Hyperthyroidism: A rare cause of pulmonary embolism: Report of two cases
A 32 year-old man, with a family history of Graves’ disease in a maternal aunt, was admitted to the hospital with a history of weight loss, excessive sweating, palpitation, tremors of the hands and irritability of sixmonths duration.\nOn clinical examination, he was found to be toxic. Pulse was 132 per minute and irregular. Blood pressure (BP) was 110/70 mmHg. He had moderate bilateral exophtalmos associated with a large elastic vascular goiter. He also had clinical signs of right heart failure, including edema of lower limbs, hepatomegaly and hepatojugular reflux. Laboratory tests revealed normocytic normochromic anemia with a hemoglobin level of 11.8 g/dL. The rest of the laboratory results were within normal range. Thyroid function tests confirmed a state of thyrotoxicosis with free T4 (FT4) of 51 pmol/L (reference range 10-24), and TSH of 0.07 μU/mL (reference range 0.4-4.5). High titer of antithyroid-stimulating antibodies confirmed the diagnosis of Graves’ disease. Electrocardiogram (ECG) showed complete arrhythmia due to atrial fibrillation (CA/FA). A cervicothoracic scan indicated a non-compressing and non-dipping homogeneous goiter.\nEchocardiography revealed dilated right cavities, mild tricuspid insufficiency, and elevated pulmonary pressure reaching 64 mmHg. There were no signs of left ventricular enlargement or reduced function.\nThe diagnosis of PE was suspected by the presence of significant pulmonary hypertension, and was confirmed by a lung perfusion-ventilation scan test that showedhypoperfusion of the left lung [].\nNo conventional venous thromboembolism risk factors were identified. Thrombophilia screen, including protein C and S, antithrombin, activated protein C resistance, lupus anticoagulant, and anti-cardiolipin antibody were negative.\nThe patient was diagnosed as Graves’ disease complicated by cardiothyreosis and PE. The patient received heparin, followed by oral anticoagulant therapy. Benzylthiouracil (Basdène®) treatment was also initiated at a dose of 225 mg daily, associated with beta-blocker propranolol. Two months later, radioactive iodine treatment (8 mCi) was administered, resulting in incomplete recovery from thyrotoxicosis. Repeated echocardiography showed normal pulmonary artery pressure (29 mmHg). The patient died of acute heart failure secondary to a chest infection 2.5 months after radioactive iodine treatment.