Thromb Haemost 1992; 68(02): 208-213
DOI: 10.1055/s-0038-1656350
Original Article
Schattauer GmbH Stuttgart

Defect of Platelet Aggregation and Adhesion Induced by Autoantibodies Against Platelet Glycoprotein IIIa

Authors

  • Carlo L Balduini

    The Department of Internal Medicine (Clinical Medicine 2), University of Pavia-IRCCS S. Matteo, Pavia, Italy
  • Giampiera Bertolino

    The Department of Internal Medicine (Clinical Medicine 2), University of Pavia-IRCCS S. Matteo, Pavia, Italy
  • Patrizia Noris

    The Department of Internal Medicine (Clinical Medicine 2), University of Pavia-IRCCS S. Matteo, Pavia, Italy
  • Franco Piovella

    The Department of Internal Medicine (Clinical Medicine 2), University of Pavia-IRCCS S. Matteo, Pavia, Italy
  • Fabiola Sinigaglia

    1   The Department of Biochemistry, University of Pavia, Pavia, Italy
  • Vittorio Bellotti

    The Department of Internal Medicine (Clinical Medicine 2), University of Pavia-IRCCS S. Matteo, Pavia, Italy
  • Anna Samaden

    The Department of Internal Medicine (Clinical Medicine 2), University of Pavia-IRCCS S. Matteo, Pavia, Italy
  • Mauro Torti

    1   The Department of Biochemistry, University of Pavia, Pavia, Italy
  • Giuliano Mazzini

    2   The Centro di Studio per I'lstochimica', Department of Animal Biology, Pavia, Italy
Further Information

Publication History

Received 01 August 1989

Accepted after revision 19 March 1992

Publication Date:
03 July 2018 (online)

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Summary

A young patient developed chronic idiopathic thrombocytopenic purpura. Prednisone therapy normalized platelet number, but bleeding symptoms did not disappear. Platelet function was severely impaired, since platelet aggregation, ATP release and adhesion to collagen and subendothelial matrix were significantly reduced. Plasma and purified immunoglobulins of the patient reproduced the functional defects in normal platelets. Immunoblotting revealed that patient’s plasma contained an antibody reacting with a component of platelets with the same electrophoretic mobility of glycoproteins IIIa of normal platelets. Moreover, patient’s plasma inhibited the binding of an anti-GPIIb/IIIa monoclonal antibody to platelet surface. Additional immunosuppressive therapy with prednisone and azathioprine normalized platelet function and induced the disappearance of bleeding symptoms.