The Contribution of Anti-prothrombin-antibodies to Lupus Anticoagulant Activity

Daniëlle A. Horbach; Erica van Oort; Ronald H. W. M. Derksen; Philip G. de Groot

doi:10.1055/s-0037-1615066

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1998; 79(04): 790-795
DOI: 10.1055/s-0037-1615066

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The Contribution of Anti-prothrombin-antibodies to Lupus Anticoagulant Activity

Discrimination between Functional and Non-functional Anti-prothrombin-antibodies

Authors

Daniëlle A. Horbach

¹From the Departments of Haematology, The Netherlands

²From the Rheumatology and Clinical Immunology, University Hospital Utrecht, The Netherlands

³From the Institute of Biomembranes, Utrecht University, The Netherlands
Erica van Oort

¹From the Departments of Haematology, The Netherlands

²From the Rheumatology and Clinical Immunology, University Hospital Utrecht, The Netherlands
Ronald H. W. M. Derksen

²From the Rheumatology and Clinical Immunology, University Hospital Utrecht, The Netherlands
Philip G. de Groot

¹From the Departments of Haematology, The Netherlands

³From the Institute of Biomembranes, Utrecht University, The Netherlands

Abstract

Summary

The presence of lupus anticoagulant (LAC) is strongly correlated with a history of thrombosis in patients with SLE. LAC activity can be caused by anti-prothrombin (FII)- and/or anti-β₂glycoprotein I (β₂GPI)-antibodies.

In the present study, the contribution of anti-FII-antibodies to LAC activity was measured in 28 LAC positive plasmas. Plasmas were incubated with prothrombin or BSA, immobilized on CNBr-activated Sepharose, to absorb all anti-FII-antibodies. In 4 out of the 28 plasmas LAC activity was completely dependent on anti-FII-antibodies. In 7 out of the 28 plasmas, anti-FII-antibodies did not contribute to LAC activity. These anti-FII-antibodies can be regarded as non-functional antibodies. In the majority (17/28) of the samples, LAC activity within a single plasma was caused by a combination of antibodies with different specificities. Both dRVVT and KCT showed comparable sensitivity for the detection of functional anti-FII-antibodies.

In conclusion, in most samples LAC activity is not caused by anti-FII-antibodies alone but by a combination of different types of antibodies. The presence of LAC activity and anti-FII-antibodies in one plasma does not automatically implicate that these antibodies are responsible for the LAC activity.

Full Text

References

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