| dc.description | Abstract: Although clinically important abnormalities of hemostasis are unusual in patients with thyroid disease, coagulation and fibrinolytic systems are, nonetheless affected by hormone alterations. Patients with hypothyroidism may present abnormal bleeding. The precise nature of the "ohemostatic defect was explained by a decrease in several coagulation factors, an increase in fibrinolytic activity and an abnormal platelet adhesiveness. If the hypercoagulable state contributes to increase the risk of thromboembolic complications in hypothyroid patients, the relatively increased fibrinolytic activity in such patients probably has a protective role. Although precise statistics are not available, thromboembolic disorders do not seem to be common in patients with hyperthyroidism. These' patients showed a specific elevation of the factors VIII and von Willebrand and a reduction in plasma fibrinolytic activity. Maybe, hyperdynamic circulation may counterbalance these potential hypercoagulable changes. One of the hypothesis for elevated anti-hemophilic factor activity in hyperthyroidism is based on the fact that epinephrine infusion in normal subjects is followed by elevated levels of hemostasis changes that have been reported and not yet adequately explained. The aim of this study was to evaluate components of contact phase, coagulation, natural factor VIII activity, and hyperthyroid subjects which have an increased sensitivity to the etfects of cathecolamines. An experimental model with dogs before and after hypothyroidism induction was performed in order to study the importance of the f3 adrenergic receptors in levels of factor VIII and von Willebrand. During the clinic phase ofthis study, we analyzed 33 untreated hyperthyroid patients (mean age 39:!:13 years old), 20 hypothyroid patients (mean age 23:t6 years). Ali patients were female. Twenty nine female euthyroid subjects (mean age 48:!:18 years) were the control Group. The following was analyzed: activated Partial Thromboplastin Time (APTT), Prothrombin Time (TP), Thrombin Time (TT), Factors V, Vil, VIll , XI and XII, Fibrinogen, Protein C (PC), Protein S (PS), Cl-inhibitor (C 1), alpha 2-macroglobulin (alpha-2), prealbumin and von Willebrand factor, Plasmatic prekallikrein (PK), triiodothyronine (T3 ), tetraiodothyronine (T 4) total and tree, TSH and TSHus. Only ~actor XII and the a. 2-macroglobulin were decreased during the contact phase in hypothyroid patients. We do not believe that tlfts decrease in factor XII levels is due to the reduction on protein synthesis. We have determined other coagulation factors; they are more sensitive to alterations in hepatic proteins synthesis, like factor Vil and PK. They were not altered in hypothyroid patients. The decrease of a. 2 macroglobulin in hypothyroid patients could represent a regulatory mechanism against fybrinolysis. Both factor VIII and von Willebrand were increased in hyperthyroid patients. These factors were similar in the hypothyroid and the control group. Final common pathway parameters and fibrinogen did not show a significant difference between the three groups...Note: The complete abstract is available with the full electronic digital thesis or dissertations | |
