Abstract 392: Recurrent ischemic strokes in a patient with ITP, case report and literature review

Introduction/Purpose Immune Thrombocytopenic purpura (ITP) is an autoimmune acquired thrombocytopenia caused by autoantibodies against platelet antigens leading to platelet destruction and platelet underproduction. Patients with ITP usually have a higher risk of bleeding compared to the general population, however thrombocytopenia in ITP is not necessarily protective against thrombosis. While the exact pathophysiology of hypercoagulability in ITP is still not fully understood and not enough data in literature guiding stroke management in patients with ITP as the primary stroke risk factor, there are multiple etiologies suggested including inflammation, antiphospholipid antibodies in some patients, or the effects of certain treatments such as glucocorticoids and Thrombopoietin receptor agonists (TPO‐RAs) Methods A single case report, literature review through PubMed Results A 65‐year‐old male with a history of unprovoked deep vein thrombosis (DVT) and pulmonary embolism (PE) while on Rivaroxaban presented with worsening headaches and cognitive dysfunction. A CT scan of the head revealed bilateral subacute frontal lobe infarcts with an embolic appearance. Initial laboratory tests showed thrombocytopenia (54,000), and a hypercoagulable workup, including tests for anticardiolipin antibodies, antiphospholipid antibodies, beta‐2 glycoprotein antibodies, factor V Leiden mutation, and Prothrombin gene mutation, returned negative. A bone marrow biopsy revealed immature megakaryocytes without morphological abnormalities. Transthoracic and transesophageal echocardiograms did not show any intracardiac or intrapulmonary shunts, and telemetry monitoring did not detect any arrhythmias. The patient was switched from Rivaroxaban to Warfarin, with an INR target of 2.0‐3.0, and was started on glucocorticoids and Rituximab. Follow‐up showed an improvement in platelet count. Eight months after discharge, the patient experienced a new right pontine infarct; at that time, his INR was 2.34, and a repeat stroke workup was inconclusive. The Warfarin dose was adjusted to achieve an INR target of 2.5‐3.5. Over a subsequent 4‐year follow‐up period, the patient did not experience any additional strokes. Conclusion Patients with immune thrombocytopenic purpura (ITP) face an increased risk of stroke, often of cryptogenic origin. While thrombocytopenia in ITP is not protective against thrombosis, it certainly increases the risk of bleeding in individuals on anticoagulant therapy, making management more complex. Further research is needed to develop guidelines for managing stroke in ITP patients particularly who lack conventional stroke risk factors Additionally, the potential role of anti‐inflammatory agents, such as glucocorticoids, in reducing stroke risk in this population warrants investigation.