Activation of Blood Coagulation and Fibrinolysis in Graves' Disease

F. Marongiu; M. Conti; M. L. Murtas; G. Mameli; G. G. Sorano; E. Martino

doi:10.1055/s-2007-1003766

Hormone and Metabolic Research, Table of Contents

Horm Metab Res 1991; 23(12): 609-611
DOI: 10.1055/s-2007-1003766

Clinical

Activation of Blood Coagulation and Fibrinolysis in Graves' Disease

F. Marongiu¹ , M. Conti¹ , M. L. Murtas² , G. Mameli¹ , G. G. Sorano¹ , E. Martino²

¹Institute of Internal Medicine, Cattedra di Clinica Medica I, University of Cagliari, Cagliari, Italy
²Cattedra di Endocrinologia, University of Cagliari, Cagliari, Italy

Abstract

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Summary

We studied blood coagulation and fibrinolysis activities in hyperthyroidism before and after methimazole or ¹³¹I.

Fibrinopeptide A and Bβ 15-42, in vivo indicators of thrombin and plasmin activity, were measured by RIA, while fibrinogen by the Clauss method. We studied 50 patients, affected by toxic diffuse goiter. We evaluated 21 of them before and after treatment. Fibrinogen, fibrinopeptide A, and Bβ 15-42 were higher in patients than in controls (p < 0.0001). There was no difference in fibrinopeptide A nor in Bβ 15-42 before or after treatment. In euthyroidism fibrinogen returned to normal values. Inflammation of the thyroid gland secondary to autoimmunity may activate blood coagulation by release of tissue factor. High fibrinogen before treatment may be explained as an aspecific response. Since it persists in euthyroidism, autoimmunity could account for high fibrinopeptide A and Bβ 15-42 after treatment.

Key words

Graves' Disease - Fibrinogen - Fibrinopeptide A - Blood Coagulation - Fibrinolysis - Bβ15-42

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