Thrombin-activatable fibrinolysis inhibitor in hypothyroidism and hyperthyroxinaemia

Chantal J. N. Verkleij; Danka J. F. Stuijver; Bregje van Zaane; Alessandro Squizzato; Dees P. M. Brandjes; Harry R. Büller; Joost C. M. Meijers; Victor E. A. Gerdes

doi:10.1160/TH12-07-0525

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2013; 109(02): 214-220
DOI: 10.1160/TH12-07-0525

Blood Coagulation, Fibrinolysis and Cellular Haemostasis

Schattauer GmbH

Thrombin-activatable fibrinolysis inhibitor in hypothyroidism and hyperthyroxinaemia

Authors

Chantal J. N. Verkleij

¹Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Danka J. F. Stuijver

²Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

³Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands
Bregje van Zaane

²Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

³Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands
Alessandro Squizzato

⁴Clinical Medicine, University of Insubria, Varese, Italy
Dees P. M. Brandjes

²Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

³Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands
Harry R. Büller

²Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Joost C. M. Meijers

¹Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

²Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Victor E. A. Gerdes

²Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

³Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands

Abstract

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.

Keywords

TAFI - thyroid - fibrinolysis - coagulation

Full Text

References

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