Serum levels of microparticles and vascular dysfunction markers in patients with systemic sclerosis

• Grant number: 18/26811-9
• Support type: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): August 01, 2019
• Effective date (End): July 31, 2020
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal researcher: Cristiane Kayser
• Grantee: Lucas Garcia Biagi
• Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Introduction: Systemic sclerosis (SSc) is a chronic disease of autoimmune etiology, characterized by vascular damage, dysregulation of the immune system and tissue fibrosis, with elevated morbidity and mortality. In the earliest stages of the disease, microvascular abnormalities are expressed mainly by Raynaud's phenomenon, which may precede cutaneous and visceral involvement for years. Platelet activation and, according to new findings, the role of microparticles, which are small membrane-bound vesicles released from activated or dying cells, have been involved in the pathogenesis of SSc. Objectives: In this study we aim at evaluating the serum levels of microparticles and markers of platelet activation and endothelial damage in patients with SSc. Methods: This will be a cross-sectional study, with 50 patients with SSc (according to the 2013 ACR/EULAR classification criteria), and 25 controls. Patients will be evaluated by measuring the levels of microparticles derived from platelets (CD42+/CD31+), endothelial cells (CD51+/CD105+) and monocytes (CD14+) using flow cytometry. von Willebrand factor (VWF) and thromboxane B2 will be assayed by ELISA. Clinical and capillaroscopy data will be collected from all patients. Correlations between serum markers and clinical and capillaroscopic abnormalities will be performed. Expected results: We expect to find a significant difference in serum levels of platelet activation and endothelial damage markers in SSc patients compared to the control group. These findings may help the overall comprehension of the mechanisms involved in SSc pathophysiology.