The IgG autoimmune response in postpartum acquired hemophilia A targets mainly the A1a1 domain of FVIII
Autor: | Géraldine Lavigne-Lissalde, J. Balicchi, Claude Granier, Caroline Pfeiffer, Hervé Levesque, Yves Gruel, Christopher Cayzac, Eve Mathieu-Dupas, Priscilla Lapalud, T. Ali, Jean-François Schved, J. Y. Borg |
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Rok vydání: | 2012 |
Předmět: |
Adult
Hemophilia A Subclass Pregnancy medicine Humans In patient health care economics and organizations Aged Autoimmune disease Aged 80 and over Alanine Factor VIII biology business.industry Postpartum Period Autoantibody Hematology Middle Aged medicine.disease Immunoglobulin G Immunology biology.protein Acquired hemophilia Female Antibody business Complication Postpartum period |
Zdroj: | Journal of thrombosis and haemostasis : JTH. 10(9) |
ISSN: | 1538-7836 |
Popis: | Summary. Background: Acquired hemophilia A (AHA) is a severe life-threatening autoimmune disease due to the development of autoantibodies that neutralize the procoagulant activity of factor VIII (FVIII). In rare cases, AHA occurs in the postpartum period as a serious complication of an otherwise normal pregnancy and delivery. Due to its rarity, little is known about the features of the antibody response to FVIII in AHA. Objectives: Our study wanted to (i) determine the epitope specificity and the immunoglobulin (Ig) subclasses of anti-FVIII autoantibodies in plasma samples from a large cohort of AHA patients, and (ii) compare the epitope specificity of anti-FVIII autoantibodies in plasma samples from postpartum AHA and other AHA patients. Patients/Methods: Seventy-three plasma samples from patients with postpartum AHA (n = 10) or associated with malignancies (n = 16) or autoimmune diseases (n = 11) or without underlying disease (n = 36) were analyzed with three multiplexed assays. Results and Conclusions: Our results showed a stronger response against the A1a1-A2a2-B fragments of FVIII and more specifically against the A1a1 domain in patients with postpartum AHA than in the other AHA groups (P |
Databáze: | OpenAIRE |
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