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Thrombin-activatable fibrinolysis inhibitor in hypothyroidism and hyperthyroxinaemia

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245
DOI: http://dx.doi.org/10.1160/TH12-07-0525
Issue: 2013: 109/2 (Feb) pp. 175-360
Pages: 214-220
Ahead of Print: ###MANUSCRIPT_aheadofprint###

Thrombin-activatable fibrinolysis inhibitor in hypothyroidism and hyperthyroxinaemia

See also Editorial by Franchini

C. J. N. Verkleij (1), D. J. F. Stuijver (2, 3), B. van Zaane (2, 3), A. Squizzato (4), D. P. M. Brandjes (2, 3), H. R. Büller (2), J. C. M. Meijers (1, 2), V. E. A. Gerdes (2, 3)

(1) Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; (2) Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; (3) Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands; (4) Department of Clinical Medicine, University of Insubria, Varese, Italy

Keywords

thyroid, fibrinolysis, coagulation, TAFI

Summary

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.

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