Thrombocytopenia in retinopathy of prematurity: A role for platelet transfusion?

Session Details

Session Title: Free Paper Session 16: Vascular Diseases & Diabetic Retinopathy IV

Session Date/Time: Friday 08/09/2017 | 16:30-18:00

Paper Time: 17:12

Venue: Room 114

First Author: : R.Liegl GERMANY

Co Author(s): :    P. Lundgren   S. Klevebro   Y. Sun   Z. Liu   L. Smith   A. Hellstrom              

Abstract Details


To investigate the role of thrombocytes on retinopathy of prematurity as a new treatment approach


Boston Children´s Hospital, Harvard Medical School, Department of Ophthalmology, Boston, Massachusetts, USA and Section for Ophthalmology, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden


We correlated ROP with platelet counts, from birth to post-menstrual age 36 weeks, in preterm infants born at gestational age <27 weeks (n=202). In vivo experiments were carried out in mice by using the oxygen induced retinopathy (OIR) model. To mimic thrombocytopenia, OIR mice were injected with a GpIbα antibody, resulting in a significantly reduced platelet count within 1 hour. Isolectin was used to stain dissected and flat-mounted retinae that were quantified with a computer aided system. In order to study a possible effect of platelet transfusion, platelets were isolated from adult wildtype mice and transfused retro-orbitally in mice that had OIR at postnatal age (P) 15 and 16. These mice were taken on P17 and the amount of vaso-obliteration as well as neovascularization was evaluated. In order to assure that platelets were successfully transfused, a count was done before transfusion and one hour after transfusion. Additionally, GFP labeled platelets were transfused and whole blood taken one hour after transfusion to locate these platelets in peripheral blood.


Any episode of thrombocytopenia (platelets < 100x109/L) at ≥30 weeks post-menstrual age (at onset of ROP) was an independent risk factor for severe ROP requiring treatment (OR 2.97, CI 95 % 1.37–6.46, p=0.006). Infants with severe ROP requiring treatment also had a lower weekly median platelet count compared to infants with less severe ROP not requiring treatment (193 × 109/L, range: 14–695 vs. 262 × 109/L, range: 17–786; p<0.001). In the mouse oxygen-induced retinopathy model of ROP, platelet counts were 30% lower at P17 (p=0.008), (the peak of neovascularization), compared to controls. Platelet transfusions at the onset of retinopathy, P15-16, suppressed neovascularization by 25% (p=0.0026) and platelet depletion increased neovascularization by 65% (p=0.0011).


Low platelet count is a risk factor in preterm infants developing severe ROP that requires treatment. In a murine model of retinopathy, platelet depletion induced neovascularization and platelet transfusion suppressed retinopathy. Platelets play an important role in the development of retinopathy of prematurity and the transfusion of platelets in an animal model suppressed retinopathy. Platelet transfusion and possibly stabilization may represent a new approach to treat ROP, a possibly blinding disease of preterm infants.

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