title: Thrombin-activatable fibrinolysis inhibitor in hypothyroidism and  hyperthyroxinaemia.
abstract: Endocrine disorders affect both the coagulation and fibrinolytic systems, and have been associated with the development of cardiovascular diseases. Thrombin-activatable fibrinolysis inhibitor (TAFI) is a link between coagulation and the fibrinolytic system. The aim of this study was to determine the effect of thyroid hormone excess and deficiency on TAFI levels and function. The effect of hyperthyroxinemia on TAFI was studied in healthy volunteers who were randomised to receive levothyroxine or no medication for 14 days in a crossover design. The effect of hypothyroidism on TAFI was studied in a multicentre observational cohort study. Blood was drawn before treatment of patients with newly diagnosed hypothyroidism and when euthyroidism was achieved. Plasma clot-lysis times, activated TAFI (TAFIa)-dependent prolongation of clot-lysis and TAFI levels were measured. Thyroid hormone excess resulted in a hypofibrinolytic condition and in an enhanced TAFIa-dependent prolongation of clot lysis. A trend towards decreased plasma TAFI levels was observed in healthy volunteers who used levothyroxine. Hypothyroidism resulted in hyperfibrinolysis and a reduced TAFIa-dependent prolongation of clot lysis. In conclusion, alterations of TAFIa-dependent prolongation of clot lysis in patients with thyroid disorders may cause an impaired haemostatic balance. The disturbed haemostatic balance in patients with hyperthyroidism might make them prone to thrombosis, while the risk for bleeding may increase in patients with hypothyroidism.
authors.affiliation: Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: Chantal J N
authors.initials: CJ
authors.lastname: Verkleij
authors.forename: Danka J F
authors.initials: DJ
authors.lastname: Stuijver
authors.forename: Bregje
authors.initials: B
authors.lastname: van Zaane
authors.forename: Alessandro
authors.initials: A
authors.lastname: Squizzato
authors.forename: Dees P M
authors.initials: DP
authors.lastname: Brandjes
authors.forename: Harry R
authors.initials: HR
authors.lastname: Büller
authors.forename: Joost C M
authors.initials: JC
authors.lastname: Meijers
authors.forename: Victor E A
authors.initials: VE
authors.lastname: Gerdes
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001777:Blood Coagulation; D025901:Carboxypeptidase B2 / Q000097:blood*; D018592:Cross-Over Studies; D005260:Female; D063285:Fibrin Clot Lysis Time; D005342:Fibrinolysis; D006470:Hemorrhage / Q000097:blood / Q000209:etiology; D006487:Hemostasis / Q000187:drug effects; D006801:Humans; D006981:Hyperthyroxinemia / Q000097:blood* / Q000150:complications; D007037:Hypothyroidism / Q000097:blood* / Q000150:complications; D008297:Male; D008875:Middle Aged; D009426:Netherlands; D016037:Single-Blind Method; D013927:Thrombosis / Q000097:blood / Q000209:etiology; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000008:administration & dosage / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D014284:Triiodothyronine; D013972:Thyrotropin; D025901:Carboxypeptidase B2; D013974:Thyroxine