Presentation Details
| Risk of Thrombosis in SGLT2 Inhibitor-Associated Erythrocytosis: A Multi-Center Propensity-Matched Analysis Meric Mericliler1, 2. 1Division of Hematology and Medical Oncology, Virginia Commonwealth University Health, Richmond, VA, USA.2Massey Cancer Center, Richmond, VA, USA |
Abstract
Background: Sodium-glucose cotransporter-2 inhibitors (SGLT2is) are increasingly utilized due to their cardiovascular and renoprotective benefits. These medications have been associated with erythrocytosis. The relationship between thrombotic risk and SGLT2i-associated erythrocytosis remains unknown. To date, no large-scale comparative studies have investigated the thrombotic outcomes in patients with SGLT2i-associated erythrocytosis. Objectives: The primary objective of this study was to investigate the risk of thrombotic outcomes in patients with SGLT2 inhibitor-associated erythrocytosis. Methods: Retrospective data of patients who developed erythrocytosis and those who did not within one month to one year following initiation of FDA-approved SGLT2is were retrieved from the TriNetX database. Erythrocytosis was defined by hemoglobin/hematocrit levels exceeding 16.5 g/dL/49% in males and 16 g/dL/48% in females. Patients with JAK2 mutations, including V617F and exon 12, were excluded. Patients were stratified based on gender. Propensity score matching (PSM) at a 1:1 ratio was performed to balance baseline characteristics. Patients were matched for age, race, and relevant comorbidities. The 1-year incidence of the following outcomes was assessed both before and after propensity score matching: venous thromboembolism, acute coronary syndrome (ACS), ischemic cerebrovascular disease (ICD) including transient ischemic attack and ischemic stroke, composite arterial events (ACS, ICD, and arterial embolism), composite thrombotic events (arterial and venous thrombosis), and mortality. Results: Patients with SGLT2i-associated erythrocytosis had significantly higher hemoglobin (16.2 ± 1.5 g/dL vs. 12.2 ± 2.1 in females; 16.9 ± 1.1 vs. 13.3 ± 2.4 in males) and hematocrit (49.3% ± 4.6 vs. 37.4% ± 6.9 in females; 50.9% ± 3.4 vs. 39.8% ± 7.9 in males) levels compared to controls. The majority of baseline comorbidities were more prevalent in patients with SGLT2i-associated erythrocytosis than in those who did not develop erythrocytosis after SGLT2-inhibitor treatment. Significant differences in race and age were also observed. After PSM, the differences in demographic characteristics and comorbidities were more balanced (Table 1). Before PSM, patients with SGLT2i-associated erythrocytosis, regardless of gender, had a significantly higher incidence of venous thromboembolism, acute coronary syndrome, ischemic cerebrovascular disease, composite arterial events, composite thrombotic events, and mortality (Table 2). Post-PSM analysis showed that patients with SGLT2i-associated erythrocytosis had a higher incidence of venous thromboembolism, composite arterial events, and composite thrombotic events. The incidence of acute coronary syndrome was similar between the groups in both the male and female cohorts. While males with SGLT2i-associated erythrocytosis had a higher incidence of ischemic cerebrovascular disease, this difference was not statistically significant in females. The post-PSM analysis showed no statistically significant differences in mortality rates (Table 3). Conclusions: The findings of this comparative study indicate an increased incidence of thrombotic events in patients with SGLT2i-associated erythrocytosis compared to those who do not develop erythrocytosis following treatment with SGLT2is. Similar results were observed even after propensity matching and controlling for relevant comorbidities. The limitations of this study include the use of retrospective aggregated patient data and reliance on diagnostic codes.
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No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.