The Importance of Platelet Glycoside Residues in the Haemostasis of Patients with Immune Thrombocytopaenia

• Published in: Journal of clinical medicine Vol. 10; no. 8; p. 1661
• Main Authors: Ramírez-López, Andrés, Álvarez Román, María Teresa, Monzón Manzano, Elena, Acuña, Paula, Arias-Salgado, Elena G, Martín Salces, Mónica, Rivas Pollmar, María Isabel, Jiménez Yuste, Víctor, Justo Sanz, Raul, García Barcenilla, Sara, Cebanu, Tamara, González Zorrilla, Elena, Butta, Nora V
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 13.04.2021; MDPI
• Subjects: Acids; Apoptosis; Binding sites; Blood & organ donations; Blood platelets; Chloride; Clinical medicine; Flow cytometry; Glycoproteins; glycoside residues; immune thrombocytopaenia; Plasma; platelet activation markers; platelet apoptosis; sialic acid; Sodium; Madrid Spain; Spain; platelet apoptosis; sialic acid; glycoside residues; immune thrombocytopaenia; platelet activation markers
• ISSN: 2077-0383; 2077-0383
• DOI: 10.3390/jcm10081661

Loss of sialic acid from the carbohydrate side chains of platelet glycoproteins can affect platelet clearance, a proposed mechanism involved in the etiopathogenesis of immune thrombocytopaenia (ITP). We aimed to assess whether changes in platelet glycosylation in patients with ITP affected platelet counts, function, and apoptosis. This observational, prospective, and transversal study included 82 patients with chronic primary ITP and 115 healthy controls. We measured platelet activation markers and assayed platelet glycosylation and caspase activity, analysing samples using flow cytometry. Platelets from patients with ITP with a platelet count <30 × 10 /µL presented less sialic acid. Levels of α1,6-fucose (a glycan residue that can directly regulate antibody-dependent cellular cytotoxicity) and α-mannose (which can be recognised by mannose-binding-lectin and activate the complement pathway) were increased in the platelets from these patients. Platelet surface exposure of other glycoside residues due to sialic acid loss inversely correlated with platelet count and the ability to be activated. Moreover, loss of sialic acid induced the ingestion of platelets by human hepatome HepG2 cells. Changes in glycoside composition of glycoproteins on the platelets' surface impaired their functional capacity and increased their apoptosis. These changes in platelet glycoside residues appeared to be related to ITP severity.