Insights into the Procoagulant Profile of Patients with Systemic Lupus Erythematosus without Antiphospholipid Antibodies.

Elena Monzón Manzano,Paula Acuña,Francisco Javier López-Longo,Nora V Butta,Ihosvany Fernández-Bello,María Teresa Álvarez Román,Raúl Justo Sanz,Ángel Robles Marhuenda,Víctor Jiménez Yuste

doi:10.3390/jcm9103297

Abstract

We aimed to identify the key players in the prothrombotic profile of patients with systemic lupus erythematosus (SLE) not mediated by antiphospholipid antibodies, as well as the potential utility of global coagulation tests to characterize hemostasis in these patients. Patients with SLE without antiphospholipid antibodies and without signs of thrombosis were included. The kinetics of clot formation were determined by ROTEM®. Platelet activation markers were determined by flow cytometry. Thrombin generation associated with Neutrophil Extracellular Traps (NETs) and microparticles (MPs) was measured by calibrated automated thrombogram (CAT). The plasma levels of PAI-1 were also determined. ROTEM® showed a procoagulant profile in SLE patients. SLE patients had activated platelets and more leukocyte/platelet aggregates at basal conditions. The plasma PAI-1 and platelet aggregates correlated with several ROTEM® parameters. The thrombin generation associated withthe tissue factor (TF) content of MPs and with NETs was increased. Our results suggest the utility of global tests for studying hemostasis in SLE patients because they detect their procoagulant profile, despite having had neither antiphospholipid antibodies nor any previous thrombotic event. A global appraisal of hemostasis should, if possible, be incorporated into clinical practice to detect the risk of a thrombotic event in patients with SLE and to consequently act to prevent its occurrence.

Highlights

Systemic lupus erythematosus (SLE) is a potentially fatal multiorgan inflammatory immune-mediated disease that primarily affects females
Up to 15% of patients with SLE have had myocardial infarction [1], and approximately 20–30% of deaths in patients with SLE are due to cardiovascular disease (CVD) [2,3]
The presence of antiphospholipid and anticardiolipin antibodies and lupus anticoagulant is correlated with the occurrence of cardiovascular events, 40% of SLE thrombosis cases are autoantibody-negative [5,6], suggesting the involvement of other factors.we aim to identify the key players in the prothrombotic profile of patients with SLE not mediated by antiphospholipid antibodies

Summary

Introduction

Systemic lupus erythematosus (SLE) is a potentially fatal multiorgan inflammatory immune-mediated disease that primarily affects females. Thrombosis contributes to substantial morbidity and mortality in patients with SLE due to a complex interplay between traditional risk factors and the dysregulation of autoimmunity. The duration of the disease correlates with the degree of cardiovascular involvement [4], suggesting that chronic exposure to immune system dysregulation contributes to the development of CDV in these patients. The presence of antiphospholipid and anticardiolipin antibodies and lupus anticoagulant is correlated with the occurrence of cardiovascular events, 40% of SLE thrombosis cases are autoantibody-negative [5,6], suggesting the involvement of other factors.we aim to identify the key players in the prothrombotic profile of patients with SLE not mediated by antiphospholipid antibodies

Objectives

Methods

Results