SUN-875 - Graves' Disease as A Reversible Cause of Unprovoked Pulmonary Embolism: Implications for Anticoagulation Duration

Background:
Pulmonary embolism (PE) is commonly associated with identifiable provoking factors such as surgery, immobilization, malignancy or inherited thrombophilia. However, a subset of patients presents with unprovoked venous thromboembolism (VTE). Emerging evidence suggests that hyperthyroidism is an underrecognized yet reversible prothrombotic state, mediated through alterations in coagulation, fibrinolysis and endothelial dysfunction and may contribute to unprovoked PE.

Case Presentation:
A 60-year-old woman with no prior medical history presented after a brief syncopal episode associated with a fall and rapidly progressive exertional dyspnea. She denied chest pain, hemoptysis, recent immobilization, travel, hormone use or smoking. Initial vitals showed tachycardia, EKG showed sinus tachycardia. Laboratory studies demonstrated marked thyrotoxicosis with suppressed thyroid-stimulating hormone and elevated free thyroxine (T4) and triiodothyronine (T3) levels and an elevated D-dimer with transient troponin elevation. Thyroid-stimulating immunoglobulin was significantly positive, consistent with Graves ’disease.
Computed tomography pulmonary angiography revealed acute bilateral pulmonary emboli involving the left main pulmonary artery and bilateral segmental branches, as well as extensive acute right lower extremity deep venous thrombosis. Transthoracic echocardiography demonstrated right atrial and ventricular dilation with hypokinesis and severe pulmonary hypertension with right heart strain. Hypercoagulable evaluation performed after discontinuation of the heparin drip and clinical stabilization revealed negative results for Protein C, Protein S, Factor V Leiden, anticardiolipin antibody, antithrombin and prothrombin gene mutation testing. Age-appropriate cancer screening was negative.
The patient was treated with intravenous unfractionated heparin followed by catheter-directed thrombolysis for PE and subsequently transitioned to apixaban. Methimazole and propranolol were initiated for management of hyperthyroidism. On follow-up, thyroid function tests normalized and the patient remained clinically stable on anticoagulation.

Conclusion:
Elevated levels of TSH increases levels of procoagulant factors including factor VIII, von Willebrand factor and fibrinogen, decreases fibrinolytic activity and enhances platelet activation. This case highlights Graves’ disease as an uncommon but clinically significant reversible risk factor for unprovoked PE, capable of causing extensive and life-threatening thromboembolism in the absence of traditional provoking factors. Thyroid function testing should be considered in patients presenting with unexplained VTE. The optimal duration of anticoagulation in thyrotoxicosis associated VTE remains undefined, underscoring the need for future guideline development

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