Autoantibodies to platelet glycoproteins in patients with disease-related immune thrombocytopenia

Authors

  • Peter Berchtold,

    1. Department of Molecular and Experimental Medicine, Research Institute of Scripps Clinic, La Jolla, California
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  • Jeffrey P. Harris,

    1. Department of Surgery/Otolaryngology, UCSD Medical Center, University of California, San Diego, California
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  • Patricia Tani,

    1. Department of Molecular and Experimental Medicine, Research Institute of Scripps Clinic, La Jolla, California
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  • Lawrence Piro,

    1. Department of Molecular and Experimental Medicine, Research Institute of Scripps Clinic, La Jolla, California
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  • Robert McMillan

    Corresponding author
    1. Department of Molecular and Experimental Medicine, Research Institute of Scripps Clinic, La Jolla, California
      Dr Robert McMillan, Department of Molecular and Experimental Medicine, Research Institute of Scripps Clinic, 10666 N. Torrey Pines Road, La Jolla, California 92037, U.S.A.
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Dr Robert McMillan, Department of Molecular and Experimental Medicine, Research Institute of Scripps Clinic, 10666 N. Torrey Pines Road, La Jolla, California 92037, U.S.A.

Summary

Although increased platelet destruction and elevated platelet-associated IgG have been shown in patients with lymphomas and various autoimmune diseases, such as systemic lupus erythematosus (SLE), there have been few studies evaluating autoantibodies against platelet-specific antigens. We evaluated 24 patients retrospectively with disease-related thrombocytopenia (12 with lymphoproliferative diseases and 12 with various autoimmune disorders) using a recently reported antigen-specific assay.

Autoantibodies against platelet GPIIb/IIIa or GPIb/IX were noted in 15 of the 24 patients (10 of 12 with autoimmune disease and five of 12 with lymphoproliferative disorders). Platelet-associated autoantibodies were present in 60% and plasma autoantibodies in 33%. Anti-GPIIb/IIIa autoantibodies were much more common than those against GPIb/IX.

In one patient each with thrombocytopenia and either SLE or myasthenia gravis, absorption of plasma with platelets completely removed the anti-GPIIb/IIIa autoantibodies, but did not affect the level of anti-cochlear autoantibody involved with immune-mediated hearing loss in the SLE patient or the anti-acetylcholine receptor autoantibody in the myasthenic patient.

These findings show that, in some cases of disease-related immune thrombocytopenia, autoantibodies against GPIIb/IIIa or GPIb/IX can be detected similar to those seen in chronic ITP. As shown in two patients with multiple autoimmune manifestations, the various autoantibodies have diverse specificities and do not crossreact.

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