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Antiphospholipid antibodies in immune thrombocytopenic purpura tend to emerge in exacerbation and decline in remission
Author(s) -
Bidot Carlos J.,
Jy Wenche,
Horstman Lawrence L.,
Ahn Eugene R.,
Jimenez Joaquin J.,
Yaniz Miriam,
Lander Gabriela,
Ahn Yeon S.
Publication year - 2005
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2004.05314.x
Subject(s) - exacerbation , medicine , immunology , antibody , platelet , thrombocytopenic purpura , immune system , thrombotic thrombocytopenic purpura
Summary Although the presence of antiphospholipid antibodies (APLA) in immune thrombocytopenic purpura (ITP) has been reported, their clinical significance is not clear. The present study investigated APLA profiles in relation to the clinical stages of ITP. We studied APLA in 40 patients in three stages of ITP: exacerbation/relapse ( n = 7), stable ( n = 14) and remission ( n = 19). Both IgG and IgM APLA to six target antigens were measured by enzyme‐linked immunosorbent assay: β 2‐glycoprotein 1 ( β 2GP1), cardiolipin, phosphatidylcholine, phosphatidylserine, phosphatidylethanolamine and factor VII/VIIa. The central finding was that APLA were common in ITP but differed significantly in disease stages, being highest in exacerbation (86% positive), intermediate in stable disease (57%) and lowest in remission (42%). In exacerbations, APLA were predominantly of IgG class, while in stable disease, IgM predominated. During remission, APLA often became undetectable. Both the frequency and titres of APLA were significantly higher during exacerbation than remission. An inverse correlation was found between platelet count and nearly all APLA (except β 2GP1). Sequential study of six patients revealed that APLA tended to emerge and rise with exacerbation, concurrently with new episodes of bleeding and became undetectable during remission. These findings raise the possibility that APLA may play a role in the exacerbation and remission of ITP or they may be a consequence of platelet destruction.