ECE2016 Guided Posters Neuroendocrinology (10 abstracts)
Endothelial damage and thrombotic response in patients with cured Cushing syndrome
Gloria Aranda Velazquez 1, , Mireia Mora Porta 1, , Irene Halperin 1, , Rebeca Fernandez 2 , Maribel Díaz-Ricart 3 , Marta Palomo 3 , Oscar Vidal 2, , Joaquim Enseñat 5 , Gregori Casals 6 & Felicia Alexandra Hanzu 1,
1Endocrinology Department, HCB, Barcelona, Spain; 2IDIBAPS-CIBERDEM, Barcelona, Spain; 3Hemostasy Department, HCB, Barcelona, Spain; 4Endocrine Surgery, HCB, Barcelona, Spain; 5Neurosurgery, HCB, Barcelona, Spain; 6Hormonal Laboratory, HCB, Barcelona, Spain.
Introduction: Clinical observational studies have reported the persistence of a high cardiovascular risk in patients with cured Cushing’s syndrome (CCS) compared with controls of the same age, gender and BMI. It is still at debated whether this is due to the persistence of comorbidities, hormone deficiencies or chronic changes induced by hypercortisolism. The aim of this translational approach was to investigate the interplay in CCS of the cardiovascular disease in vivo and the endothelial activation and thrombogenicity in vitro occurring in response to sera of CCS.
Methods: Cross-sectional study in CS patients and controls and in vitro endothelial damage atherothrombotic model. Subjects: I. Cured CS (CCS) (n=10) at minimum 2 years after cure and without hormone deficiencies and II. Active CS (ACS) (n=10), III. Controls (CTR) (n=10) matched for age, sex, sexual hormonal status (females, premenopausal) and also by BMI and cardiometabolic profile. We evaluated in vivo: the cardiometabolic clinical and analytical profile; endothelial dysfunction (FMD) and body composition (DEXA). Endothelial cells (EC) were exposed for 24 h or have been cultured for 7 days with the different seras (groups I, II, III) to evaluate the inflammatory EC response (VCAM, ICAM; NfKB) and the reactivity (VWF) of the extracellular matrix (ECM).
Results: Active CS patients have a clinical, subclinical and in vitro proatherothrombotic phenotype. EC exposed to CCS sera displayed augmented expression of ICAM1 (P=0.04), VCAM1 (P=0.05), a higher synthesis of sub-endothelial VWF (P=0.03) and a higher EC reactivity towards circulating platelets: platelet adhesion (P=0.04) than CTRs of the same sex, age and BMI. NFκB is activated downstream.
Conclusion: This is the first translational study demonstrating that the sera of patients with cured CS have a deleterious atherothrombotic NFκB dependent potency on the endothelium inducing endothelial inflammatory activation and increased thrombogenicity.
Article tools
My recent searches
My recently viewed abstracts
Authors
Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
© Bioscientifica 2024 |
Privacy policy |
Cookie settings
BiosciAbstracts
Bioscientifica Abstracts is the gateway to a series of products that provide a permanent, citable record of abstracts for biomedical and life science conferences.
Find out more