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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
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Published on: November 1, 2015

The inflammation and coagulation cross-talk in patients with systemic lupus erythematosus

Eelco W Meesters1, Hjalmar Hansen, Henri M H Spronk

  • 1Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands.

Blood Coagulation & Fibrinolysis : an International Journal in Haemostasis and Thrombosis
|December 21, 2006
PubMed

Insights

Systemic lupus erythematosus (SLE) patients show increased resistance to activated protein C (APC), a key factor in thrombosis. This acquired resistance, linked to inflammation and lower free protein S, highlights a critical link between SLE and clotting risk.

Area of Science:

  • Rheumatology
  • Hematology
  • Immunology

Background:

  • Systemic lupus erythematosus (SLE) is associated with high cardiovascular disease and venous thromboembolism risks.
  • Prothrombotic autoantibodies and endothelial dysfunction contribute to these risks in SLE patients.
  • Understanding the mechanisms of thrombosis in SLE is crucial for patient management.

Purpose of the Study:

  • To investigate the prevalence and causes of activated protein C (APC) resistance in female SLE patients.
  • To explore the relationship between inflammation, coagulation status, and APC resistance in SLE.
  • To identify potential determinants of thrombosis risk in SLE.

Main Methods:

  • A case-control study comparing female SLE patients with age- and sex-matched healthy controls.
  • Assessment of plasma inflammatory markers, coagulation status (prothrombin fragment 1+2, D-dimer), and APC resistance.
  • Evaluation of APC resistance using thrombin generation and activated partial thromboplastin time-based methods.

Main Results:

  • SLE patients exhibited significantly higher plasma inflammatory markers compared to controls.
  • Overall coagulation status (prothrombin fragment 1+2, D-dimer) did not differ between groups.
  • Increased APC resistance was observed in SLE patients, independent of Factor V Leiden or oral contraceptive use.
  • This acquired APC resistance correlated with lower free protein S levels and proinflammatory changes.

Conclusions:

  • Acquired APC resistance is a significant finding in SLE patients.
  • The defect appears linked to inflammatory processes and reduced free protein S levels.
  • This acquired APC resistance may be a key factor contributing to thrombosis risk in SLE, mediated by inflammation-coagulation crosstalk.

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