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Fetal and Neonatal Alloimmune Thrombocytopenia
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
The fetus inherits paternal human platelet antigens (HPA) that are not present on maternal platelets. Maternally produced anti-HPA IgG antibodies can cross the placenta resulting in destruction of fetal platelets and thrombocytopenia. Maternal platelet count and function is normal (although 10% of women with NAIT may have gestational thrombocytopenia). Although around 1 in 42 pregnancies is incompatible for HPA antigens, FNAIT develops in only 1 of 10 of these cases [2, 3].
Cellular Components of Blood
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Platelets have specific surface antigens, human platelet antigen (HPA) 1–5, and they also express ABO and HLA (human leukocyte antigen) class I antigens. Thus, platelet antibodies may be found in patients after multiple transfusions. The presence of platelet antibodies may shorten the survival of transfused platelets and reduce their efficacy.
Hospital transfusion practice
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
Platelet antigens, deriving from genetic polymorphisms among surface glycoproteins, can give rise to antibodies, complicating transfusion. There are eight well-defined systems of human platelet antigens (HPA-1 to HLA-8), each with a pair of alleles (designated ‘a’ or ‘b’) to which antibodies can arise in antigen-negative people, and several other rare antigens, not all associated with true membrane proteins.69 There are two types of clinical response. In post-transfusion purpura (PTP), typical cases occur in people who have been sensitized by past transfusion or more usually by pregnancy, often decades previously. Some days after receiving another transfusion containing platelets (even effete ones, as in red cell preparations), the patient’s own platelets seem to become involved as bystanders in a delayed immune response, resulting in thrombocytopenia. The treatment of choice is intravenous immunoglobulin.
Phagocytosis of platelets opsonized with differently glycosylated anti-HLA hIgG1 by monocyte-derived macrophages
Published in Platelets, 2023
Thijs L. J. van Osch, Juulke Steuten, Jan Nouta, Carolien A. M. Koeleman, Arthur E. H. Bentlage, Sebastiaan Heidt, Arend Mulder, Jan Voorberg, S. Marieke van Ham, Manfred Wuhrer, Anja ten Brinke, Gestur Vidarsson
Platelet transfusions are a frequently administered therapy to reduce mortality and hemorrhagic complications in patients with thrombocytopenia. A major problem in the setting of platelet transfusions is platelet refractoriness (PR), which refers to a recurring inadequate platelet count increment after multiple platelet transfusions. The incidence of PR ranges from 5% to 15% and varies depending on both patient characteristics and platelet product preparation [1–4]. In approximately 20% of PR cases platelet clearance is immune mediated, predominantly caused by the presence of alloantibodies directed against class I human leukocyte antigens (HLA) and occasionally human platelet antigens (HPA) [5–9]. Opsonization of donor platelets with these alloantibodies can result in clearance shortly after transfusion, via antibody dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC) and/or antibody dependent cellular phagocytosis (ADCP) [10–16]. The major management strategy currently available for heavily transfused alloimmunized patients is extensive matching of platelet transfusion products to prevent PR and subsequent worse clinical outcomes [7–9]. Interestingly, not all alloimmunized patients develop PR to unmatched platelet transfusions [17,18], suggesting variation in qualitative traits of the HLA specific IgG responses between patients.
Biomarkers of Complement and Platelet Activation are not correlated with the One or Twenty-Four Hours Corrected Count Increments in Prophylactically Platelet Transfused Hematological Patients: a Prospective Cohort Study
Published in Platelets, 2022
Alexander Åkesson, Marcus Ljungkvist, Myriam Martin, Anna M. Blom, Jenny Klintman, Ulf Schött, Eva Zetterberg, Thomas Kander
Platelet transfusion refractoriness is a serious clinical concern that complicates the management of patients in need of platelets. It is associated with adverse clinical outcomes and is frequently related to nonimmune platelet consumption, e.g. secondary to infections, drugs, graft-versus-host disease or splenomegaly [1]. However, alloimmunization against human leukocyte antigens (HLA) and human platelet antigens (HPA) are important immunological causes reported in approximately one third of the cases [2]. In patients recently diagnosed with nonimmune platelet transfusion refractoriness (defined as absence of alloimmunization), it is difficult to single out one definite causative factor, particularly in patients currently not burdened with apparent risk factors and who previously have responded successfully to transfusions.
Platelet increment is not associated with endothelial damage in haematological patients: a prospective observational study
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2019
S. Benediktsson, T. Kander, S. R. Ostrowski, P. I. Johansson, O. D. Thomas, U. Schött
All patients 18 years and older who were treated in the Haematology Department at Skåne University Hospital in Lund, Sweden, between 12th of February and 28th of September 2016 and needing platelet transfusions during office hours, were eligible for inclusion (Table 2). Bleeding patients were excluded. The known presence of human leukocyte antigen antibodies or human platelet antigen antibodies requiring matched platelet transfusion was also exclusion criterion, however not tested for in all patients. Other exclusion criteria included conditions and treatments with a very high demand for platelet transfusions, further described in the main study [6]. All included patients gave informed and written consent to participate.