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SAT0304 Coagulation Factor XIII Might Be A Promising Marker for Predicting Atherosclerosis in SLE
  1. I. Matsuura1,2,
  2. E. Lourenco1,
  3. J. Grossman1,
  4. B. Skaggs1,
  5. M. McMahon1
  1. 1Rheumatology, UCLA David Geffen School of Medicine, Los Angeles, United States
  2. 2Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, United Kingdom

Abstract

Background Several traditional and non-traditional risk have been implicated in the development of atherosclerosis in systemic lupus erythematosus (SLE). However, while growing evidence demonstrates that blood coagulation factor XIII (FXIII) may play an essential role in atherothrombotic disease in patients with primary antiphospholipid syndrome, the role of this coagulation factor in atherothrombotic disease and overall disease activity in patients with SLE is still poorly understood. Plasma FXIII cross-links fibrin with itself and with the endothelium, making clots resistant to fibrinolysis. Intracellular FXIII in monocytes also cross-links Type I angiotensin receptor dimer, which increases monocyte adhesion to endothelial cells and accelerates atherosclerosis. We investigated whether FXIII was associated with intima media thickness (IMT) of carotid arteries or disease activity in patients with SLE.

Objectives to evaluate clinical significance of FXIII in SLE.

Methods the study involved 50 consecutive patients with SLE enrolled in a longitudinal study on atherosclerosis biomarker from 2008 through 2015 at UCLA. Plasma FXIII activity (FXIIIa) was measured in the blood samples by ELISA. B-mode and Doppler Scanning was performed to measure IMT at baseline and 24–36 month.

Results Table1 shows the correlation with plasma level of FXIIIa and variables that were independently associated with SLE activity and atherosclerosis. There was a strong inverse correlation with the SLE Disease Activity Index (SLEDAI), physician global assessment (PGA), and dsDNA antibody, whereas there was a significant positive correlation between FXIIIa and C3 and IMT at the follow-up ultrasound (Figure1). In patients with high plasma FXIIIa (>143%), the mean SLEDAI was significantly lower, (2.17± 3.7 vs. 4.1 ± 3.2, p=0.009) and IMT at follow-up was significantly higher (0.61 ± 0.17 vs. 0.51 ± 0.14, p=0.009).

Table 1.

Correlations between FXIII and variables in SLE

Conclusions Although further confirmatory testing is underway, FXIII might be a novel marker for increased IMT in SLE.

  1. McMahon M, Skaggs BJ, Grossman JM, Sahakian L, Fitzgerald J, Wong WK, et al. A panel of biomarkers is associated with increased risk of the presence and progression of atherosclerosis in women with systemic lupus erythematosus. Arthritis Rheumatol. 2014;66(1):130–9.

  2. Ames PR, Iannaccone L, Alves JD, Margarita A, Lopez LR, Brancaccio V. Factor XIII in primary antiphospholipid syndrome. The Journal of rheumatology. 2005;32(6):1058–62.

  3. Muszbek L, Bereczky Z, Bagoly Z, Shemirani AH, Katona E. Factor XIII and atherothrombotic diseases. Seminars in thrombosis and hemostasis. 2010;36(1):18–33.

Disclosure of Interest None declared

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