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格雷夫斯病中血液凝固和纤维蛋白溶解的激活。

Activation of blood coagulation and fibrinolysis in Graves' disease.

作者信息

Marongiu F, Conti M, Murtas M L, Mameli G, Sorano G G, Martino E

机构信息

Institute of Internal Medicine, University of Cagliari, Italy.

出版信息

Horm Metab Res. 1991 Dec;23(12):609-11. doi: 10.1055/s-2007-1003766.

Abstract

We studied blood coagulation and fibrinolysis activities in hyperthyroidism before and after methimazole or 131I. Fibrinopeptide A and B beta 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 B beta 15-42 were higher in patients than in controls (p less than 0.0001). There was no difference in fibrinopeptide A nor in B beta 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 B beta 15-42 aftertreatment.

摘要

我们研究了甲巯咪唑或¹³¹I治疗前后甲状腺功能亢进患者的凝血和纤溶活性。通过放射免疫分析法(RIA)检测凝血酶和纤溶酶活性的体内指标纤维蛋白肽A和Bβ15 - 42,而纤维蛋白原采用克劳斯法测定。我们研究了50例毒性弥漫性甲状腺肿患者。对其中21例患者在治疗前后进行了评估。患者的纤维蛋白原、纤维蛋白肽A和Bβ15 - 42水平高于对照组(p < 0.0001)。治疗前后纤维蛋白肽A和Bβ15 - 42均无差异。甲状腺功能正常时,纤维蛋白原恢复到正常水平。自身免疫继发的甲状腺炎症可能通过释放组织因子激活凝血。治疗前纤维蛋白原水平高可解释为一种非特异性反应。由于其在甲状腺功能正常时持续存在,自身免疫可能是治疗后纤维蛋白肽A和Bβ15 - 42水平高的原因。

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