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.
Bardin
Nathalie
N
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
Alessi
Marie Christine
MC
Dignat-George
Francoise
F
Vague
Irene Juhan
IJ
Sampol
Jose
J
Harlé
Jean Robert
JR
Sanmarco
Marielle
M
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