Background: Lipoprotein apheresis is an important therapeutic option in homozygous familial hypercholesterolemia, progressive atherosclerosis, or when depletion of lipoprotein(a) is indicated. It is generally regarded as safe, but drops in platelet counts as well as sporadic episodes of thrombocytopenia have been reported. We assessed the influence of platelet desialylation, which may be induced by endogenous or pathogen-derived neuraminidases, on platelet adhesion to polyacrylate-based adsorbents for whole blood lipoprotein apheresis.
Methods: Medical grade platelet concentrates were incubated with neuraminidase in vitro and were circulated over adsorbent columns downscaled from clinical application.
Results: Cleavage of terminal sialic residues resulted in platelet activation with significantly elevated expression of platelet factor 4 (PF4) and in enhanced platelet adhesion to the adsorbent, accompanied by a pronounced drop in platelet counts in the column flow-through.
Conclusion: Alterations in endogenous neuraminidase activity or exogenous (pathogen-derived) neuraminidase may trigger enhanced platelet adhesion in whole blood lipoprotein apheresis.
Keywords: Platelets; adsorption; glycosylation; sialylation.