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- Circulating Platelet Antibodies
- Indirect Platelet Antibodies
- Platelet Antibodies, Qualitative
Antibodies to HLA class I antigens and platelet-specific glycoproteins IIb/IIIa, Ib/IX, Ia/IIa, and GP-IV.
Screen for the presence of circulating antibodies to platelets (not bound to the platelet surface), that may be associated with the destruction of platelets.
This assay is not designed to detect antibodies associated with heparin-induced thrombocytopenia (HIT), the most common drug-induced immune thrombocytopenia, nor other drug-associated thrombocytopenias. Some low titer, low avidity antibodies may not be detected using this assay.
Solid-phase enzyme-linked immunoassay
Platelet antibodies can be autoimmune (directed against endogenous, i.e., the patient's own platelet antigens) or alloimmune (directed against antigens on exogenous platelets encountered through pregnancy or transfusion). Platelet antibodies may be directed to a number of antigenic “targets” carried on platelet cytoplasmic membranes.1-6 This platelet antibody profile is designed to detect antibodies to HLA class I and platelet glycoprotein IV (CD36) antigens, and to polymorphic epitopes on the platelet GPs IIb/IIIa, Ib/IX, and Ia/IIa.4 Platelet glycoprotein (GP) IV antigen deficiency is rare in Caucasians but frequent in Asians and Africans.4,7,8 The IIb/IIIa glycoprotein complex plays a central role in platelet adhesion by binding fibrinogen, fibronectin, vitronectin, and von Willebrand factor.2 Glycoprotein Ib/IX is the main receptor for von Willebrand factor and glycoprotein Ia/IIa is involved in collagen adhesion.2 The congenital absence of IIb/IIIa results in Glanzmann thrombasthenia and the absence of Ib/IX causes Bernard-Soulier syndrome.
Platelet antibodies may be involved in several clinical situations described below3,9:
Immune Thrombocytopenic Purpura (ITP), formerly referred to as idiopathic thrombocytopenic purpura, occurs when platelet autoantibodies with broad reactivity against common epitopes on platelet glycoprotein complexes destroy an individual's platelets and result in a persistent thrombocytopenia.3,9-11 Antiplatelet autoantibodies also are thought to impair platelet production by megakaryocytes.9,12,13 ITP in children often can be associated to a transient viral infection. Approximately 15% of childhood ITP cases become chronic.2 ITP in adults often has an insidious onset, resulting in chronic thrombocytopenia that rarely remits spontaneously.1,2 This condition can be idiopathic, or in some cases, associated with another autoimmune condition (e.g., SLE) or malignancy.1 The majority of autoantibodies identified in patients with ITP are directed against components of platelet glycoprotein IIb/IIIa. Antibodies to glycoprotein Ib/IX also are observed. Some authors have found that identification of platelet associated antibodies has prognostic significance in ITP and can help in understanding the underlying mechanism of thrombocytopenia.14-16 According to the American Society for Hematology practice guideline, routine evaluation for platelet reactive antibodies in the evaluation of ITP is not recommended while testing for HIV and HCV should be considered in all patients with acute ITP.11
Neonatal alloimmune thrombocytopenia (NAIT) typically occurs when fetal platelets have an antigen from the father that is absent in the mother.1,5,17 In this condition, which can be considered to be the platelet equivalent of hemolytic disease of the newborn (HDN), maternal antibodies cross the placenta and destroy fetal platelets. This condition occurs in 1 in 1200 live births in the Caucasian population, and unlike HDN, frequently occurs during the first pregnancy.1,2 Affected infants may have severe thrombocytopenia and are at increased risk for intracranial bleeding.1,18 As a component of the work-up, diagnostic testing of the mother's blood is performed for the presence of platelet antibody. Evaluation should also include typing maternal and paternal platelet glycoproteins. In Caucasians, 80% of NAIT is caused by alloimmunization to HPA-1a (a component of platelet glycoprotein IIb/IIIa) in HPA-1a-negative mothers.5 Other antigens, including HPA 2, 3, 4, 5, and 15, are less frequently implicated.18,19 The majority of platelet reactive antibodies identified in patients with NAIT are directed against components of platelet glycoprotein IIb/IIIa, most commonly HPA-1a.1 Antibodies to HPA-5b (detected as anti-Ia/IIa) are frequently observed in pregnancy but tend to be associated with milder thrombocytopenia.1 Antibodies to HLA also have been associated with NAIT.1 Platelet antigen incompatibility is necessary but not sufficient to cause NAIT.18 Neonatal serum or plasma samples are less sensitive for circulating antibody detection than maternal samples since the antibodies may be attached to platelets or cleared.
Post-transfusion purpura (PTP) is a rare condition where a patient suffers from an acute episode of severe immune-mediated thrombocytopenia that occurs 5 to 14 days after a platelet-containing transfusion.1,2,20,21 The patient's own platelets also are destroyed along with transfused platelets, a phenomenon thought to be caused by panreactive platelet reactive antibodies.20,22 Antigen sensitization can frequently be traced to exposure to exogenous platelet antigen either through pregnancy or previous transfusion. Like NAIT, the majority of autoantibodies identified in patients with PTP are directed against components of platelet glycoprotein IIb/IIIa, most commonly HPA-1a.1,2
Platelet transfusion refractoriness is a condition characterized by the lack of expected platelet count increment after a platelet transfusion.1 As many as 70% of patients receiving multiple platelet transfusions for thrombocytopenia will exhibit some degree of refractoriness.1,23 This condition is most common in patients treated for malignant hematopoietic disorders.1 While platelet antibody production can cause platelet refractoriness, other potential causes include sepsis, disseminated intravascular coagulation (DIC), or drug-induced thrombocytopenia. Immune-mediated platelet refractoriness is most commonly caused by antibodies to HLA antigens but has also been observed in association with antibodies to platelet-specific antigens.1,2,23-25
Red-top tube or gel-barrier tube
Separate serum from red cells. Transfer serum to a plastic transport tube.
Refrigerate for up to 48 hours, freeze if longer storage is needed.
Causes for Rejection
Hemolysis; serum not separated from cells
If a newborn child has a significantly low platelet count and the physician suspects neonatal alloimmune thrombocytopenia purpura (NAIT), a serum platelet antibody test should be ordered on both the mother and the child (patient). The work-up for NAIT is best accomplished by not only evaluation for platelet reactive antibodies, but also typing maternal and paternal platelet glycoproteins.
- 1. Roback JD, Grossman BJ, Harris T, et al, eds. American Association of Blood Banks. Technical Manual. 17th ed. Bethesda, Md: AABB Press; 2011.
- 2. Norton A, Allen DL, Murphy MF. Review: Platelet alloantigens and antibodies and their clinical significance. Immunohematology. 2004;20(2):89-102.15373657
- 3. Lochowicz A, Curtis B. Clinical applications of platelet antibody and antigen testing. Lab Med. 2011;42:687-692.
- 4. Hayashi T, Hirayama F. Advances in alloimmune thrombocytopenia: perspectives on current concepts of human platelet antigens, antibody detection strategies, and genotyping. Blood Transfus. 2015;13(3):380-390.26057488
- 5. Peterson JA, McFarland JG, Curtis BR, Aster RH. Neonatal alloimmune thrombocytopenia: pathogenesis, diagnosis and management. Br J Haematol. 2013 Apr;161(1):3-14.23384054
- 6. Metcalfe P, Watkins NA, Ouwehand WH, et al. Nomenclature of human platelet antigens. Vox Sang. 2003 Oct;85(3):240–245.14516468
- 7. Curtis BR, Ali S, Glazier AM, Ebert DD, Aitman TJ, Aster RH. Isoimmunization against CD36 (glycoprotein IV): description of four cases of neonatal isoimmune thrombocytopenia and brief review of the literature. Transfusion. 2002 Sep;42(9):1173-1179.12430674
- 8. Lee K, Godeau B, Fromont P, et al. CD36 deficiency is frequent and can cause platelet immunization in Africans. Transfusion. 1999 Aug;39(8):873-879.10504124
- 9. McMillan R. Antiplatelet antibodies in chronic immune thrombocytopenia and their role in platelet destruction and defective platelet production. Hematol Oncol Clin North Am. 2009 Dec;23(6):1163-1175.19932426
- 10. Davoren A, Bussel J, Curtis BR, Moghaddam M, Aster RH, McFarland JG. Prospective evaluation of a new platelet glycoprotein (GP)-specific assay (PakAuto) in the diagnosis of autoimmune thrombocytopenia (AITP). Am J Hematol. 2005 Mar;78(3):193–197.15726595
- 11. Neunert C, Lim W, Crowther M, et al. The American society of hematology 2011 evidence-based practice guideline for immune thrombocytopenia. Blood. 2011. Apr 21;117(16):4190-4207.21325604
- 12. Iraqi M, Perdomo J, Yan F, Choi PY, Chong BH. Immune thrombocytopenia: antiplatelet autoantibodies inhibit proplatelet formation by megakaryocytes and impair platelet production in vitro. Haematologica. 2015 May;100(5):623-632.25682608
- 13. Nugent D, McMillan R, Nichol JL, Slichter SJ. Pathogenesis of chronic immune thrombocytopenia: increased platelet destruction and/or decreased platelet production. Br J Haematol. 2009 Sep;146(6):585-596.19466980
- 14. Fabris F, Scandellari R, Ruzzon E, Randi ML, Luzzatto G, Girolami A. Platelet-associated autoantibodies as detected by a solid-phase modified antigen capture ELISA test (MACE) are a useful prognostic factor in idiopathic thrombocytopenic purpura. Blood. 2004 Jun 15;103(12):4562-4564.14976036
- 15. Go RS, Johnston KL, Bruden KC. The association between platelet autoantibody specificity and response to intravenous immunoglobulin G in the treatment of patients with immune thrombocytopenia. Haematologica. 2007 Feb;92(2):283-284.17296593
- 16. Cantoni S, Carpenedo M, Nichelatti M, et al. Clinical relevance of antiplatelet antibodies and the hepatic clearance of platelets in patients with immune thrombocytopenia. Blood. 2016 Oct 27;128(17):2183-2185.27601463
- 17. Bussel JB, Sola-Visner M. Current approaches to the evaluation and management of the fetus and neonate with immune thrombocytopenia. Semin Perinatol. 2009 Feb;33(1):35-42.19167580
- 18. Arnold DM, Smith JW, Kelton JG. Diagnosis and management of neonatal alloimmune thrombocytopenia. Transfus Med Rev. 2008 Oct;22(4):255-267.18848153
- 19. Glade-Bender J, McFarland JG, Kaplan C, Porcelijn L, Bussel JB. Anti-HPA-3A induces severe neonatal alloimmune thrombocytopenia. J Pediatr. 2001 Jun;138(6):862-867.11391330
- 20. Taaning E, Tonnesen F. Pan-reactive platelet antibodies in post-transfusion purpura. Vox Sang. 1999;76(2):120-123.10085529
- 21. Shtalrid M, Shvidel L, Vorst E, Weinmann EE, Berrebi A, Sigler E. Post-transfusion purpura: a challenging diagnosis. Isr Med Assoc J. 2006 Oct;8(10):672-674.17125110
- 22. Curtis BR, McFarland JG. Detection and identification of platelet antibodies and antigens in the clinical laboratory. Immunohematology. 2009;25(3):125-135.20406019
- 23. Kiefel V, Konig C, Kroll H, Santoso S. Platelet alloantibodies in transfused patients. Transfusion. 2001 Jun;41(6):766-770.11399817
- 24. Rebulla P. A mini-review on platelet refractoriness. Haematologica. 2005 Feb;90(2):247-253.15710579
- 25. Pavenski K, Freedman J, Semple JW. HLA alloimmunization against platelet transfusions: pathophysiology, significance, preventionand management. Tissue Antigens. 2012 Apr;79(4):237-245.22385314
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|117150||Platelet Antibody Profile||014087||HLA Class 1 Antibody||48501-1|
|117150||Platelet Antibody Profile||014088||IIb/IIIa Antibody||48505-2|
|117150||Platelet Antibody Profile||014089||Ib/IX Antibody||48506-0|
|117150||Platelet Antibody Profile||014090||Ia/IIa Antibody||47084-9|
|117150||Platelet Antibody Profile||117151||Glycoprotein IV Antibody||43302-9|