Coexistence of Trisomy 8 and 13 in a Newly Diagnosed Patient with Diffuse Large B Cell Non-Hodgkin's Malignant Lymphoma and Acute Myeloblastic Leukemia Secondary to Primary Myelofibrosis

Bumbea H1,2, Popov VM3*, Tomuleasa C4,5, Omer M3, Dobrea C1, Manea I6, Zurac S1,7, Popp C7, Dumitru I2, Simoiu M8 and Mastalier B1,9

1Department of Medicine, UMF Carol Davila, 020021 Bucharest, Romania 2Department of Hematology, Emergency University Hospital, 050098 Bucharest, Romania 3Department of Hematology, Colentina Clinical Hospital, 020125 Bucharest, Romania 4Department of Medicine, UMF Iuliu Hatieganu, 400012 Cluj Napoca, Romania 5Department of Hematology, IOCN Chiricuta, 400015 Cluj Napoca, Romania 6Department of Nuclear Medicine, Colentina Clinical Hospital, 020125 Bucharest, Romania 7Department of Morphopathology, Colentina Clinical Hospital, 020125 Bucharest, Romania 8Department of Infectious Disease, M Bals Institute, 021105 Bucharest, Romania 9Department of Surgery, Colentina Clinical Hospital, 020125 Bucharest, Romania

^*Correspondance to: Popov VM 

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Abstract:

Background: Concomitant diagnosis of Non-Hodgkin lymphoma (NHL) and acute myeloid leukemia secondary chronic Myeloproliferative Neoplasms (MPNs) is rarely reported. Patients with MPNs may have a second neoplasm; the risk of lymphoid line neoplasms is 2.5 to 3.5 times. The explanation for this association is the genetic instability of hematopoietic progenitors in MPNs. Case Report: Patient man 80 years old, Caucasian, known with much comorbidity, presents for physical asthenia, sweating, and right inguinal adenopathy with a diameter of 5 cm to 6 cm, partial mobility, and pain (appearing 1 month before the examination). The patient was diagnosed concomitantly with DLBCL and AML secondary to Primary Myelofibrosis (PMF) and presented a complex karyotype - trisomy 8 and 13 and triple-negative PMF status. The patient initially received 2 well-tolerated R mini CHOP series, this type of treatment was selected to treat DLBCL for one unfit patient for intensive chemotherapy due to his age and comorbidities. R mini CHOP administration was followed by severe aplasia that lasted approximately 2 weeks followed by severe thrombocytosis that reached 4000 x 109/L and thromboreductin recommendation was mandatory. The result of the treatment was a partial response but with severe adverse events neutropenia G4, due to the delay of the treatment the patient lost the response. It was mandatory to select another treatment line and the chosen was Venetoclax, it was selected for the simultaneous treatment of DLBCL and the underlying AML. It was obtained a significant reduction in the size of the inguinal lymph node block in 2 weeks of the treatment. Severe neutropenia was diagnosed and complicated with sepsis. The evolution is unfavorable with the installation of multiple organ dysfunctions. Conclusion: The presence of a complex karyotype (trisomy 8, trisomy 13) in a patient with myeloid metaplasia with triple-negative PMF was associated with blast transformation and severe thrombocytosis. The patient was diagnosed concomitantly with DLBCL, making the therapeutic decision difficult. Venetoclax has been shown to be useful in the treatment of DLBCL but has been associated with severe neutropenia, which has led to infectious complications.

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Cite the Article:

Bumbea H, Popov VM, Tomuleasa C, Omer M, Dobrea C, Manea I, et al. Coexistence of Trisomy 8 and 13 in a Newly Diagnosed Patient with Diffuse Large B Cell Non-Hodgkin's Malignant Lymphoma and Acute Myeloblastic Leukemia Secondary to Primary Myelofibrosis. Ann Clin Case Rep. 2022; 7: 2123.