Prothrombotic changes due to an increase in thyroid hormone levels

Area of Science:

• Endocrinology
• Hematology
• Cardiovascular Medicine

Background:

• Case-control studies suggest a link between higher free thyroxine levels and increased venous thromboembolism risk.
• Previous research on thyroid hormones and hemostasis in thyrotoxicosis has yielded inconclusive results.
• Thyroid hormones significantly influence metabolic processes, including those affecting blood coagulation.

Purpose of the Study:

• To evaluate multiple markers of hemostasis and fibrinolysis in a paired design.
• To assess changes in hemostatic balance during induced shifts in thyroid hormone levels.
• To investigate the impact of levothyroxine (lT4) suppression treatment on coagulation parameters.

Main Methods:

• A paired study design involving 90 patients undergoing total thyroidectomy.
• Analysis of hemostasis and fibrinolysis markers before radioiodine remnant ablation and 6 weeks after levothyroxine (lT4) suppression treatment.
• Comparison of paired data using the Wilcoxon's signed-rank test to detect significant changes.

Main Results:

• Significant increases in fibrinogen, von Willebrand factor, factor VIII, and plasminogen activator inhibitor 1 were observed during lT4 treatment (P<0.001).
• Platelet function analyzer (PFA-100) closure times, reflecting platelet adhesion and aggregation, were significantly shortened with epinephrine and ADP stimulation (P<0.001).
• These findings indicate a shift towards a hypercoagulable and hypofibrinolytic state.

Conclusions:

• Increased thyroid hormone levels induce a prothrombotic hemostatic balance.
• The observed hemostatic changes may contribute to the elevated cardiovascular morbidity and mortality associated with even mild thyrotoxicosis.
• This study provides robust evidence linking thyroid hormone fluctuations to significant alterations in blood coagulation and fibrinolysis.