The Impact of Hemostatic Alterations in Manifest and Subclinical Hypothyroidism on Endothelial Dysfunction

Abstract

Autoimmune thyroiditis (AIT) with progression to hypothyroidism is frequently accompanied by systemic vascular and hemostatic abnormalities that contribute to increased cardiovascular risk. This study aimed to explore the relationship between endothelial dysfunction and hemostasis alterations in patients with subclinical and manifest hypothyroidism. A total of 87 participants were enrolled, including 20 healthy controls, 38 with subclinical hypothyroidism, and 29 with manifest hypothyroidism. Laboratory assessment comprised classical coagulation markers such as prothrombin index (PTI), activated partial thromboplastin time (APTT), fibrinogen, platelet count, and D-dimer, along with endothelial indicators including von Willebrand factor (vWF), endothelin-1 (ET-1), and soluble intercellular adhesion molecule-1 (sICAM-1). The results revealed progressive endothelial dysfunction in hypothyroid groups, manifested by a decline in vWF levels and significant elevation of ET-1 and sICAM-1. Concurrently, hemostatic imbalance was evident, with prolonged APTT, increased fibrinogen concentration, and higher D-dimer values compared with controls. Correlation analysis demonstrated strong positive associations between endothelial and coagulation parameters, most notably between ET-1 and sICAM-1 (r = 0.81, p < 0.001). These findings indicate that both subclinical and manifest hypothyroidism are characterized by distinct but interconnected vascular and coagulation disturbances. Importantly, alterations emerge even at the subclinical stage, underscoring the need for early identification and monitoring to reduce thrombotic risk in autoimmune thyroid disease.