Track: Case Reports

Abstract:

A 54-year-old male with a 10-year history of pruritic red plaques and scales on the trunk and extremities, previously diagnosed with psoriasis without biopsy, received topical corticosteroids and traditional Chinese medicine with limited improvement. One year ago, secukinumab was initiated, partially relieving symptoms. Six months ago, scalp and facial nodules developed with progressive cervical, axillary, and inguinal lymphadenopathy. Biopsy of a scalp nodule showed nodular dermal and subcutaneous lymphohistiocytic infiltrates with epidermotropic mononuclear cells. Immunohistochemistry revealed CD3+, CD4+, CD30+, Ki-67 80%, and positive T-cell receptor gene rearrangement. Trunk plaques had similar features but were CD30- with Ki-67 30%. PET-CT demonstrated hypermetabolic lymphadenopathy; laboratory results included elevated LDH (582 U/L) and β2-microglobulin (17.3 mg/L), with peripheral blood flow cytometry and bone marrow negative for involvement. Folliculotropic mycosis fungoides was diagnosed. Brentuximab vedotin plus gemcitabine induced marked tumor reduction for 3 months before progression; the patient died 6 months later. IL-17 inhibitors, especially secukinumab, have rarely been linked to cutaneous T-cell lymphoma (CTCL). Proposed mechanisms include disruption of IL-17-mediated anti-tumor immunity, imbalance of Th17/Treg and Th1/Th2 responses, and compensatory increases in IL-23 and IL-17F, which may promote tumor progression through angiogenesis, reduced cytotoxic T-cell infiltration, and enhanced tumor survival. This case highlights the need for vigilance and prompt biopsy of atypical or progressive skin lesions in patients receiving IL-17 inhibitors.