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Increased thrombin generation and activity in patients with systemic lupus erythematosus and anticardiolipin
J S Ginsberg1, C Demers, P Brill-Edwards
1Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Insights
Patients with systemic lupus erythematosus (SLE) and anticardiolipin antibodies (ACA) show biochemical evidence of a prothrombotic state. This indicates an increased risk of blood clots in SLE patients with ACA.
Area of Science:
- Rheumatology
- Hematology
- Clinical Chemistry
Background:
- Systemic lupus erythematosus (SLE) is an autoimmune disease associated with an increased risk of thrombosis.
- Anticardiolipin antibodies (ACA) are frequently found in SLE patients and are linked to thromboembolic events.
- The prothrombotic state in these patients requires further biochemical investigation.
Purpose of the Study:
- To determine if SLE patients with ACA exhibit biochemical markers of an ongoing prothrombotic state.
- To correlate ACA presence with specific indices of thrombin generation and activity.
Main Methods:
- Cross-sectional analysis of 43 SLE outpatients.
- Clinical evaluation including warfarin use, thromboembolic history, and disease activity (LACC).
- Laboratory evaluation of prothrombin fragments (F1+2), fibrinopeptide A (FPA), and ACA on two separate occasions.
Main Results:
- ACA-positive (ACA+) patients had significantly higher mean levels of F1+2 and FPA compared to ACA-negative (ACA-) patients.
- Elevated F1+2 and FPA levels were observed even after excluding patients with prior thromboembolism or active disease.
- ACA+ patients showed higher F1+2 and FPA levels than patients on warfarin therapy.
Conclusions:
- The presence of ACA in SLE patients is associated with biochemical evidence of an ongoing prothrombotic state.
- These findings support the hypothesis that ACA contributes to hypercoagulability in SLE.
- Further research into anticoagulant strategies for ACA-positive SLE patients is warranted.
Abstract:
The objective of this study is to determine whether patients with systemic lupus erythematosus (SLE) and anticardiolipin antibodies (ACA) have biochemical evidence of an ongoing prothrombotic state. Using a cross-sectional analysis of a cohort design in an outpatient SLE clinic setting, 43 consecutive patients with SLE participated. Patients underwent clinical and laboratory evaluations on two separate occasions at least 3 months apart. As part of the clinical evaluation, the following were ascertained: (1) the ongoing use of warfarin therapy; (2) the presence of prior venous and arterial thromboembolic disease by history, critical review of objective tests, and examination for reflux in the deep veins of the legs as an indicator of venous thrombosis; and (3) disease-related activity by performing a lupus activity criteria count (LACC). As part of the laboratory evaluation, blood was taken on both occasions and assayed for prothrombin fragments (F1 + 2) and fibrinopeptide A (FPA), as indices of thrombin generation and activity, respectively, and ACA. For the analyses, patients were classified as ACA+ if the assay was abnormal on both occasions and ACA- if the assay was negative on both occasions or negative on one occasion and positive on the other. ACA+ patients had: (1) a significantly higher mean level of F1 + 2 (1.07 nmol/L) than ACA- patients (0.79 nmol/L; P = .02) and patients receiving warfarin (0.47 nmol/L; P = .009) and (2) a significantly higher mean level of FPA (1.01 nmol/L) than ACA- patients (0.45 nmol/L; P = .02). When patients with prior thromboembolism were excluded from the analysis, significant differences in the mean levels of F1 + 2 and FPA between ACA+ and ACA- patients were still seen, whereas when patients with prior thromboembolism and/or active disease were excluded from the analysis, a significant difference in the mean level of FPA and a nonsignificant trend in the mean level of F1 + 2 were seen. The results of this study support the hypothesis that the presence of ACA in SLE patients is associated with an ongoing prothrombotic state.