S Shieh1, D L Mikkola, G S Wood. 1. Department of Internal Medicine, Case Western Reserve University, Cleveland, Ohio, USA.
Abstract
BACKGROUND: Pityriasis lichenoides chronica (PLC) and pityriasis lichenoides et varioliformis acuta (PLEVA) are benign T-cell diseases that share several overlapping clinicopathologic features, leading many to believe that they exist as a spectrum rather than as single entities. Previous molecular studies have shown that PLEVA is a clonal lymphoproliferative disorder. To further characterize the immunohistologic features of PLC and to determine whether PLC demonstrates clonality, we studied 6 cases of PLC using a frozen section-immunoperoxidase technique and polymerase chain reaction/denaturing gradient gel electrophoresis. OBSERVATIONS: All 6 cases showed a mild to moderate superficial and deep perivascular infiltrate composed predominantly of CD4(+) T cells, admixed with Langerhans cells and macrophages; most were associated with an HLA-DR(+) epidermis. Three of 6 cases involved monoclonal T-cell receptor gamma (TCR gamma) gene rearrangements detected by V gamma 1-8/J gamma 1-2 and V gamma 9/J gamma 1-2 primers. CONCLUSIONS: Our findings enhance existing data showing that PLC shares many immunohistologic features with PLEVA and indicating that PLC is frequently a clonal T-cell disease. This provides further evidence that PLC and PLEVA are interrelated processes within the larger group of T-cell lymphoproliferative disorders.
BACKGROUND:Pityriasis lichenoides chronica (PLC) and pityriasis lichenoides et varioliformis acuta (PLEVA) are benign T-cell diseases that share several overlapping clinicopathologic features, leading many to believe that they exist as a spectrum rather than as single entities. Previous molecular studies have shown that PLEVA is a clonal lymphoproliferative disorder. To further characterize the immunohistologic features of PLC and to determine whether PLC demonstrates clonality, we studied 6 cases of PLC using a frozen section-immunoperoxidase technique and polymerase chain reaction/denaturing gradient gel electrophoresis. OBSERVATIONS: All 6 cases showed a mild to moderate superficial and deep perivascular infiltrate composed predominantly of CD4(+) T cells, admixed with Langerhans cells and macrophages; most were associated with an HLA-DR(+) epidermis. Three of 6 cases involved monoclonal T-cell receptor gamma (TCR gamma) gene rearrangements detected by V gamma 1-8/J gamma 1-2 and V gamma 9/J gamma 1-2 primers. CONCLUSIONS: Our findings enhance existing data showing that PLC shares many immunohistologic features with PLEVA and indicating that PLC is frequently a clonal T-cell disease. This provides further evidence that PLC and PLEVA are interrelated processes within the larger group of T-cell lymphoproliferative disorders.