What is the pathophysiology of pityriasis lichenoides?

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

Mucha-Habermann disease is not a vasculitic process despite reports of immunoglobulin and complement deposition in vessels. Fibrin is not present in the walls of vessels, and thrombi are not found in the lumen. A cell-mediated mechanism has been proposed based on a T-lymphocytic infiltrate with a cytotoxic/suppressor phenotype, diminished epidermal Langerhans cells, and a reduction of the CD4/CD8 ratio. CD30 (Ki-1) cells, which are associated with large cell lymphoma, have been identified in the infiltrate of both lymphomatoid papulosis and Mucha-Habermann disease, leading some authors to view this as a self-limited self-healing lymphoproliferative disease. [3, 4] One study suggests that pityriasis lichenoides is a form of a T-cell dyscrasia, based on the presence of intraepithelial atypical lymphocytes, phenotypic abnormalities, and TCR-gamma rearrangements. [5]


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