Submitted June 21, 2007
Accepted December 13, 2007
Galactosylation does not prevent the rapid clearance of long-term 4°C stored platelets
Hans H Wandall, Karin M Hoffmeister, Anne Louise Sorensen, Viktoria Rumjantseva, Henrik Clausen, John H Hartwig, and Sherrill J Slichter*
ZymeQuest, Inc., Beverly, MA, United States
Division of Hematology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States
Department of Cellular and Molecular Medicine, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
Puget Sound Blood Center, and University of Washington School of Medicine, Seattle, WA, United States
* Corresponding author; email: sjslichter{at}psbc.org.
Cold storage of platelets for transfusion is desirable to extend platelet storage times and to prevent bacterial growth. However, the rapid clearance of cold stored platelets prevents their use. A novel method for preventing the rapid clearance of cold stored platelets has previously been developed in a murine model.1 Cold storage induces the clustering and recognition of exposed
-N-acetylglucosamine (
GlcNAc) on platelet surfaces. Glycosylation of
GlcNAc residues with UDP-galactose results in the normal survival of short-term (2h) 0°C stored murine platelets.1 Based on this finding, we developed a similar glycosylation process by adding UDP-galactose to human apheresis platelets. A phase I clinical trial was conducted transfusing radiolabeled autologous apheresis platelets stored for 48 hours at 4°C with or without pre-treatment with UDP-galactose. In contrast to the murine study, galactosylation of human platelets did not prevent the accelerated platelet clearance routinely observed after 4°C storage. We next developed a murine model of platelet storage for 48 hours at 4°C and showed that UDP-galactose treatment of murine platelets also did not prevent their rapid clearance in agreement with the human platelet study. We conclude that different mechanisms of clearance may exist for short and long term cold stored platelets.