Plasmablastic transformation of plasma cell myeloma with heterotropic expression of CD3 and CD4: a case report

Abstract

Plasmablastic lymphoma (PBL) can rarely be seen as a transformation from plasma cell myeloma (PCM), especially in late stages of the disease where it portends a poorer prognosis and a different line of management for the patient. When unrelated to PCM, PBL is considered to be a separate aggressive variant of B-cell lymphoma typically seen in the oral cavity of immunocompromised adults. We describe a case of plasmablastic transformation having a pan T-cell phenotype with CD3 and CD4 positivity, in an immunocompetent elderly lady diagnosed with PCM. This 60-year-old lady presented with worsening backache and a 2-cm skin nodule in the left cervical region, while she was on treatment with vincristine, cyclophosphamide, dexamethasone (VCD), and bortezomib. On biopsy, the skin nodule showed an infiltrating lymphoid tumor composed of immunoblastic cells with brisk mitosis and apoptosis. On Immunohistochemistry (IHC), lymphoid cells revealed plasma cell markers CD38, CD138, CD56, and MUM1. Pan-T-cell markers CD3 and CD4 were also diffusely expressed in tumor cells. B-cell markers CD20 and PAX5 were not expressed; c-Myc IHC and EBER by in situ hybridization (ISH) were negative in the tumor. Mitotic index by Ki67 was >95%. Thus, a diagnosis of plasmablastic transformation in a known PCM case was made. This is the first case, to the best of our knowledge, with a heterotropic T-cell phenotype in a plasmablastic transformation from PCM. It is critical to correctly diagnose such cases as they may occasionally be misinterpreted as T-cell neoplasms. Clinically, a more aggressive treatment is indicated for such patients. Further studies in these cases may enhance our understanding of complex underpinnings of lymphoma biology.

Keywords:

• Plasmablastic lymphoma
• Plasma cell myeloma
• Heterotropic T-cell phenotype

Acknowledgements

The authors deeply appreciate Mrs Uma and Mrs Janet from immunohistochemistry section of the Dept of Pathology, TMC, for their excellent technical support. Our deep gratitude is also due to Dr Hari Menon for his invaluable clinical insights into the case. We would also like to appreciate the contributions of Mr Sandeep, Mr Vinayak, and Ms Sonali for carrying out the in situ hybridization test. The support for molecular study would not have been possible without the help of Dr Omshree Shetty and Dr Trupti Pai from Molecular Diagnostic Laboratory of this hospital.