Abstrakt
Objective With increasing free thyroxine levels, a gradually rising risk of venous thromboembolism has been described in case-control studies. However, reports on the influence of thyroid hormones on haemostasis, while suggesting a hypercoagulable state in thyrotoxicosis, have often been inconclusive.
The present study evaluates multiple markers of haemostasis and fibrinolysis in a paired design, making it more sensitive to changes in thyroid hormone levels. Design We analysed multiple variables in patients who shifted from severe hypothyroidism to mild hyperthyroidism during thyroid cancer treatment.
Those with possible residual disease were excluded. Methods Ninety patients following total thyroidectomy were tested on two occasions: (a) before radioiodine remnant ablation and (b) 6 weeks later, on levothyroxine suppression treatment, and the results were compared using the Wilcoxon test for paired data.
Results During levothyroxine treatment, significant increases (all p<0.001) in fibrinogen (from median 3.4 to 3.8 g/l), von Willebrand factor (from 85 to 127%), factor VIII (from 111 to 148%), and plasminogen activator inhibitor-1 (from 6.5 to 13.9 µg/l) were observed. In addition, the activation times of platelet adhesion and aggregation stimulated with collagen and epinephrine/adenosine diphosphate (ADP), i.e. closure times in platelet function analyzer (PFA-100), were significantly shortened (p<0.001): for epinephrine from median 148 to 117 s and for ADP from 95 to 80 s.
Changes in other tests were less prominent or insignificant. Conclusions An increase in thyroid hormone levels shifts the haemostatic balance towards a hypercoagulable, hypofibrinolytic state.
This may contribute to the increased cardiovascular morbidity and mortality observed even in mild thyrotoxicosis.
