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P117 Exploring mechanisms behind thrombosis in systemic lupus erythematosus
  1. Mads L Larsen1,2,
  2. Laura Nørgaard1,
  3. Petrus Linge3,
  4. Julie B Larsen4,5,
  5. Henrik Z Langkilde6,7,
  6. Ellen M Hauge2,5,
  7. Steffen Thiel1,
  8. Anne Voss6,7,
  9. Anders Bengtsson3 and
  10. Anne Troldborg1,2,5
  1. 1Dept. of Biomedicine, Aarhus University, Aarhus, Denmark
  2. 2Dept. of Rheumatology, Aarhus University Hospital, Aarhus, Denmark
  3. 3Dept of Clinical Sciences, Rheumatology, Lund University, Skåne University Hospital, Lund, Sweden
  4. 4Dept. of Clinical Biochemistry, Regional Hospital Horsens, Horsens, Denmark
  5. 5Dept. of Clinical Medicine, Aarhus University, Aarhus, Denmark
  6. 6Dept. of Clinical Research, University of Southern Denmark, Odense, Denmark
  7. 7Dept. of Rheumatology, Odense University Hospital, Odense, Denmark

Abstract

Objective This systematic review seeks to survey existing literature concerning systemic lupus erythematosus (SLE)-related thrombosis risk mechanisms within six pro-coagulable categories: autoantibodies (including antiphospholipid antibodies (aPL)), the complement system, platelets, the endothelium, the coagulation system, and fibrinolysis. Patients with SLE face an approximately 50% thrombosis risk after diagnosis, However, the underlying mechanisms are intricate, and anticoagulation recommendations are lacking.

Methods The review was conducted in accordance with the preferred reporting items for systematic reviews and meta-analyses (PRISMA) statements. PubMed and Embase were searched without time restrictions to identify studies evaluating mechanisms of thrombosis based on the six mentioned pro-coagulable categories in SLE.

Results Thirty-one studies were included. Figure 1 illustrates the literature search process. Thirty studies employed in vitro investigations utilizing a case-control design, and one animal study was identified. Autoantibodies (mainly aPL) were the subject of investigation in 80% of studies. The studies highlighted pro-coagulable interactions between autoantibodies and all other investigated pro-coagulable categories. Ten studies identified cross reactivity between aPL and other SLE autoantibodies. There was a paucity of studies exploring the impact of anti-inflammatory or anti-thrombotic treatments within the investigated mechanisms.

Conclusions The thrombosis risk mechanisms mediated by aPL in SLE are well-documented. These mechanisms may also be shared with other autoantibodies in SLE, potentially explaining the increased thrombosis risk observed in aPL-negative SLE patients. Interactions between the pro-coagulable categories were frequently reported in the literature and appear pivotal in SLE thrombosis risk. Further research is warranted to elucidate the effects of different treatments on thrombosis mechanisms in SLE.

Abstract P117 Figure 1
Abstract P117 Figure 1

Flow diagram of the literature search for studies included in this review according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement

http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ .

https://doi.org/10.1136/lupus-2024-el.171

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