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Platelet aggregation response in immune thrombocytopenia patients treated with romiplostim

Authors
  • Al-Samkari, Hanny1
  • Van Cott, Elizabeth M.2
  • Kuter, David J.1
  • 1 Harvard Medical School, Division of Hematology, Massachusetts General Hospital, Zero Emerson Place, Suite 118, Boston, MA, 02114, USA , Boston (United States)
  • 2 Harvard Medical School, Department of Pathology, Massachusetts General Hospital, Boston, MA, USA , Boston (United States)
Type
Published Article
Journal
Annals of Hematology
Publisher
Springer-Verlag
Publication Date
Nov 17, 2018
Volume
98
Issue
3
Pages
581–588
Identifiers
DOI: 10.1007/s00277-018-3556-6
Source
Springer Nature
Keywords
License
Yellow

Abstract

The thrombopoietin receptor agonist romiplostim is used for the long-term treatment of chronic immune thrombocytopenia (ITP). ITP patients have an increased thrombotic risk, which could be exacerbated if romiplostim increased platelet hyperreactivity or caused spontaneous platelet aggregation. To investigate this possibility, this study examined platelet function in romiplostim-treated ITP patients and healthy subjects. Light transmission platelet aggregometry utilizing arachidonic acid, collagen, epinephrine, ristocetin, ADP, and saline (to assess spontaneous aggregation) was performed for each subject. In addition, the ADP AC50 (ADP concentration that induced half-maximal aggregation) was determined for each patient as a sensitive measurement of altered platelet reactivity. Fifteen ITP patients and 7 healthy subjects entered the study. All ITP patients had active disease and were receiving weekly romiplostim as the sole ITP-directed therapy. Platelet aggregation in response to the strong agonists arachidonic acid, collagen, and ristocetin was not significantly different between ITP patients and healthy subjects (P = 0.2442, P = 0.0548, and P = 0.0879, respectively). Platelet aggregation in response to weak agonists was significantly reduced in ITP patients compared with that in healthy subjects: median (range) aggregation to ADP, 45% (15–84%) versus 89% (70–95%) (P = 0.0010), and epinephrine, 21% (1.6–90%) versus 88% (79–94%) (P = 0.0085). The median AC50 of ADP was threefold higher in ITP patients versus that in healthy subjects (6.3 μM vs 2.1 μM) (P = 0.0049). Significant spontaneous aggregation was not observed in any patient. Platelets from romiplostim-treated ITP patients do not show evidence for spontaneous aggregation or hyperreactivity, but instead have a modestly reduced aggregation response to ADP and epinephrine.

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