MYELOMA VERSUS PLASMABLASTIC LYMPHOMA IN A FRAIL ELDERLY PATIENT: A CASE REPORT OF A DIAGNOSTIC AND THERAPEUTIC CHALLENGE
- 1Instituto de Oncologia Ciências Médicas (IONCM-CMMG), Belo Horizonte, MG, Brazil
- 2Faculdade Ciências Médicas de Minas Gerais (FCM-MG), Belo Horizonte, MG, Brasil, Belo Horizonte, MG, Brazil
Abstract
Background: Plasma cell neoplasms with plasmablastic morphology and plasmablastic lymphoma may show substantial morphologic and immunophenotypic overlap, making their differential diagnosis particularly challenging. This distinction may be even more difficult in elderly patients with limited tolerance to intensive lymphoma-directed therapy, in whom diagnostic uncertainty directly affects therapeutic decision-making. Case report: An 81-year-old man with hypertension and negative HIV serology presented with an infiltrative left lateral chest-wall mass (11.0 × 5.0 × 3.8 cm) with destruction of the fourth costal arch. Biopsy showed a hematolymphoid neoplasm with plasmablastic features. Immunohistochemistry demonstrated CD138+, MUM1+, CD56+, Ki-67 ∼90%, CD20-, CD30-, and HHV-8-. An expanded panel showed CD79a+, PAX5-, ALK-, CD19-, diffuse Kappa with rare Lambda expression, Cyclin D1-, MYC protein-, and CD117+, supporting a clonal plasma cell phenotype. EBER in situ hybridization could not be performed because the assay was not available at the evaluating laboratory. Bone marrow aspirate contained 21.5% atypical plasma cells. Flow cytometry identified 7.41% monoclonal plasma cells (CD45-/CD38++/CD138++/CD56+++/CD117+, Kappa-restricted, CD19/CD20/CD27-). Cytogenetics showed 46,XY[20]. Bone marrow biopsy demonstrated ∼20% plasmacytic infiltration, CD138+/CD79a+/CD117+/CD56+, with a Kappa ratio >10:1. The combination of substantial clonal marrow plasma cell involvement, destructive osseous disease, and plasma cell immunophenotype favored a plasma cell neoplasm with plasmablastic morphology, although PBL could not be definitively excluded. Given the patient’s advanced age, ECOG 3, comorbidities, and limited tolerance to intensive lymphoma-directed therapy, CODOX-IVAC, dose-adjusted EPOCH, and HyperCVAD were considered unsuitable. After multidisciplinary discussion, bortezomib, thalidomide, and dexamethasone were initiated with radiotherapy to the symptomatic lesion. Discussion: Plasmablastic myeloma and PBL may both show plasmablastic morphology, loss of mature B-cell markers, plasma cell-associated antigens, high proliferative activity, and light-chain restriction. In this case, Kappa restriction established clonality but was not independently discriminatory, and a normal conventional karyotype did not resolve the diagnosis. EBER status could not be assessed because of local laboratory unavailability, representing an additional limitation in the differential diagnosis. Conversely, significant clonal marrow plasma cell infiltration together with destructive bone involvement favored a plasma cell neoplasm. Conclusion: Distinguishing plasmablastic myeloma from PBL may remain challenging despite extensive morphologic, immunophenotypic, and marrow evaluation. Here, the overall clinicopathologic findings favored a plasma cell neoplasm with plasmablastic morphology, while PBL could not be fully excluded. A bortezomib-based regimen plus local radiotherapy was therefore selected as an individualized, tolerability-driven strategy primarily directed toward a plasma cell neoplasm while retaining potential activity against a plasmablastic lymphoma phenotype.
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BibTeX
@article{anastacio2026myeloma,
title = {{MYELOMA VERSUS PLASMABLASTIC LYMPHOMA IN A FRAIL ELDERLY PATIENT: A CASE REPORT OF A DIAGNOSTIC AND THERAPEUTIC CHALLENGE}},
author = {Lucas de Barros ANASTÁCIO and Pedro Henrique Rodrigues VIANA and Marcia Torresan DELAMAIN},
journal = {Hematology, Transfusion and Cell Therapy},
year = {2026},
month = oct,
doi = {10.1016/j.htct.2026.107903},
url = {https://doi.org/10.1016/j.htct.2026.107903},
note = {CC BY},
}
RIS
TY - JOUR
TI - MYELOMA VERSUS PLASMABLASTIC LYMPHOMA IN A FRAIL ELDERLY PATIENT: A CASE REPORT OF A DIAGNOSTIC AND THERAPEUTIC CHALLENGE
AU - Lucas de Barros ANASTÁCIO
AU - Pedro Henrique Rodrigues VIANA
AU - Marcia Torresan DELAMAIN
PY - 2026
DA - 2026/10/23
JO - Hematology, Transfusion and Cell Therapy
DO - 10.1016/j.htct.2026.107903
UR - https://doi.org/10.1016/j.htct.2026.107903
AB - Background: Plasma cell neoplasms with plasmablastic morphology and plasmablastic lymphoma may show substantial morphologic and immunophenotypic overlap, making their differential diagnosis particularly challenging. This distinction may be even more difficult in elderly patients with limited tolerance to intensive lymphoma-directed therapy, in whom diagnostic uncertainty directly affects therapeutic decision-making. Case report: An 81-year-old man with hypertension and negative HIV serology presented with an infiltrative left lateral chest-wall mass (11.0 × 5.0 × 3.8 cm) with destruction of the fourth costal arch. Biopsy showed a hematolymphoid neoplasm with plasmablastic features. Immunohistochemistry demonstrated CD138+, MUM1+, CD56+, Ki-67 ∼90%, CD20-, CD30-, and HHV-8-. An expanded panel showed CD79a+, PAX5-, ALK-, CD19-, diffuse Kappa with rare Lambda expression, Cyclin D1-, MYC protein-, and CD117+, supporting a clonal plasma cell phenotype. EBER in situ hybridization could not be performed because the assay was not available at the evaluating laboratory. Bone marrow aspirate contained 21.5% atypical plasma cells. Flow cytometry identified 7.41% monoclonal plasma cells (CD45-/CD38++/CD138++/CD56+++/CD117+, Kappa-restricted, CD19/CD20/CD27-). Cytogenetics showed 46,XY[20]. Bone marrow biopsy demonstrated ∼20% plasmacytic infiltration, CD138+/CD79a+/CD117+/CD56+, with a Kappa ratio >10:1. The combination of substantial clonal marrow plasma cell involvement, destructive osseous disease, and plasma cell immunophenotype favored a plasma cell neoplasm with plasmablastic morphology, although PBL could not be definitively excluded. Given the patient’s advanced age, ECOG 3, comorbidities, and limited tolerance to intensive lymphoma-directed therapy, CODOX-IVAC, dose-adjusted EPOCH, and HyperCVAD were considered unsuitable. After multidisciplinary discussion, bortezomib, thalidomide, and dexamethasone were initiated with radiotherapy to the symptomatic lesion. Discussion: Plasmablastic myeloma and PBL may both show plasmablastic morphology, loss of mature B-cell markers, plasma cell-associated antigens, high proliferative activity, and light-chain restriction. In this case, Kappa restriction established clonality but was not independently discriminatory, and a normal conventional karyotype did not resolve the diagnosis. EBER status could not be assessed because of local laboratory unavailability, representing an additional limitation in the differential diagnosis. Conversely, significant clonal marrow plasma cell infiltration together with destructive bone involvement favored a plasma cell neoplasm. Conclusion: Distinguishing plasmablastic myeloma from PBL may remain challenging despite extensive morphologic, immunophenotypic, and marrow evaluation. Here, the overall clinicopathologic findings favored a plasma cell neoplasm with plasmablastic morphology, while PBL could not be fully excluded. A bortezomib-based regimen plus local radiotherapy was therefore selected as an individualized, tolerability-driven strategy primarily directed toward a plasma cell neoplasm while retaining potential activity against a plasmablastic lymphoma phenotype.
SN - 2531-1379
SN - 2531-1387
ER -