Drug-induced reversible lymphoid dyscrasia: A clonal lymphomatoid dermatitis of memory and activated T cells
Certain systemic conditions predispose patients to excessive lymphocyte responses to immune-perturbing drugs, which may progress to malignant lymphoma. Many pathologists and clinicians believe that differentiation of pseudolymphoma from cutaneous T cell lymphoma (CTCL) can be reliably made through phenotypic and molecular analysis. We encountered 15 cases of atypical cutaneous T-cell lymphoid hyperplasia in the setting of drug therapy. We explored phenotypic anomalies using antibodies to CD2, 3, 4, 7, 8, 20, 30 and CD62 K and sought T-cell receptor gene rearrangements by a polymerase chain reaction methodology. The lymphoid infiltrates showed reproducible CD7 and/or CD62 K deletion in concert with T cell clonality and variable CD30 positivity-findings similar to those of CTCL-but the rashes resolved or improved substantially after drug modulation. We hypothesize that the infiltrates represent an unrepressed expansion of CD7- and CD62 K-negative activated memory T lymphocytes in response to antigenic triggers. We propose the term "drug-induced reversible lymphoid dyscrasia" to describe this entity.