Thromb Haemost 1999; 82(03): 1028-1032
DOI: 10.1055/s-0037-1614324
Letters to the Editor
Schattauer GmbH

The Effects of Low-intensity Warfarin on Coagulation Activation in Patients with Antiphospholipid Antibodies and Systemic Lupus Erythematosus

James D. Douketis
1   From the Departments of Medicine, Toronto, Canada
,
Mark A. Crowther
1   From the Departments of Medicine, Toronto, Canada
,
James A. Julian
2   Clinical Epidemiology and Biostatistics, McMaster University, Hamilton Canada, Canada
,
Katheryne Stewart
1   From the Departments of Medicine, Toronto, Canada
,
Dianne Donovan
1   From the Departments of Medicine, Toronto, Canada
,
Elzbieta A. Kaminska
1   From the Departments of Medicine, Toronto, Canada
,
Carl A. Laskin
3   Department of Medicine, The Toronto Hospital, University of Toronto, Toronto, Canada
,
Jeffrey S. Ginsberg
1   From the Departments of Medicine, Toronto, Canada
› Author Affiliations
Supported by a Grant-in-Aid from the Medical Research Council of Canada. Dr. Ginsberg is a recipient of a Career Investigator Award from the Heart and Stroke Foundation of Ontario; Dr. Crowther is a recipient of a Research Fellowship from the Medical Research Council of Canada.
Further Information

Publication History

Received 03 February 1999

Accepted after resubmission 19 April 1999

Publication Date:
09 December 2017 (online)

Summary

The optimal intensity of oral anticoagulant therapy for the prevention of thromboembolism in patients with antiphospholipid antibodies (APLA) and systemic lupus erythematosus is controversial. Retrospective studies have suggested that patients with APLA are resistant to oral anticoagulant therapy, with a targeted International Normalization Ratio (INR) of 2.0 to 3.0, and that a higher intensity of anticoagulation (INR: 2.6 to 4.5) is required to prevent recurrent thromboembolism. To investigate if patients with APLA are resistant to the anticoagulant effect of low intensities of warfarin therapy, we performed a randomized trial in which 21 patients with APLA and systemic lupus erythematosus were allocated to receive one of three intensities of warfarin (INR: 1.1 to 1.4, 1.5 to 1.9 or 2.0 to 2.5) or placebo for four months. The main outcome was the effect of each intensity of warfarin therapy on prothrombin fragment 1+2 level (F1+2), that was used as a marker of coagulation activation. When F1+2 levels in patients allocated to the three warfarin intensities were compared to F1+2 levels in the placebo group, there was a statistically significant decrease (p <0.05) in the patient group receiving warfarin with a targeted INR of 2.0 to 2.5 at two, three and four months, and in the patient group with a targeted of INR 1.5 to 1.9 at three months. We conclude that in patients with APLA and systemic lupus erythematosus, warfarin therapy, with a targeted INR of 2.0 to 2.5, is effective in suppressing coagulation activation, and therefore, might be effective in preventing thromboembolism.

 
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