Acquired thrombasthenia due to inhibitory effect of glycoprotein Iibiia autoantibodies

Dorit Blickstein, Rima Dardik, Esther Rosenthal, Judith Lahav, Yair Molad, Aida Inbal*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Background: A 75 year old patient presenting with mucocutaneous bleeding was diagnosed with acquired thrombasthenia. The diagnosis was based on lack of platelet aggregation with adenosine diphosphate (ADP), arachidonic acid and collagen, and normal aggregation induced by ristocetin. Objective: To study the mechanism of platelet function inhibition in a patient with acquired thrombasthenia. Methods: Aggregation assays of platelets from the patient and healthy controls were performed. In addition, antiglycoprotein (GP) IIbIIIa antibodies binding to normal platelets in the presence or absence of the patient's serum was studied by flow cytometry. Results: Aggregation of normal platelets in the presence of patient's plasma was inhibited four- and 2.5-fold in the presence of ADP and arachidonic acid respectively, while collagen-induced aggregation was completely abolished. Ristocetin-induced aggregation was normal. The patient's serum inhibited binding of commercial anti-glycoprotein IIbIIIa antibodies to normal platelets twofold by flow cytometry. Treatment with anti-CD20 monoclonal antibody (rituximab) normalized the patient's platelet aggregation. Conclusions: These results suggest that the patient developed inhibitory anti-GPIIbIIIa autoantibodies that caused acquired thrombasthenia.

Original languageEnglish
Pages (from-to)307-310
Number of pages4
JournalIsrael Medical Association Journal
Issue number5
StatePublished - May 2014
Externally publishedYes


  • Acquired thrombasthenia
  • Anti-GPIIbIIIa antibodies
  • Platelet aggregation
  • Rituximab


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