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We present a case of a 61-year-old woman with relapse/refractory multiple myeloma post-autologous peripheral blood stem cell transplantation who presented with recurrent febrile episodes and infection. Worsening thrombocytopenia during lenalidomide-based therapy for early biochemical relapse warranted further investigations. Even though it was initially attributed to lenalidomide and relapse/refractory multiple myeloma, there was not much improvement in her counts despite adjustment of her medications. Subsequent serial bone marrow results and cytogenetic evolution eventually revealed therapy-related myelodysplastic syndrome progressing to therapy-related acute myeloid leukemia. In view of her age and comorbidities, she was treated with subcutaneous azacytidine with palliative intent which resulted in transient disappearance of blasts in the peripheral blood. She subsequently succumbed to progressive therapy-related acute myeloid leukemia and relapse/refractory multiple myeloma. This case highlights the complexity in diagnosing therapy-related myelodysplastic syndrome earlier as prompt diagnosis is crucial in delaying its progression to therapy-related acute myeloid leukemia. Managing therapy-related acute myeloid leukemia in the setting of relapse/refractory multiple myeloma post-autologous peripheral blood stem cell transplantation is challenging in terms of balancing the treatment toxicity and providing the best possible quality of life.

Diffuse large B-cell lymphoma (DLBCL) is a type of non-Hodgkin Lymphoma commonly presenting as a solid tumor either by nodal or extra-nodal manifestations. Here we describe two atypical presentations of lymphoma, finally resulting in the diagnosis of DLBCL. Case 1: A 53-year-old man with a previous history of nasopharyngeal carcinoma presented with a two-week history of B-symptoms and hyperleukocytosis. Peripheral blood film showed 78% abnormal mononuclear cells. Immunohistochemical stain showing Ki-67 of 90%, negative c-myc, BCL2 and BCL6, and negative c-MYC with fluorescence in-situ hybridization studies on the trephine biopsy, concluded the diagnosis of CD5+ DLBCL of ABC subtype. He received intravenous cyclophosphamide and oral prednisolone for cytoreduction, followed by 6 cycles of chemo-immunotherapy. However, he succumbed due to severe sepsis after the completion of therapy. Case 2: A 56-year-old lady who was initially investigated for pyrexia of unknown origin was noted to have hemophagocytosis upon bone marrow aspirate examination. The bone marrow trephine biopsy revealed some atypical clusters of B-cells positive for CD20 which was inconclusive. PET-CT scan noted an enlarged hypermetabolic spleen without lymphadenopathy. Splenic biopsy with immunohistochemical studies revealed DLBCL of ABC subtype. The diagnosis was consistent with primary splenic DLBCL. She became unwell post splenic biopsy and was admitted to the intensive care unit where she passed away 2 weeks later from Candida and Sternotrophomonas septicemia. These cases highlight the atypical presentations of a common subtype of NHL in our center. Arriving at the definitive diagnosis can be difficult especially when patients are acutely ill, hampering the necessary invasive procedures for diagnosis. The outcomes of both cases are briefly discussed hoping to spread awareness among clinicians on the rare and acutely critical presentations of DLBCL.