Does the anti-prothrombin antibodies measurement provide additional information in patients with thrombosis?
The aim of this study is to get new insight into the relevance of IgG anti-prothrombin antibodies in patients with thrombosis and to determine whether human prothrombin alone (aPT) or complexed to phosphatidylserine (aPS/PT) should be preferentially used for measuring these antibodies by enzyme-linked immunosorbent assay (ELISA). To this end, prevalence of anti-prothrombin antibodies, their characteristics in terms of avidity and heterogeneity, and their relationship with anti-beta2 glycoprotein I antibodies (abeta2GPI) were studied in 152 patients with thrombosis. Patients were divided into two groups according to the presence or absence of antiphospholipid antibodies (aPL), called aPL+ or aPL-, respectively. In the aPL- group (n=90), the prevalence of anti-prothrombin antibodies was substantial (10%) but not significantly different from that of control (5%). In the aPL+ group (n=62), lupus anticoagulant (LA) or anticardiolipin antibodies (aCL) positive, 61% were positive for anti-prothrombin antibodies with no statistical difference between aPT and aPS/PT prevalence (42% vs. 55%, respectively). In the whole thrombotic population, 19% were only aPT and 34% only aPS/PT suggesting the presence of different antibodies. Absorption experiments confirmed the heterogeneity of aPT and aPS/PT. No difference in their avidity was demonstrated. From the aPL+ group, 60 were LA positive. Among them, 18% were negative for abeta2GPI and anti-prothrombin antibodies showing that the detection of these antibodies could not substitute for LA determination. In conclusion, our data show that the screening of the different anti-prothrombin antibodies is not warranted in the aPL+ group since these antibodies do not provide additional information compared to aCL, LA and/or abeta2GPI measurement. Nevertheless, the substantial prevalence of anti-prothrombin antibodies in the aPL- group should be further explored in a large prospective study.
Fédération Autoimmunité et Thrombose, Lab. Immunologie, Hôpital de la Conception, 27 bd jean Moulin 13005, and INSERM U608, UFR de Pharmacie, Université de la Méditerranée, Marseille, France. nathalie.bardin@mail.ap-hm.fr
Nathalie
N
Bardin
Marie Christine
MC
Alessi
Francoise
F
Dignat-George
Irene Juhan
IJ
Vague
Jose
J
Sampol
Jean Robert
JR
Harlé
Marielle
M
Sanmarco
D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood / Q000276:immunology; D017152:Antibodies, Antiphospholipid / Q000097:blood* / Q000276:immunology; D000915:Antibody Affinity; D001323:Autoantibodies / Q000097:blood* / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D016682:Lupus Coagulation Inhibitor / Q000097:blood / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010718:Phosphatidylserines / Q000276:immunology*; D011516:Prothrombin / Q000276:immunology*; D013927:Thrombosis / Q000276:immunology*; D053482:beta 2-Glycoprotein I / Q000276:immunology
D017153:Antibodies, Anticardiolipin; D017152:Antibodies, Antiphospholipid; D001323:Autoantibodies; D016682:Lupus Coagulation Inhibitor; D010718:Phosphatidylserines; D053482:beta 2-Glycoprotein I; D011516:Prothrombin