Endocrine Abstracts

While increasing levels of thyroxine may be a risk factor for venous thromboembolism (van Zaane et al. Blood 2010 115(22) 4344–4349), there is a relative lack of detailed data on the effect of thyroid hormones on haemostatic system. We analyzed multiple markers of haemostasis in a cohort of patients shifting from severe hypothyroidism to mild hyperthyroidism during their differentiated thyroid cancer treatment.

In 94 patients following total thyroidectomy for cancer, selected tests were performed on two occasions: i) before the radioiodine remnant ablation, in hypothyroidism (TSH, median 92.2 mIU/l; interquartile range 72.2–135.9), and ii) 6–8 weeks later on levothyroxine treatment, with low-normal to suppressed TSH (0.29 mIU/l; 0.11–0.82).

While the values for D-dimer (medians, 0.34 and 0.32 mg/l, respectively), antithrombin (100 and 109.5%), and tissue plasminogen activator (2.9 and 2.8 μg/l) were not changed during levothyroxine treatment, other markers, i.e. fibrinogen (3.5 and 3.9 g/l; Wilcoxon P<0.001), plasminogen activator inhibitor 1 (6.8 and 13.2 μg/l; P<0.001), von Willebrand factor (95.141%; P<0.001) and factor VIII (105.184%; P<0.001) were increased significantly, suggesting a shift towards pro-coagulation activities in the haemostatic balance. Also, the activation times of primary haemostasis (i.e. platelet adhesion and aggregation), evaluated by the PFA-100 System after stimulation with collagen and epinephrine (136 and 116 s; P=0.002) or with collagen and ADP (89 and 82 s; P=0.017), were significantly shortened.

Increasing saturation with thyroid hormones is thus associated with multiple changes in haemostatic balance, suggestive of haemostatic system activation.