Departments of Endocrinology Hematology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Avenue Hippocrate, 10, B-1200 Brussels, Belgium.
Eur J Endocrinol. 2011 Apr;164(4):599-603. doi: 10.1530/EJE-10-0837. Epub 2011 Jan 21.
Several hemostatic abnormalities have been described in hypothyroidism, such as modification of coagulation proteins and bleeding tendency. Although thyroid hormone deficiency is considered to be responsible for these changes, the underlying mechanisms have not yet been established.
To evaluate the respective influence of peripheral thyroid hormones (free thyroxine) and TSH on blood clotting by assessing coagulation parameters in patients with a history of total thyroidectomy for thyroid cancer, under three different conditions: induced hypothyroidism, euthyroid state, and following recombinant human TSH (rhTSH) administration.
Coagulation parameters (platelet count, fibrinogen, international normalized ratio, prothrombin time, thrombin time, activated partial thromboplastin time (APTT), factor VIII activity ((FVIII:C), as well as von Willebrand factor antigen (VWF:Ag) and VWF activity using collagen binding assay (VWF:CBA)) were measured in patients with severe hypothyroidism following withdrawal of thyroid hormone replacement therapy, and in the same patients with euthyroidism after restoring replacement treatment (group A), and before and after administering rhTSH (group B).
FVIII:C, VWF:Ag, and VWF:CBA were significantly decreased (P<0.001), whereas APTT was significantly increased (P<0.001) in patients with severe hypothyroidism compared with patients in the euthyroid state. No changes in clotting parameters were observed in patients who received rhTSH therapy.
This prospective study shows that severe short-term hypothyroidism is associated with significantly lower levels of VWF:Ag, VWF:CBA, and FVIII:C. Administration of exogenous TSH has no effect on coagulation parameters. These findings suggest that thyroid hormone deficiency is likely to be the main cause of coagulation alterations in patients with hypothyroidism.
甲状腺功能减退症可导致多种止血异常，如凝血蛋白的改变和出血倾向。尽管甲状腺激素缺乏被认为是这些变化的原因，但潜在的机制尚未确定。
通过评估患有甲状腺癌病史的患者在三种不同情况下（诱导性甲状腺功能减退症、甲状腺功能正常和接受重组人促甲状腺激素（rhTSH）治疗）的外周甲状腺激素（游离甲状腺素）和 TSH 对凝血的各自影响，来评估凝血参数。
在停止甲状腺激素替代治疗后出现严重甲状腺功能减退症的患者中测量凝血参数（血小板计数、纤维蛋白原、国际标准化比值、凝血酶原时间、凝血酶时间、活化部分凝血活酶时间（APTT）、VIII 因子活性（FVIII:C）以及 von Willebrand 因子抗原（VWF:Ag）和使用胶原结合测定法（VWF:CBA）测量 VWF 活性），并在同一患者甲状腺功能正常后恢复替代治疗时（组 A），以及在使用 rhTSH 治疗之前和之后（组 B）测量。
与甲状腺功能正常的患者相比，严重甲状腺功能减退症患者的 FVIII:C、VWF:Ag 和 VWF:CBA 显著降低（P<0.001），而 APTT 显著增加（P<0.001）。接受 rhTSH 治疗的患者凝血参数没有变化。
这项前瞻性研究表明，严重的短期甲状腺功能减退症与 VWF:Ag、VWF:CBA 和 FVIII:C 的水平显著降低有关。外源性 TSH 的给药对凝血参数没有影响。这些发现表明，甲状腺激素缺乏可能是甲状腺功能减退症患者凝血改变的主要原因。
