Laboratory workup largely is a function of the acuity of the disease. A patient presenting with febrile ulceronecrotic pityriasis lichenoides et varioliformis acuta (PLEVA) requires an entirely different approach than a patient presenting with pityriasis lichenoides chronica (PLC).

The following laboratory tests address both implicated causes of Mucha-Habermann disease and other disorders in the differential diagnosis; tailor the workup to each patient's presentation:

  • Antistreptolysin O titers

  • EBV IgM/IgG viral capsid antigen and nuclear antigen antibody

  • Erythrocyte sedimentation rate

  • Hepatitis B surface antigen, antisurface antibody, and anticore IgM

  • Hepatitis C virus antibody

  • HIV screening

  • Monospot or heterophil antibody test

  • Rapid plasma reagin

  • Throat cultures

  • Toxoplasma Sabin-Feldman dye test, enzyme-linked immunoassay, and indirect immunofluorescence/hemagglutination


Other Tests

A punch biopsy of 4 mm or larger or shave biopsy should be strongly considered to ensure the diagnosis and rule out lymphomatoid papulosis.

T-cell gene rearrangement studies to test for clonality may aid in the diagnosis of a lymphoma. It should be noted, however, that benign dermatoses also may show T-cell gene restriction and that the discovery of a clone is not a sine qua non of a lymphoma diagnosis. Several studies have shown a significant portion of pityriasis lichenoides cases have a T-cell clone. [5, 31]


Histologic Findings

Ackerman has established histopathologic criteria for fully developed lesions of PLEVA and PLC. [32] Early lesions in both variants are smooth, since areas of parakeratosis initially are overlain by a normal cornified layer with a basket-woven appearance.

PLEVA lesions are characterized by a wedge-shaped superficial and deep dermal lymphohistiocytic infiltrate with intravascular margination of neutrophils, a confluent parakeratotic scale crust, thinning of the granular layer, basilar necrosis of keratinocytes, vacuolar interface dermatitis with a lymphocyte in nearly every vacuole, erythrocyte extravasation, and dermal edema.

Rare cases of γδ T-cell–predominant disease may mimic more aggressive lymphomas histologically. [33, 34]

PLC lesions are characterized by a superficial dermal infiltrate, focal parakeratosis, preservation of the granular layer, and focal disappearance of the dermal-epidermal interface.