Posttransplant lymphoproliferative disorders following hematopoietic stem cell transplantation: a clinicopathological study of a large single-center cohort.
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Posttransplant lymphoproliferative disorder (PTLD) is a serious complication of hematopoietic stem cell transplantation (HSCT) and is typically driven by immunosuppression and Epstein-Barr virus infection. This study analyzed the clinicopathological spectrum and outcomes of PTLD in a large single-center cohort. We retrospectively reviewed 37 PTLD patients who were diagnosed post-HSCT (2017-2024). Histopathological classification was conducted in accordance with the 5th Edition of the World Health Organization Classification of Hematolymphoid Tumors (WHO-HAEM5). Immunohistochemistry, EBV-encoded RNA in situ hybridization, fluorescence in situ hybridization, and clonality assays were performed. Clinical data, treatment responses, and survival outcomes were collected and analyzed. The PTLD incidence was 2.4% among allo-HSCT recipients, with a male predominance (2.36:1). The median time to onset post-HSCT was 3 months (range: 1-21 months), with 81.1% of cases occurring within 6 months. The pathological types of PTLD included hyperplasias (9 cases), polymorphic PTLD (20 cases), and lymphoma (8 cases; all diffuse large B-cell lymphomas). First-line management include reduced immunosuppression, rituximab, and antiviral therapy. Prebiopsy rituximab in 5 patients caused CD20 loss, complicating the diagnosis. The mortality rate was 27%, primarily from infectious complications following PTLD-directed therapy. The median postdiagnosis survival was 3.5 months. PTLD post-HSCT is a serious complication that often follows an aggressive clinical course. While the direct contribution of PTLD to mortality was challenging to establish, its development frequently triggered intensive interventions (e.g., rituximab and immunosuppression reduction), which in turn led to fatal infectious complications in more than one-quarter of our cohort. Therefore, the high mortality in these patients was largely indirect and attributable to treatment-related infectious complications in profoundly immunocompromised hosts.