HistoryThis section has been translated automatically.
HPA was originally identified in patients who showed refractoriness to platelet transfusions (Bruhn 2007).
DefinitionThis section has been translated automatically.
Human platelet antigens (HPA) are polymorphisms in the platelet antigens that can be bound by antibodies. These antigens are localized almost exclusively on platelet glycoproteins. They represent so-called thrombocytic blood group systems (Ostendorf 2024).
The antigen determinants can induce the formation of platelet antibodies (Urban 2013).
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ClassificationThis section has been translated automatically.
A distinction is made between the following antigen determinants on the surface of platelets:
- Type I antigens
- Type II antigens (Böck 2024)
HPA is a type II antigen. They represent genetically determined polymorphisms and are usually inherited in an autosomal codominant manner. In the meantime, HPA has been detected not only on thrombocytes, but also in very low concentrations in endothelial cells and smooth muscle cells. A distinction is now made between more than 30 HP antigens (Böck 2024).
Of particular clinical significance are:
- HPA- 1 a with a phenotype frequency of 97 %
- HPA- 1 b with a phenotype frequency of 31 %
- HPA- 2 a with a phenotype frequency of 99.8
- HPA- 2 b with a phenotype frequency of 12
- HPA- 3 a with a phenotype frequency of 86
- HPA- 3 b with a phenotype frequency of 63
- HPA- 4 a with a phenotype frequency of > 99.9
- HPA- 4 b with a phenotype frequency of < 0.1 %
- HPA- 5 a with a phenotype frequency of > 98.8 %
- HPA- 5 b with a phenotype frequency of 21 % (Böck 2024 / Urban 2013)
HPA 1a and HPA 5b are particularly responsible for neonatal alloimmune thrombocytopenia and post-transfusion purpura (Böck 2024).
General informationThis section has been translated automatically.
HPA plays a role in transfusion therapy in particular, as alloantibodies can be formed against foreign HPA. These alloantibodies can react with the corresponding platelets and destroy them immunologically (Ostendorf 2024).
During a transfusion or during pregnancy, the mother may become sensitized to platelet antigen 1. The development of alloantibodies against platelets can lead to immune thrombocytopenia (ITP) , also known as post-transfusion thrombocytopenia or post-transfusion purpura. (Herold 2021).
HPA is of great importance during pregnancy when the mother forms alloantibodies against the unborn child's HPA and this triggers thrombocytopenia in the child. Alloimmune thrombocytopenia is usually only discovered at birth (Ostendorf 2024).
OccurrenceThis section has been translated automatically.
HPA- 1 a/a genotypes are found in 74% of blood donors, HPA- 1a / b in 16% and HPA- 1 b / b in 10% (Jacobs 2005).
DiagnosticsThis section has been translated automatically.
Platelet antigens are detected by molecular genetics using the polymerase chain reaction (Böck 2024).
Complication(s)This section has been translated automatically.
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Immune thrombocytopenia:
- 1. post-transfusion thrombocytopenia:
- This occurs relatively rarely. It primarily affects women > 50 years of age. In 85 %, sensitization to the HPA- 1 antigen has previously occurred, e.g. through transfusions or pregnancy (Herold 2021). The thrombocytopenia that occurs after a delay of 7 - 10 days should be treated with intravenous immunoglobulins to neutralize the effector antibodies (Kasper 2015).
- 2 Neonatal alloimmune thrombocytopenia:
- This is found in approx. 0.2 % of all newborns. The cause is a feto-maternal incompatibility of thrombocytic antigens, which is triggered by HPA- 1 a antibodies in approx. 85 % of cases. In such a case, the mother is HPA- 1 b homozygous (Herold 2021).
- Therapeutically, i.v. immunoglobulins and prednisone are administered prenatally (Bussel 2021)
- 3. passive alloimmune thrombocytopenia:
- This can occur immediately after (Schwenzer 2000) a transfusion of plasma containing HPA-A (Herold 2021). Treatment consists of the administration of platelet concentrates (Karges 2009).
Patients who are carriers of the HPA- 1 b genotype show a higher rate of myocardial infarction or restenosis (Bruhn 2007).
LiteratureThis section has been translated automatically.
- Böck M (2024) Lecture Transfusion Medicine. Basic knowledge for students. Doi: https://www.transfusionsmedizin-vorlesung.de/vorlesung-transfusionsmedizin/blutgruppen-thrombozyten-und-granulozyten/blutgruppen-auf-thrombozyten/das-hpa-system-human-platelet-antigen-system/
- Bruhn H D, Schambeck C M, Hach- Wunderle V (2007) Hemostaseologie für die Praxis: Sicher durch den klinischen Alltag. Schattauer GmbH Stuttgart 375 - 376
- Bussel J B, Vander Haar E L, Berkowitz R L (2021) New developments in fetal and neonatal alloimmune thrombocytopenia. Am J Obstet Gynecol. 225 (2) 120 - 127
- Herold G et al (2021) Internal medicine. Herold Publishing House 146
- Jacobs C (2005) The "human platelet antigen-1" (HPA- 1) polymorphism does not influence the effects of glycoprotein IIb / IIIa inhibitors. Dissertation for the degree of Doctor of Medicine of the Medical Faculty of the Heinrich Heine University Düsseldorf
- Karges W, Al Dahouk S (2009) Internal medicine ... in 5 days. Springer Medizin Verlag Heidelberg 293
- Kasper D L, Fauci A S, Hauser S L, Longo D L, Jameson J L, Loscalzo J et al. (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 138 e5
- Ostendorf N, Antwerpes F, Walensi M (2024) Human platelet antigen. DocCheck Flexikon. doi: https://flexikon.doccheck.com/en/Humanes_Pl%C3%A4ttchenantigen
- Schwenzer N, Ehrenfeld M (2000) Surgical basics. Georg Thieme Verlag Stuttgart / New York 211
- Urban E, Liebscher U M, Tonn T (2013) Diagnostics of immunologically induced thrombocytopenia. Hemotherapy 32 - 43 doi: file:///Users/leah/Downloads/beitrag4_haemotherapie_20.pdf