Pityriasis lichenoides-like drug reaction: A clinical histopathologic study of 10 cases

Abstract

Figure 3. A) Phenotypic studies highlighting the infiltrate by the CD3 pan T-cell marker (200%). There is a predominance of B) CD8, (200%), to C) CD4, (200%). D) There is a marked reduction in the expression of CD7 (200%).

Pityriasis lichenoides chronica in a patient on tafasitamab and lenalidomide therapy for diffuse large B-cell lymphoma

“…A clinical histopathologic study that reviewed 10 cases of pityriasis lichenoides-like drug reaction reported a paucity of inflammatory cells, with eosinophils noted in 1 case. 4 The histopathologic findings in our case align with the histologic characteristics of drug- and chemo-induced PLC, showing infiltration of lymphocytes in the papillary dermis and interface dermatitis with apoptotic parakeratosis, and a lack of eosinophils.…”

“… 5 One case report presents the case of an 83-year-old woman who developed PLC after receiving an anti-CCR4 monoclonal antibody. 4 Similar to our patient, she experienced symptoms months after initiating tafasitamab/lenalidomide therapy and her symptoms were exacerbated with each infusion.…”

“…1 More rarely, PLC may be seen as a paraneoplastic phenomenon or a reaction to a medication. 3 , 4 Some researchers label PLC as a lymphoproliferative disorder given that these patients have demonstrated T-cell clonality, but this is highly debated in the literature. 1 , 2 , 5 Herein, we present a case of PLC in a patient with diffuse large B-cell lymphoma (DLBCL) who developed a rash after initiating tafasitamab/lenalidomide therapy.…”

Pityriasis lichenoides et varioliformis acuta in a patient treated with cevostamab

“…On histopathology, PLEVA demonstrates a T-cell dominant infiltrate, 4 and a dominant T-cell clone has been found in a majority of cases. 3 Magro et al 5 argued that PLEVA and PLC represent a form of T-cell dyscrasia based on the reduced expression of CD7 and CD62L, along with the presence of clonality. They also cited cases which evolved into mycosis fungoides as evidence of an underlying T-cell process.…”

Utility of IL‐36 immunostaining in distinguishing psoriasis from pityriasis rosea and pityriasis lichenoides

“…17 The etiology of PL remains unclear, though several hypotheses exist in the literature, including an inflammatory response to infection, an immune-complex mediated hypersensitivity vasculitis, and an indolent T-cell lymphoproliferative disorder that can show T-cell monoclonality. [18][19][20][21][22][23][24][25][26][27] In any case, IL-36 does not appear to be a significant driver of inflammation in most cases of this disease.…”