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Hemostasis in Overt and Subclinical Hyperthyroidism
Arash Ordookhani1, Kenneth D Burman2
1Endocrine Section, Department of Internal Medicine, Providence Hospital, Washington, DC, 20017.
International Journal of Endocrinology and Metabolism
|December 5, 2017
Summary
Hyperthyroidism may cause a hypercoagulable state, increasing venous thromboembolism (VTE) risk. However, definitive clinical confirmation of this hemostatic change is still needed.
Area of Science:
- Endocrinology
- Hematology
- Thrombosis Research
Background:
- Conflicting data exists regarding hyperthyroidism's impact on hemostasis.
- Limited population-based studies hinder understanding of clinical implications, particularly venous thromboembolism (VTE) risk.
- This review examines hemostatic alterations in both overt and subclinical hyperthyroidism.
Purpose of the Study:
- To review and synthesize current knowledge on hemostatic changes in hyperthyroidism.
- To evaluate the potential link between hyperthyroidism and an increased risk of VTE.
Main Methods:
- A systematic literature search was performed using the MEDLINE database.
- Keywords included hyperthyroidism, thyrotoxicosis, Graves disease, goiter, hemostasis, coagulation factors, blood coagulation disorders, VTE, bleeding, and fibrinolysis.
- Relevant articles linking hyperthyroidism and hemostasis were included.
Main Results:
- Hyperthyroidism, both overt and subclinical, is generally associated with a hypercoagulable state.
- This may stem from elevated levels of coagulation factors (e.g., FVIII, FX, FIX, vWF, fibrinogen).
- Hypofibrinolysis is also observed, indicated by decreased plasmin/plasmin activator or increased PAI-1 and TAFI.
Conclusions:
- While many studies suggest a hypercoagulable state in overt hyperthyroidism at a biochemical level.
- The clinical significance of these findings regarding the actual occurrence of VTE remains unconfirmed.
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