Thyroid pathology and platelet functional activity

Abstract

Thyroid pathology is the second largest disease after diabetes in endocrinology. In patients with thyroid dysfunction an increase in bleeding time, activated partial thromboplastin time (aPTT) activated recalcification time (ATS), the clotting time are observed. The most important role in the physiology and pathology of coagulation platelets play. Hypothyroidism can alter platelet function, changing Adenozin diphosphate-induced aggregation. Violations of activation platelets: slowing or stopping the adhesion and aggregation, increased disaggregation can lead to severe hemorrhage. According to the study in patients with thyroid dysfunction are observed: lengthening of APTT, increased levels of fibrinogen, reflecting a tendency to anticoagulation, reducing the total number of platelets, decreased platelet aggregation activity, growth of aggregation speed, reduction of the maximum aggregate size and elongation of maximum speed value. Patients with elongation of APTT and fibrinogen increase indicate a rapid continuous intravascular coagulation, accompanied by moderate hypocoagulation of consumption – reducing the number of platelets allows to suggest the consumption. More significant are hemostatic changes in patients with multinodular non-toxic goiter with respect to shifts in patients with hypothyroidism. More important changes are in clotting and platelet activation in patients with the simultaneous occurrence of hypothyroidism and nontoxic multinodular goiter. The presence of signs of acceleration of intravascular coagulation, as measured by the fibrinogen content, allows to suggest that hypocoagulation is not associated with the property of thyroid hormones to reduce the activity or production of plasma-coagulation factors, or increase anticoagulant blood potential. More likely, hypocoagulation is secondary - due to the activation of the WTF, leading to accelerated consumption of clotting factors. Decreased platelet content shows the consumption. Thus, in patients with impaired thyroid function coagulation system is under stress, expressed by the development of signs of DIC with a chronic course, these changes are manifested more deeply in patients with uninodule nontoxic goiter.