Assessment of Time-Dependent Platelet Activation Using Extracellular Vesicles, CD62P Exposure, and Soluble Glycoprotein V Content of Platelet Concentrates with Two Different Platelet Additive Solutions.

Novel analytical measures are needed to accurately monitor the properties of platelet concentrates (PCs). Since activated platelets produce platelet-derived extracellular vesicles (EVs), analyzing EVs of PCs may provide additional information about the condition of platelets. The prospect of using EVs as an auxiliary measure of platelet activation state was investigated by examining the effect of platelet additive solutions (PASs) on EV formation and platelet activation during PC storage.

Autoimmune heparin-induced thrombocytopenia of delayed onset: a clinical challenge.

Background: Heparin-induced thrombocytopenia (HIT) usually appears at 5 to 10 days after initiation of heparin. Autoimmune HIT can arise after discontinuation of heparin treatment (delayed-onset HIT) or without any preceding heparin exposure (spontaneous HIT syndrome).

Case Report: This case presents a course of autoimmune HIT with delayed onset.

Maternal HLA genotyping is not useful for predicting severity of fetal and neonatal alloimmune thrombocytopenia.

Lack of reliable laboratory parameters is the main challenge in the management of fetal and neonatal alloimmune thrombocytopenia (FNAIT). Despite the long-known association between the HLA-DRB3*01:01 allele and human platelet antigen 1a (HPA-1a) alloimmunisation, maternal human leucocyte antigen (HLA) typing has been of little clinical value. Recently, other DRB3 allele variants have been suggested to predict the severity of FNAIT.

Great discrepancy in antithrombin activity measured using five commercially available functional assays.

Introduction: Congenital antithrombin (AT) deficiency is an inherited thrombophilia with high thrombosis prevalence. It has been reported that functional laboratory tests have varying potential in recognizing type II defects, and that there is discrepancy between thrombin inhibition based and factor Xa inhibition based methods.

Materials And Methods: Patients with known AT deficiency (n=374) were interviewed and their current AT status was tested in a new blood sample (n=214).

Fetal intracranial haemorrhages caused by fetal and neonatal alloimmune thrombocytopenia: an observational cohort study of 43 cases from an international multicentre registry.

Objective: To characterise pregnancies where the fetus or neonate was diagnosed with fetal and neonatal alloimmune thrombocytopenia (FNAIT) and suffered from intracranial haemorrhage (ICH), with special focus on time of bleeding onset.

Design: Observational cohort study of all recorded cases of ICH caused by FNAIT from the international No IntraCranial Haemorrhage (NOICH) registry during the period 2001-2010.

Setting: 13 tertiary referral centres from nine countries across the world.

Significance of quantitative measurement of heparin-induced platelet antibodies.

Background: Heparin-induced thrombocytopenia (HIT) is a prothrombotic immune-mediated adverse drug reaction. Antigen and platelet activation assays are used for detection of antibodies. Quantitative results from platelet factor 4 (PF4)-dependent immunoassays may lead to inter-laboratory standardization of measurements.

Alloantibodies against low-frequency human platelet antigens do not account for a significant proportion of cases of fetomaternal alloimmune thrombocytopenia: evidence from 1054 cases.

Background: Maternal alloantibodies against the five common human platelet antigen (HPA) systems (HPA-1 to -3, -5, and -15) are found in only 20% of cases referred for fetal and neonatal thrombocytopenia (FMAIT) investigations. The question asked was whether mismatches for the remaining 11 low-frequency HPAs (HPA-4 and -6bw to -17bw) might in part explain the remaining 80% of cases.

Study Design And Methods: A total of 1054 paternal DNA samples from referred FMAIT cases (among which 223 cases where antibodies against a common HPA were found) were genotyped for 11 low-frequency HPAs as well as a recently discovered polymorphism (ITGA2B-C2320T).

Soluble glycoprotein V as a quality marker of platelet concentrates stressed by transportation.

Background: Despite ongoing improvements in storage conditions for platelet concentrates (PCs) for clinical use, leukoreduced platelets (PLTs) undergo subtle changes that are partly due to PLT activation. As PLTs are activated, the expression of P-selectin (CD62P) increases, and soluble glycoprotein V (sGPV) is released. GPV, part of the GPIbIXV complex, has been suggested as a marker of PLT activation.