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Persistent High Levels of IgM Antiphospholipid Antibodies in a Patient with Recurrent Pregnancy Losses and Rheumatoid Arthritis
Author(s) -
Ota Kuniaki,
Dambaeva Svetlana,
Lee Jennifer,
GilmanSachs Alice,
Beaman Kenneth,
KwakKim Joanne
Publication year - 2014
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.12196
Subject(s) - isotype , immunology , medicine , cardiolipin , antiphospholipid syndrome , autoantibody , antibody , rheumatoid arthritis , immunoglobulin m , pregnancy , serology , immunoglobulin g , biology , monoclonal antibody , phospholipid , membrane , genetics
Objective Recurrent pregnancy losses ( RPL ) and unexplained infertility ( UI ) are often associated with the presence of antiphospholipid antibodies ( APA ). We report one case with RPL , UI , and persistent IgM APA without B‐cell isotype switch. Method of study (i) A case report of a woman with RPL and UI who eventually developed rheumatoid arthritis and B‐cell phenotype study of the case and controls by flow cytometric analysis; (ii) a retrospective cohort study of 1067 subjects with APA test. Results A 44‐year‐old woman with a history of RPL and UI was revealed to have high levels of APA , primarily of IgM isotype: IgM autoantibodies were specific to cardiolipin, phosphatidylglycerol, phosphatidylserine, and phosphatidylinositol. The monitoring of the patient's serological characteristics for 28 months did not reveal the development of IgG APA . B‐cell phenotype analysis revealed decreased switched and double negative memory B cells and increased non‐switched memory B cells in comparison with normal controls and reported ranges. A retrospective analysis of APA test revealed that total five patients (5/1067, 0.47%) with similar persistent IgM‐only pattern were detected. Conclusion Persistent IgM APA without isotype switch may be a rare variant form of APA manifestation, which is associated with dysregulated B‐cell subsets.

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