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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

Chantal J. N. Verkleij
1   Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
,
Danka J. F. Stuijver
2   Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
3   Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands
,
Bregje van Zaane
2   Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
3   Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands
,
Alessandro Squizzato
4   Clinical Medicine, University of Insubria, Varese, Italy
,
Dees P. M. Brandjes
2   Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
3   Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands
,
Harry R. Büller
2   Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
,
Joost C. M. Meijers
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
,
Victor E. A. Gerdes
2   Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
3   Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands
› Author Affiliations Financial support:This work was supported in part by a grant from the Dutch Diabetes Research Foundation (Grant 2005.00.016 to J.C.M.M.).
Further Information

Publication History

Received: 29 July 2012

Accepted after major revision: 28 October 2012

Publication Date:
29 November 2017 (online)

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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
 

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