Adverse effects of glucocorticoids: coagulopathy

Abstract

Hypercortisolism is associated with various systemic manifestations, including central obesity, arterial hypertension, glucose intolerance/diabetes mellitus, dyslipidemia, nephrolithiasis, osteoporosis, gonadal dysfunction, susceptibility to infections, psychiatric disorders, and hypercoagulability. The activation of the hemostatic system contributes to the development of atherosclerosis and subsequent cardiovascular morbidity and mortality. Previous studies have identified an increased risk of both unprovoked and postoperative thromboembolic events in patients with endogenous and exogenous Cushing's syndrome (CS). The risk for postoperative venous thromboembolism in endogenous CS is comparable to the risk after total hip or knee replacement under short-term prophylaxis. The mechanisms that are involved in the thromboembolic complications in hypercortisolism include endothelial dysfunction, hypercoagulability, and stasis (Virchow's triad). It seems that at least two factors from Virchow's triad must be present for the occurrence of a thrombotic event in these patients. Most studies have demonstrated that this hypercoagulable state is explained by increased levels of procoagulant factors, mainly factors VIII, IX, and von Willebrand factor, and also by an impaired fibrinolytic capacity, which mainly results from an elevation in plasminogen activator inhibitor 1. Consequently, there is a shortening of activated partial thromboplastin time and increased thrombin generation. For these reasons, anticoagulant prophylaxis might be considered in patients with CS whenever they have concomitant prothrombotic risk factors. However, multicenter studies are needed to determine which patients will benefit from anticoagulant therapy and the dose and time of anticoagulation.

Translational evidence of prothrombotic and inflammatory endothelial damage in Cushing syndrome after remission

“…Platelet adhesion and VWF are classical key players in the onset of acute cardiovascular events, with strong evidence indicating the relationship between elevated levels of VWF, platelet dysfunction and an increased risk of arterial thrombosis, including myocardial infarction and ischaemic stroke. Increased levels of VWF and platelet number, as well as alteration of platelet functionality, have been frequently observed and implicated in CS haemostasis alterations in CS …”

“…The mechanisms by which patients with CS in stable remission maintain subclinical atherosclerotic damage appear to be multifactorial, including the persistence of deleterious humoural and cellular sera factors, such as pro‐inflammatory adipokines, altered coagulation and thrombosis factors, platelet function and endothelial activation and dysfunction …”

Coagulation Profile Dynamics in Pediatric Patients with Cushing Syndrome: A Prospective, Observational Comparative Study

“…16 Similarly, hyperlipidemia also is associated with Cushing syndrome, yet another risk factor for VTE. 15,17 …”

Substances and methods prohibited in sport

“…Jako leki stosowane są: w astmie, alergii, stanach zapalnych i przewlekłych urazach układu mięśniowo-szkieletowego. Jako doping poprawiają sprawność wytrzymałościową poprzez działanie neurostymulujące, przeciwzapalne i metaboliczne [39]. Działania niepożądane to: osteoporoza, otyłość, zmniejszenie masy mięśniowej, nadciśnienie, cukrzyca posterydowa, hepatotoksyczność, zaburzenia psychiczne, depresje oraz koagulopatia [40].…”