endothelium-associated proteins in thyroid disease. Acta Endocrinol 1992;126:399-403. Plasma concentrations of endothelium-derived proteins (fibronectin and von Willebrand factor), liver synthesized proteins (haptoglobin, transferrin, ceruloplasmin, \g=a\1-antitrypsin, antithrombin III and factor VIII-coagulant) and plasma arginine-vasopressin (AVP) were measured in 12 hyperthyroid, 9 hypothyroid and 1 5 age-and sex-matched normal controls. In hyperthyroid patients the plasma concentrations of AVP and endothelium-associated proteins (EAP) were significantly higher than in the control group (p <0.05 and p <0.01 respectively). Rendering hyperthyroid patients into the euthyroid state significantly lowered AVP (p<0.01), fibronectin (p<0.05) and von Willebrand factor (p<0.01) compared with pretreatment levels. Hypothyroid patients were studied at diagnosis and after replacement therapy with levothyroxine. Compared with pretreatment values, significant increases were noted in plasma concentrations of von Willebrand factor, fibronectin and AVP (p<0.01). With the exception of factor VIII-coagulant, the concentrations of hepatic synthesized proteins did not deviate from normal values in hyperthyroid and hypothyroid patients. Significant correlations were found beween serum-free thyroxine on the one hand and the plasma concentrations of fibronectin (p<0.005), von Willebrand factor (p<0.001) and AVP (p<0.0001). Similarly, there was significant correlation between the plasma concentrations of AVP on the one hand and fibronectin (p <0.002) and von Willebrand factor (p<0.01). The results demonstrate elevated plasma levels of AVP in hyperthyroid patients and an increase during levothyroxine treatment of hypothyroid patients. The increase in EAP (fibronectin and von Willebrand factor) was dependent on thyroid hormone, and correlated with the increase in the plasma AVP concentrations. The mechanism(s) underlying the interrelation between AVP, EAP and thyroid hormones is (are) yet to be defined.Endothelial cells are metabolically active tissue (1, 2) known to synthesize and release a variety of proteins, such as tissue-plasminogen activator, fibronectin and von Willebrand factor, which are involved in blood coagulation and the fibrinolytic process. Alterations in components of both the fibrinolytic enzyme system and the coagulation mechanism have been reported in both hyper-and hypothyroidism, and include in hyperthyroid patients a rise in von Willebrand factor (3), fibronectin (1,4) and tissue-plasminogen activator (1, 5).The mechanism responsible for the hyperthyroidismassociated increase in endothelially synthesized proteins, i.e. endothelium-associated proteins (EAP) including fibronectin and von Willebrand factor, remains unknown. A jS-adrenergic mechanism has been pro¬ posed as a mediator for the increase of EAP in hyperthyroidism. However, the increase of EAP was not prevented by ß-blocker agents, suggesting that a mechanism(s) other than the ß-adrenergic system is respon¬ sible for the elevation of EAP in hyperthyroidism ...