The Hypercoagulable state in Hyperthyroidism is mediated via the Thyroid Hormone β Receptor pathway

Area of Science:

• Endocrinology
• Hematology
• Molecular Biology

Background:

• Hyperthyroidism is linked to a hypercoagulable state, but the mechanism remains unclear.
• Resistance to thyroid hormone (RTH) involves defective thyroid hormone receptor beta (TRβ), leading to elevated thyroid hormones (TH) with tissue refractoriness.
• This study investigates if TRβ mediates the hypercoagulable state observed in hyperthyroidism.

Purpose of the Study:

• To determine if the thyroid hormone receptor beta (TRβ) mediates the hypercoagulable state associated with hyperthyroidism.
• To compare coagulation and fibrinolysis markers in hyperthyroid patients, RTH patients, and euthyroid controls.

Main Methods:

• A cross-sectional study was conducted in the Netherlands and the UK from November 2013 to January 2015.
• Participants included patients with RTH due to defective TRβ (n=18), hyperthyroid patients (n=16), and euthyroid subjects (n=18).
• Measurements included thyroid hormone concentrations and markers of coagulation and fibrinolysis.

Main Results:

• Hyperthyroid patients exhibited significantly higher levels of von Willebrand factor (VWF), factor VIII, fibrinogen, and D-dimer compared to RTH patients.
• Both hyperthyroid and RTH patients had elevated free thyroxine (FT4) levels compared to euthyroid controls.
• No significant differences in coagulation and fibrinolysis markers were observed between RTH patients and euthyroid controls.

Conclusions:

• The procoagulant effects seen in hyperthyroidism are mediated via the TRβ.
• Elevated FT4 levels in RTH patients, without defective TRβ, do not lead to a hypercoagulable state.
• TRβ plays a crucial role in thyroid hormone-mediated regulation of coagulation and fibrinolysis.