The role of platelets in retinopathy of prematurity

The review discusses the factors affecting the development of retinopathy of prematurity, namely, the role of low platelet count in the pathogenesis of the disease and association with its severe forms. Recently, platelets have been revealed to play a key role in angiogenesis and the delivery of regulatory proteins. This pathogenetic association may be attributed to two factors. Firstly, children with retinopathy of prematurity and low platelet count develop disrupted delivery of regulatory proteins necessary to maintain optimal platelet count. Secondly, excess vascular endothelial growth factor A is absorbed incompletely, which contributes to overstimulation of endothelial cells, their proliferation, and hence retinopathy of prematurity. Thus, the main pathogenetic mechanisms of platelet count effect on the development of retinopathy of prematurity may be associated with the fact that they locally stimulate or inhibit angiogenesis. Low platelet count in peripheral blood slows down normal vasculogenesis of the peripheral retina. However, platelet transfusions and partial hemolysis result in release of bioactive substances regulating angiogenesis, including vascular endothelial growth factor and hypoxia Inducible factor, from platelet granules, which leads to abnormal vasoproliferation. That is why further studies of platelet count management are warranted to determine the preferred timing and quantities of infusion therapy, which can provide clinical benefit. The need for platelet transfusion in patients with retinopathy of prematurity and thrombocytopenia is still a matter for discussion.