• PDF / 152,875 Bytes
• 1 Pages / 595.245 x 841.846 pts (A4) Page_size
• 74 Downloads / 157 Views

DOWNLOAD

REPORT

---

1 S

Cytokine release syndrome: case report In a trial (NCT02735291), a 34-year-old man developed cytokine release syndrome (CRS) during with anti-cd19-transduced-tcells for relapsed/refractory acute B-cell lymphoblastic leukaemia (B-ALL). The man, who was diagnosed with chronic myeloid leukaemia (CML) for 1 year and acute lymphoblastic lesion for 8 months admitted for the CAR-T therapy due to relapse for 2 months. In January 2017, he visited an external hospital for treatment of splenauxe and subsequently, he was diagnosed with CML. After the confirmed diagnosis, he had received imatinib, and the results of subsequent regular blood routine re-examinations were normal. In May 2017, WBC increased again. A further morphological examination of bone marrow cells showed CML with acute lymphoblastic lesion. Subsequently, fusion gene detection revealed BCR-ABL p210/ABL 25.67%; drug resistance gene detection revealed the existence of E355G mutation. He was diagnosed with relapsed and refractory B-ALL. Therefore, imatinib was replaced by dasatinib. At the same time, complete remission (CR) was achieved after induction chemotherapy with IVLP, which included idarubicin, vindesine, pegaspargase and dexamethasone. Later, dasatinib was continued and he was sequentially given the IVP regimen including idarubicin, vindesine and dexamethasone, CAM regimen including cyclophosphamide, cytarabine, mercaptopurine [6- purinethol] and methotrexate and pegaspargase. In December 2017, his WBC count increased again. Bone marrow cell morphology revealed acute leukaemia myelogram. Fusion gene detection revealed BCR-ABL p210/ABL 5.70%; drug resistance gene detection revealed the existence of T315I mutation, with no E355G mutation detected. Considering the relapse of primary disease, his dasatinib therapy was stopped and he was given the IVP regimen, which included idarubicin, vindesine and dexamethasone for another induction chemotherapy but this time he did not achieve remission. In January 2018, he admitted for the anti-cd19-transduced-t-cells [CAR-T therapy]. After admission, 100mL of peripheral blood was collected, and anti-cd19-transduced-t-cells was amplified and cultured by separation and transfection in vitro. Before the back-transfusion, he received fludarabine from day 1 to day 3 and cyclophosphamide from day 1 to day 3 as pretreatment. After an interval of 2 days, 100 mL of the third-generation anti-cd19-transduced-t-cells was transfused back on 05 February 2018. From day 3 of anti-cd19-transduced-t-cells infusion, he developed intermittent fever, which was generally in the afternoon or at night with a body temperature of 38.5–40.0°C. The body temperature normalized on day 10 after unspecified symptomatic treatment. On Day 3 after anti-cd19-transduced-t-cells infusion, the re-examinations of both interleukin (IL)-6 and ferritin revealed a significant elevation. On day 10 after the back transfusion, IL-6 normalised but ferritin still remained at a high level. He developed grade 1 CRS as adverse reaction secondary to anti-cd19-transdu