[CD19 CAR-T treatment for B-lymphoblastic lymphoma complicated with disseminated intravascular coagulation: a case report and literature review]
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Updated: May 24, 2025

A Syngeneic Mouse B-Cell Lymphoma Model for Pre-Clinical Evaluation of CD19 CAR T Cells
Published on: October 16, 2018
1Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China Hubei Clinical and Research Centre of Thrombosis and Hemostasis, Wuhan 430022, China.
Abstract:
Objective: To explore the clinical manifestations, pathogenesis, and therapeutic approaches of disseminated intravascular coagulation (DIC) associated with chimeric antigen receptor T-cell (CAR-T) therapy for B-lymphoblastic lymphoma. Methods: Retrospective collection and analysis were conducted on the clinical data of a patient with B-lymphoblastic lymphoma who received CAR-T therapy in the Hematology Department of Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, in April 2020. To review the literatures, Chinese databases (CNKI, Wanfang Database) and PubMed were searched form database inception up to November 2024 using the retrieval entries "chimeric antigen receptor T-cell therapy", "CAR-T", "coagulation", "bleeding", and "thrombosis" . Results: The patient, a 32-year-old male, diagnosed with B-lymphoblastic lymphoma for over 10 months, relapsed after three cycles of chemotherapy and allogeneic hematopoietic stem cell transplantation, with bone marrow cytology indicating 20.24% abnormal phenotype B-lineage precursor cells. After CAR-T cell infusion at a dose of 4×10(6)/kg, the patient developed grade 2 cytokine release syndrome (CRS) on day 2, nasal bleeding on day 4, high fever again on day 9, with worsening coagulation parameters, DIC and persistent hypofibrinogenemia. After treatment with tocilizumab, corticosteroids to counteract CRS, and active replacement therapy such as administration of blood product and fibrinogen, the patient's CRS and coagulation abnormalities gradually improved. The patient was followed up for 16 months regularly after CAR-T therapy, with CAR-T cells sustained and minimal residual disease remained negative as assessed by bone marrow flow cytometry. Subsequently, the patient stopped taking oral immunosuppressants on his own, which aggravated rejection reaction complicated with infection. The patient and his family requested to be discharged and lost the follow-up. A total of 20 relevant English articles and 6 Chinese articles were retrieved from the literature search. Conclusion: CAR-T-associated coagulopathy occurs alongside CRS. It is characterized by hypofibrinogenemia, and is life-threatening when progressing to DIC. Anti-CRS and replacement therapies have proven to be effective treatment strategies.
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