PB0362 - Coagulation monitoring on treatment with Inotuzumab Ozogamicin in children with relapsed/refractory B-cell precursor acute lymphoblastic leukemia

Sunday, June 23, 2024

13:45 – 14:45 ICT

Room: Exhibition Hall

Co-Author(s)

DE

Dmitrii Evstratov

PhD, Hematologist
Dmitry Rogachev National Medical Research Center Of Pediatric Hematology, Oncology and Immunology
Moscow, Moskva, Russia

Presenting Author(s)

Elena A. Seregina, PhD

Leading Researcher
Dmitry Rogachev National Medical Research Centеr of Pediatric Hematology, Oncology and Immunology
Moscow, Moskva, Russia

Co-Author(s)

ES

Ekaterina Sitnova

Resident
Dmitry Rogachev National Medical Research Center Of Pediatric Hematology, Oncology and Immunology
Moscow, Moskva, Russia
LV

Ludmila Vavilova

Hematologist
Dmitry Rogachev National Medical Research Center Of Pediatric Hematology, Oncology and Immunology
Moscow, Moskva, Russia
NM

Natalia Myakova

MD Prof. Oncohematology Dpt.
Dmitry Rogachev National Medical Research Center Of Pediatric Hematology, Oncology and Immunology
Moscow, Moskva, Russia
PZ

Pavel Zharkov

Doctor of Science, Head of Hemostasis Pathology Unit
Dmitry Rogachev National Medical Research Center Of Pediatric Hematology, Oncology and Immunology
Moscow, Moskva, Russia

Background: Inotuzumab ozogamicin (InO) is an anti-CD22 bispecific antibody conjugated with the cytotoxic agent calicheamicin. It is associated with the increased risk of Veno-Occlusive Disease.

Aims: Evaluation of hemostatic changes on treatment with InO.

Methods: Patients < 18 years, treated with InO (0.8 mg/m2 1 day, 0.5 mg/m2 8 and 15 days) were prospectively included in our study. Coagulation monitoring included activated partial thromboplastin time, prothrombin Quick, fibrinogen, thrombin time, D-dimer, antithrombin III, protein S, Protein C, von Willebrand factor (VWF) activity and antigen (VWF:AG). Time points of monitoring were before the first InO dose (“0”), before the second (“1”), before the third (“2”) and a week after the third dose (“3”). Comparison of numerical variables was performed with Wilcoxon test. P-value < 0.05 was considered as significant.

Results: 18 patients were included in our study. In one patient therapy was withdrawn after the first infusion of InO due to hepatic toxicity.
There were no significant differences in values of activated partial thromboplastin time, prothrombin Quick, fibrinogen, thrombin time, D-dimer, antithrombin III, protein S, protein C, VWF activity in time point “0” compared with “1”, “2” and “3”.
Median value of VWF:AG in points “0”, “1”, “2” and “3” was 155% (IQR: 123-230%), 197,5% (IQR: 144.6-243.8%), 227.9% (IQR: 186-244.3%), 225.1% (IQR: 175.3-236.7%), respectively. In 3 patients value of VWF:AG in point “3” was not available. Value in point “2” in these patients and in point “1” in patient with interrupted therapy was considered as the value after the end of therapy. Mean value of VWF:AG before treatment (169.1±68.4%) was significantly lower than after the end of therapy (234±98.9%), p=0.002.

Conclusion(s): In our study value of VWF:AG increased on treatment with InO, possibly due to endothelial activation.