Massive pulmonary thromboembolism combined with transient thyrotoxicosis in an 18 year old girl

Abstract

Background: Pulmonary thromboembolism (PTE) is thought to usually stem from deep vein thrombosis (DVT). However, evidence of DVT could not be found in many cases. Furthermore, transient thyrotoxicosis is a rare but potentially life-threatening emergency involving a systemic hypercoagulable state. We report on an 18 year-old-girl with transient thyrotoxicosis with massive PTE without DVT. Case presentation: An 18-year-old girl was admitted to the hospital with syncope. Patient had no history of trauma, any known underlying disease or oral contraceptives use. Chest computed tomography (CT) showed massive PTE in both central pulmonary arteries and diffuse goiter. However, a low extremity Doppler sonogram did not detect DVT. To manage the PTE, we administered low molecular weight heparin. On the other hands, thyroid function test indicated a state of thyrotoxicosis. In addition, patient had a partial protein S deficiency but no other immunologic abnormality. Therefore, the patient was diagnosed with massive PTE, thyrotoxicosis, and partial protein S deficiency. Patient was discharged with oral warfarin and methimazole. A follow-up echocardiogram obtained 3 months after anticoagulation therapy demonstrated normal dimensions and systolic function. After thyrotoxicosis was treated with methimazole for a month, a euthyroid state was achieved and the goiter decreased to a normal size. The methimazole was gradually tapered off and stopped at 4 months. At a 6-month follow up visit, PTE and pulmonary hypertension had disappeared but the patient still had a partial protein S deficiency. We decided to stop all medication with careful monitoring. During a 4year follow-up period after the episode, she was asymptomatic without any evidence of recurrent systemic thromboembolism or hyperthyroidism. Conclusions: Early recognition and appropriate treatment of PTE combined with transient thyrotoxicosis were vital to preventing other complications.

Venous Thromboembolism and Thymic Hyperplasia in the Setting of Silent Graves' Disease

“…Activation of thyroid hormone receptor beta (THRB) is one of the leading hypotheses with respect to exactly how thyroid hormone causes a hypercoagulable state [ 6 , 7 ]. Supporting this potential mechanism is the finding that patients with thyroid hormone resistance with defective THRB do not tend to develop increased coagulation factors, this being in spite of increased thyroid hormone.…”

Upper extremity deep venous thrombosis secondary to thyrotoxic periodic paralysis with accompanying hyperphosphatemia and severe hypomagnesemia

“…9 One proposed mechanism of this effect is by way of the thyroid hormone receptor β affecting gene transcription of coagulation and fibrinolytic proteins. 10 Another possible mechanism is via altered clot structure/lysis, as hyperthyroidism has been associated with increased density of clots and resistance to clot lysis. 11 These effects normalize after return to a euthyroid state.…”