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Presentation Details
Cytokine Release Syndrome and Thrombosis Risk after CAR-T Therapy

Courtney Crawford1, Parmis Sahrapima1, Joseph Shatzel2, 3, Corinne Lavasseur2, 3.

1Department of Internal Medicine, Oregon Health and Sciences University, Portland, OR, USA, Portland, OR, USA.2Division of Hematology and Medical Oncology, Oregon Health and Sciences University, Portland, OR, USA, Portland, OR, USA.3Knight Cancer Institute, Portland, OR, USA

Abstract


Background: Cytokine release syndrome (CRS) is a systemic inflammatory response triggered by infections and certain medical treatments, most notably chimeric antigen receptor (CAR) T-cell therapy. Thrombotic complications are common in severe inflammatory states and are increasingly recognized after CAR-T therapy, with reported rates of 6-10%; however, the extent to which CRS contributes to thrombotic risk after CAR-T remains poorly defined.   Objectives: The aim of this study is to characterize the incidence and risk of thrombosis in patients who develop CRS after CAR-T therapy.  Methods: We are conducting a large retrospective cohort study comparing thrombotic events in CAR-T patients who do and do not develop CRS. The is an ongoing study involving individualized chart review of 350-400 patients treated at Oregon Health & Science University from 2017-2025. The primary clinical outcome is venous or arterial thrombotic event within 90 days of CAR-T administration, identified through longitudinal follow-up. We are collecting data on patient demographics, hematologic malignancy, CAR-T product, antithrombotic and antiplatelet use, immune effector cell-associated neurotoxicity syndrome (ICANS) incidence and grade, and established thrombotic risk factors (infection history, body mass index, and concurrent malignancies), and all-cause mortality. Results: To date, we have reviewed 100 charts, and patient characteristics are shown in Table 1. Eighty of 100 patients developed CRS with a median time to onset of 4 days. In the CRS group, 11 patients experienced a thrombotic event within 90 days of CAR-T, whereas no thrombotic events occurred in those without CRS (p=0.086). Among the other variables collected, infection within 90 days of CAR-T therapy administration was associated with an increased thrombotic risk in the preliminary analysis. Twenty patients developed an infection after CAR-T therapy and of whom 7 experienced a thrombotic event (p<0.001).  Conclusions: Preliminary findings have demonstrated an increased absolute rate of thrombosis in patients who develop CRS after CAR-T therapy. Completion of the 350-400 patient cohort analysis will allow for more definitive estimates of thrombosis risk associated with CRS after CAR-T therapy. 

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