Endocrine Abstracts

Patients with active Cushing’s syndrome (CS) have an increased coagulability and thrombotic tendency. High glucocorticoids concentrations increase plasma clotting factors, especially von Willebrand factor (vWf) and reduced fibrinolytic capacity. Thromboemobolic complications, mainly in the postsurgical phase, have been reported.

Aim of this longitudinal study was to evaluate haemostatic and fibrinolytic markers in patients with active Cushing’s syndrome during the activity and after the remission or the persistency of the disease.

Forty patients (32 women and 9 men) with CS were enrolled in the study: 36 were affected by ACTH-secreting pituitary adenoma and 4 by an adrenal adenoma. All patients, at the starting of the study, had an active CS. All patients were re-evaluated after 12–24 months after surgery: 27 presented the remission of the disease (Group 1), 13 had persistent hypercortisolism (Group 2). Haemostatic and fibrinolytic markers were evaluated in all patients during the activity of the disease and after surgery. No patients were taking drugs to affect coagulations tests.

von Willebrand factor (P<0.0001), plasminogen activator inhibitor (PAI-1) activity (P=0.003), antithrombin III (P=0.0002) and plasmin–antiplasmin complex (P=0.006) were statistically different in Group 1. No differences between active and remission patients were observed in other markers (fibrinogen, prothrombin fragment 1+2, factor V, factor VII, factor IX, factor XII, activated partial thromboplastin time, thrombin–antithrombin complex, plasminogen, and D-dimer). No statistical differences of haemostatic and fibrinolytic markers were observed between patients of Group 2.

The study confirms that CS is associated with a thrombophilic state and to the alteration of the fibrinolytic system. Recent studies provide evidence that polymorphisms in the vWf and PAI-1 can influence the corticosteroid-mediated transcriptional regulation of these factors. Therefore, further studies are necessary to define the modifications of coagulation cascade in hypercortisolism.