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Galectin-3-binding protein is a novel predictor of venous thromboembolism in systemic lupus erythematosus
A.S.R. Peretz1, N.S. Rasmussen2, S. Jacobsen3, C. Sjöwall4, C.T. Nielsen5
- Center for Rheumatology and Spine Diseases, Gentofte, Copenhagen University Hospital, Denmark.
- Copenhagen Lupus and Vasculitis Clinic, Center for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen University Hospital, Denmark.
- Copenhagen Lupus and Vasculitis Clinic, Center for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen University Hospital, Denmark.
- Department of Rheumatology, and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
- Copenhagen Lupus and Vasculitis Clinic, Center for Rheumatology and Spine Diseases, Rigshospitalet, Copenhagen University Hospital, Denmark. christoffer.tandrup.nielsen.01@regionh.dk
CER13889
2021 Vol.39, N°6
PI 1360, PF 1368
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PMID: 33337998 [PubMed]
Received: 03/08/2020
Accepted : 19/11/2020
In Press: 18/12/2020
Published: 25/11/2021
Abstract
OBJECTIVES:
Venous (VTE) and arterial (AT) thrombosis in systemic lupus erythematosus (SLE) are poorly explained and difficult to predict. Leptin and tumour necrosis factor-like weak inducer of apoptosis (TWEAK) have been linked to subclinical atherosclerosis and galectin-3-binding protein (G3BP) to type I interferon activation and a pro-thrombotic environment. Thus, we explore serum G3BP, interferon gamma-induced protein 10 (IP-10), soluble CD163 (sCD163), TWEAK and leptin as predictors of VTE and AT, damage accrual, and all-cause mortality during follow-up in a Swedish SLE cohort.
METHODS:
Baseline data were available from 162 SLE patients. VTE (deep vein thrombosis and/or pulmonary embolism), AT (myocardial infarction and/or stroke), damage accrual, and survival data were the main study outcomes and available at follow-up (median of five years). Baseline serum G3BP, IP-10, sCD163, TWEAK and leptin were measured and analysed by univariable and multivariable methods for association to the study outcomes.
RESULTS:
During the follow-up, 10 (6%) VTE and 13 (8%) AT events occurred. The SLICC/ACR Damage Index increased in 78 (48%) patients, and 19 (12%) patients died. In the univariable regression analysis G3BP levels were significantly associated with an increased risk of VTE (hazard ratio (HR) 1.11, 95% confidence interval (CI): 1.01–1.22, p=0.03). This persisted in the adjusted multivariable analyses (HR 1.18, 95% CI: 1.05-1.33, p=0.007). The other biomarkers were not associated with AT/VTE, damage accrual, or all-cause mortality.
CONCLUSIONS:
Our study identifies serum G3BP as a novel predictor of VTE in SLE. Further studies are needed to understand the role of G3BP in VTE and translate this into clinical practice.