Dataset Information

What is the role of hydroxychloroquine in reducing thrombotic risk in patients with antiphospholipid antibodies?

ABSTRACT: A 35-year-old man presents with an acute unprovoked deep vein thrombosis of the left lower extremity. He is treated with anticoagulation and elects to discontinue treatment after 6 months. He subsequently develops polyarthralgias, fatigue, and a malar rash, and a diagnosis of systemic lupus erythematosus is made based on laboratory and clinical findings. Additional laboratory testing reveals persistent triple positive antiphospholipid antibodies, including lupus anticoagulant, high titer anticardiolipin antibodies, and anti-?2-glycoprotein I antibodies. The patient is reinitiated on anticoagulation, and the patient's rheumatologist inquires if the addition of hydroxychloroquine could help to prevent recurrent thrombosis.

SUBMITTER: Wang TF

PROVIDER: S-EPMC6142483 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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What is the role of hydroxychloroquine in reducing thrombotic risk in patients with antiphospholipid antibodies?

Wang Tzu-Fei TF Lim Wendy W

Hematology. American Society of Hematology. Education Program 20161201 1

A 35-year-old man presents with an acute unprovoked deep vein thrombosis of the left lower extremity. He is treated with anticoagulation and elects to discontinue treatment after 6 months. He subsequently develops polyarthralgias, fatigue, and a malar rash, and a diagnosis of systemic lupus erythematosus is made based on laboratory and clinical findings. Additional laboratory testing reveals persistent triple positive antiphospholipid antibodies, including lupus anticoagulant, high titer anticar ...[more]

PMID: 27913551

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Project description:Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by pregnancy morbidity or thrombosis and persistent antiphospholipid antibodies (aPL) that bind to the endothelium and induce endothelial activation, which is evidenced by the expression of adhesion molecules and the production of reactive oxygen species (ROS) and subsequent endothelial dysfunction marked by a decrease in the synthesis and release of nitric oxide (NO). These endothelial alterations are the key components for the development of severe pathological processes in APS. Patients with APS can be grouped according to the presence of other autoimmune diseases (secondary APS), thrombosis alone (thrombotic APS), pregnancy morbidity (obstetric APS), and refractoriness to conventional treatment regimens (refractory APS). Typically, patients with severe and refractory obstetric APS exhibit thrombosis and are classified as those having primary or secondary APS. The elucidation of the mechanisms underlying these alterations according to the different groups of patients with APS could help establish new therapies, particularly necessary for severe and refractory cases. Therefore, this study aimed to evaluate the differences in endothelial activation and dysfunction induced by aPL between patients with refractory obstetric APS and other APS clinical manifestations. Human umbilical vein endothelial cells (HUVECs) were stimulated with polyclonal immunoglobulin-G (IgG) from different groups of patients n = 21), including those with primary (VTI) and secondary thrombotic APS (VTII) and refractory primary (RI+), refractory secondary (RII+), and non-refractory primary (NR+) obstetric APS. All of them with thrombosis. The expression of adhesion molecules; the production of ROS, NO, vascular endothelial growth factor (VEGF), and endothelin-1; and the generation of microparticles were used to evaluate endothelial activation and dysfunction. VTI IgG induced the expression of adhesion molecules and the generation of microparticles and VEGF. RI+ IgG induced the expression of adhesion molecules and decreased NO production. RII+ IgG increased the production of microparticles, ROS, and endothelin-1 and reduced NO release. NR+ IgG increased the production of microparticles and endothelin-1 and decreased the production of VEGF and NO. These findings reveal differences in endothelial activation and dysfunction among groups of patients with APS, which should be considered in future studies to evaluate new therapies, especially in refractory cases.

Dataset Information

What is the role of hydroxychloroquine in reducing thrombotic risk in patients with antiphospholipid antibodies?

Publications

What is the role of hydroxychloroquine in reducing thrombotic risk in patients with antiphospholipid antibodies?

Similar Datasets

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