Premium
Autoantibodies to Factor XII and Kininogen‐Dependent Antiphosphatidylethanolamine Antibodies in Patients with Recurrent Pregnancy Loss Augment Platelet Aggregation
Author(s) -
Sato Yoshihiro,
Sugi Toshitaka,
Sakai Rie
Publication year - 2015
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12402
Subject(s) - factor xii , antibody , autoantibody , platelet , thrombin , kininogen , prekallikrein , medicine , chemistry , endocrinology , coagulation , immunology , kallikrein , biochemistry , enzyme
Problem Numerous studies have suggested that factor XII ( FXII ) deficiency, autoantibodies to FXII (anti‐ FXII ), and antiphosphatidylethanolamine antibodies ( aPE ) are associated with recurrent pregnancy loss ( RPL ). aPE in RPL patients recognize the LDC 27 peptide of kininogen domain 3. Anti‐ FXII in RPL patients recognizes the heavy chain of FXII , especially the amino‐terminal sequences IPP 30 peptide. Previous studies suggested that LDC 27 and IPP 30 are the responsible sites competing for the same binding site on platelets and inhibiting augmentation of thrombin‐induced platelet aggregation. Our aim was to study the influence of antibodies to LDC 27 and IPP 30 on platelet aggregation. Methods of study In fifteen healthy volunteers, platelet aggregation induced by γ‐thrombin in the presence or absence of antibodies to LDC 27 and IPP 30 was measured. Sixteen RPL patients who were positive for anti‐ FXII were measured for spontaneous small platelet aggregate ( SSPA ) formation. Results and Conclusions Antibodies to LDC 27 and IPP 30 markedly increased aggregation of normal platelets stimulated by γ‐thrombin. Augmentation of SSPA formation was more frequent in the patients with RPL who were positive for anti‐ FXII than in the control group ( P = 0.003). This study strongly supports the hypothesis that aPE and anti‐ FXII may cause RPL due to disruption of the normal antithrombotic effects of kininogens and FXII .