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[Thrombophilia in systemic lupus erythematosus: A case-control study]
N Belfeki1, M S Khanfir1, F Said1
1Service de médecine interne, CHU la Rabta de Tunis, rue Jbel Lakhdar,La Rabta Jebbari, 1007 Tunis, Tunisie.
Insights
Systemic lupus erythematosus (SLE) patients show higher rates of thrombotic abnormalities. Protein C deficiency and acquired protein C resistance are linked to thrombosis in SLE, not antiphospholipid antibodies.
Area of Science:
- Rheumatology
- Hematology
- Immunology
Background:
- Systemic lupus erythematosus (SLE) is associated with an increased risk of thrombosis.
- Understanding thrombotic tendencies in SLE patients is crucial for risk stratification and management.
Purpose of the Study:
- To investigate thrombotic risk factors in SLE patients.
- To evaluate congenital and acquired abnormalities predisposing to thrombosis in SLE.
Main Methods:
- 53 SLE patients and 53 age/sex-matched healthy controls were assessed.
- Evaluated antiphospholipid antibodies (aCL, aβ2GP, LAC), Protein C (PC), Protein S (PS), Antithrombin (AT), acquired activated protein C resistance, and homocysteinemia.
- Compared frequencies of thrombophilic markers and thrombosis incidence between groups using Chi-squared and student tests.
Main Results:
- 17.0% of SLE patients had positive antiphospholipid antibodies, compared to 0% in controls (P=0.01).
- Protein S deficiency (32.1%) and hyperhomocysteinemia (30.2%) were significantly more frequent in SLE patients.
- Venous thrombosis occurred in 9.4% of SLE patients; significantly associated with Protein C deficit (P=0.02) and acquired activated protein C resistance (P=0.04), but not antiphospholipid antibodies.
Conclusions:
- Thrombophilic abnormalities are more prevalent in SLE patients than in healthy individuals.
- Protein C deficiency and acquired protein C resistance are significant risk factors for thrombosis in SLE.
- Antiphospholipid antibodies did not show a significant correlation with thrombosis in this SLE cohort.
Introduction:
To investigate the thrombotic tendency in patients with systemic lupus erythematosus (SLE) by evaluating congenital and acquired abnormalities with an increased risk of thrombosis.
Patients And Methods:
A total of 53 patients with SLE were included in the study. Fifty-three healthy controls paired by age and sex were assessed. Anticardiolipin antibodies (aCL), anti β2 glycoprotein (aβ2GP), lupus anticoagulant (LAC), protein C (PC), protein S (PS), antithrombin (AT), acquired activated protein C, and homocysteinemia were evaluated. Comparisons for categorical variables were analyzed by Chi2 and student tests.
Results:
The patients were all female and had a mean age of 30.6 years (16/58). The healthy controls were all female and their mean age was 30.8 years (17/56). Five patients (9.4%) developed venous thrombosis during the 24 months of follow-up. The antiphospholipid antibodies were positive in 17 patients (32.1%) and negative in all healthy controls (P=0.01). PS deficiency was noted in 17 patients (32.1%) and in 5 controls (P=0.004). Hyperhomocysteinemia was noted in 16 patients (30.2%) versus 3 controls (5.6%) (P=0.002). Test for PC deficiency and acquired activated protein C showed no significant difference between the two groups. No AT deficiency was found in the patients. The study of clinical and biological correlations based on the presence and absence of thrombophilic parameters concluded to a significant association between Protein C deficit and thrombosis (P=0.02) and acquired activated protein C resistance and thrombosis (P=0.04). There was no significant association between the APL and thrombosis.
Conclusion:
Thrombophilic abnormalities were significantly more frequent in lupus patients than in healthy controls. Thrombotic events were significantly associated with PC deficit and acquired protein C resistance. There was no correlation between antiphospholipid antibodies and thrombosis.
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