Journal article
Platelet production and platelet destruction: assessing mechanisms of treatment effect in immune thrombocytopenia
- Barsam, Sarah J. Department of Haematology, University College London Hospital, London, United Kingdom;
- Psaila, Bethan Department of Haematology, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom;
- Forestier, Marc Department of Medicine, Laboratory for Thrombosis Research, Kantonsspital Baden, Baden, Switzerland;
- Page, Lemke K. Platelet Disorders Center, Department of Pediatrics, Weill-Cornell Medical College, New York, NY;
- Sloane, Peter A. Platelet Disorders Center, Department of Pediatrics, Weill-Cornell Medical College, New York, NY;
- Geyer, Julia T. Department of Pathology and Laboratory Medicine, Weill-Cornell Medical College, New York, NY; and
- Villarica, Glynis O. Platelet Disorders Center, Department of Pediatrics, Weill-Cornell Medical College, New York, NY;
- Ruisi, Mary M. Platelet Disorders Center, Department of Pediatrics, Weill-Cornell Medical College, New York, NY;
- Gernsheimer, Terry B. Puget Sound Blood Centre, University of Washington School of Medicine, Seattle, WA
- Beer, Juerg H. Department of Medicine, Laboratory for Thrombosis Research, Kantonsspital Baden, Baden, Switzerland;
- Bussel, James B. Platelet Disorders Center, Department of Pediatrics, Weill-Cornell Medical College, New York, NY;
Published in:
- Blood. - American Society of Hematology. - 2011, vol. 117, no. 21, p. 5723-5732
English
Abstract
This study investigated the immature platelet fraction (IPF) in assessing treatment effects in immune thrombocytopenia (ITP). IPF was measured on the Sysmex XE2100 autoanalyzer. The mean absolute-IPF (A-IPF) was lower for ITP patients than for healthy controls (3.2 vs 7.8 × 109/L, P < .01), whereas IPF percentage was greater (29.2% vs 3.2%, P < .01). All 5 patients with a platelet response to Eltrombopag, a thrombopoietic agent, but none responding to an anti-FcγRIII antibody, had corresponding A-IPF responses. Seven of 7 patients responding to RhoD immuneglobulin (anti-D) and 6 of 8 responding to intravenous immunoglobulin (IVIG) did not have corresponding increases in A-IPF, but 2 with IVIG and 1 with IVIG anti-D did. This supports inhibition of platelet destruction as the primary mechanism of intravenous anti-D and IVIG, although IVIG may also enhance thrombopoiesis. Plasma glycocalicin, released during platelet destruction, normalized as glycocalicin index, was higher in ITP patients than controls (31.36 vs 1.75, P = .001). There was an inverse correlation between glycocalicin index and A-IPF in ITP patients (r2 = −0.578, P = .015), demonstrating the relationship between platelet production and destruction. Nonresponders to thrombopoietic agents had increased megakaryocytes but not increased A-IPF, suggesting that antibodies blocked platelet release. In conclusion, A-IPF measures real-time thrombopoiesis, providing insight into mechanisms of treatment effect.
- Language
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- English
- Open access status
- green
- Identifiers
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- DOI 10.1182/blood-2010-11-321398
- ISSN 0006-4971
- Persistent URL
- https://folia.unifr.ch/global/documents/249442
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