Increased thrombin-activatable fibrinolysis inhibitor and decreased tissue factor pathway inhibitor in patients with hypothyroidism.
Various abnormalities of coagulation-fibrinolytic system have been reported in patients with thyroid dysfunction. Several studies indicate that coagulation and fibrinolytic system is disturbed in the patients with hypothyroidism. Also, the influence of hypothyroidism on hemostasis is controversial; both hypocoagulable and hypercoagulable states have been reported. The levels of plasma thrombin-activatable fibrinolysis inhibitor (TAFI) antigen and tissue factor pathway inhibitor (TFPI) have been investigated only once in patients with hypothyroidism. Therefore, the main purpose of this study was to evaluate the profile of coagulation and fibrinolytic parameters including TAFI and TFPI in patients with hypothyroidism. Fifteen patients with untreated hypothyroidism and 15 age-matched healthy controls were included in the study. Factors V(FV), VII (FVII), VIII (FVIII) activities, von Willebrand factor (vWF), protein C, protein S, thrombomodulin (TM), TFPI, and TAFI were measured. The relationships between serum thyroid hormones and these hemostatic parameters were examined. Compared with the control subjects, FVII activity, and TM Ag and TAFI Ag levels were significantly increased in patients with hypothyroidism, whereas FV, FVIII, vWF, protein C and protein S activities, and TFPI Ag levels were significantly decreased. We did not find any significant correlation between serum thyroid hormones and the hemostatic parameters that we measured. In conclusion, we found some important differences in the hemostatic parameters between the patients with hypothyroidism and healthy controls. Increased FVII, TM, and TAFI and decreased FV, FVIII, vWF, protein C, protein S, and TFPI in these patients represent a potential hypercoagulable and hypofibrinolytic state, possible endothelial dysfunction, which might augment the risk for atherosclerotic and atherothrombotic complications. Thus, disturbances of the hemostatic system may contribute to the excess mortality due to cardiovascular disease seen in patients with hypothyroidism.
Erem
Cihangir
C
Department of Internal Medicine, Karadeniz Technical University, 61080, Trabzon, Turkey. cihangirerem@hotmail.com
Ucuncu
Ozge
O
Yilmaz
Mustafa
M
Kocak
Mustafa
M
Nuhoglu
Irfan
I
Ersoz
Halil Onder
HO
D000328:Adult; D001777:Blood Coagulation / Q000502:physiology; D001778:Blood Coagulation Disorders / Q000097:blood / Q000209:etiology; D025901:Carboxypeptidase B2 / Q000097:blood*; D016022:Case-Control Studies; D005260:Female; D006490:Hemostatics; D006801:Humans; D007037:Hypothyroidism / Q000097:blood* / Q000150:complications; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D018180:Thrombomodulin / Q000097:blood; D013963:Thyroid Hormones / Q000097:blood
D006490:Hemostatics; D008074:Lipoproteins; D018180:Thrombomodulin; D013963:Thyroid Hormones; C051928:lipoprotein-associated coagulation inhibitor; D025901:Carboxypeptidase B2