Platelet Antibody

Platelets Antibody test is used to evaluate Thrombocytopenia and exclude an immune-associated etiology.


Immune-mediated destruction of platelets may be caused by either autoantibodies directed against antigens located on the same person’s platelets or alloantibodies that develop after exposure to transfused platelets received from a donor. These antibodies are usually directed to an antigen on the platelet membrane, such as human leukocyte antigen (HLA) or platelet-specific antigen (e.g., PLA1, PLA2). Many different laboratory techniques can be used to demonstrate the antiplatelet antibodies. These tests can directly identify the immunoglobulin with the use of radioimmunoassay (RIA) or immunofluorescence. Quantitative measurements are possible with cytofluorometry. Other tests identify complement binding on the affected platelet membrane. Most antiplatelet antibody testing is now performed using immunologic assays.


Antibodies directed to platelets will cause early destruction of the platelets and subsequent thrombocytopenia. Immunologic thrombocytopenia includes the following:

  1. Idiopathic thrombocytopenia purpura (ITP) is a term that describes a group of disorders characterized by immune-mediated destruction of the platelets within the spleen or other reticuloendothelial organs. Platelet-associated immunoglobulin (Ig) G antibodies are detected in 90% of these patients.
  2. Posttransfusion purpura is a rare syndrome characterized by the sudden onset of severe thrombocytopenia a few hours to a few days after transfusion of red blood cells (RBCs) or platelets. This is usually associated with an antibody to AB, B, and O (ABO), HLA, or PLA antigens on the RBC. In most situations the blood recipient has previously been sensitized to a PLA1 antigen during previous transfusions or during previous pregnancy. Once these antibodies form, they destroy the donor’s PLA1-positive platelets and the recipient’s PLA-negative platelets.
  3. Maternal-fetal platelet antigen incompatibility (neonatal thrombocytopenia) occurs when the fetal platelet contains a PLA1 antigen that is absent in the mother. Just like Rh RBC incompatibility, the mother creates anti-PLA1 antibodies that cross the placenta and destroy the fetal platelets. The mother is not thrombocytopenic. Neonatal thrombocytopenia can also occur if the mother has ITP autoantibodies that are passed through the placenta and destroy the fetal platelets.
  4. Drug-induced thrombocytopenia. While a host of drugs are known to induce autoimmune-mediated thrombocytopenia, heparin is the most common and causes heparin-induced thrombocytopenia (HIT). There are two types of HIT, type I and II, that may develop. Type I HIT is generally considered a benign condition and is not antibody mediated. In type II HIT, thrombocytopenia is usually more severe and is antibody mediated. Type II HIT is caused by an IgG antibody and usually occurs after 6 to 8 days of intravenous heparin therapy. Although platelet counts may be low, bleeding is unusual. Rather, paradoxical thromboembolism is the most worrisome complication and may be attributable to platelet activation caused by the anti–H-PF4 antibody complex instigating platelet aggregation.
    HIT occurs in about 1% to 5% of patients taking heparin for 5 to 10 days, and heparin-induced thrombosis occurs in one third to one half of these patients. Cessation of heparin is mandatory, and alternative anticoagulation is initiated. The diagnosis is suspected based on clinical symptoms, recent heparin administration, and low platelet counts. The diagnosis is confirmed by identifying heparin-induced thrombocytopenia antibodies (HIPA). This test uses an enzyme-linked immunosorbent assay to detect HIT-specific antibodies to heparin-PF4 complex. This assay can detect IgG, IgM, and IgA antibodies, and has a sensitivity of approximately 80% to 90%.
    Other drugs known to cause antiplatelet antibodies include cimetidine, analgesics (salicylates, acetaminophen), antibiotics (cephalosporins, penicillin derivatives, sulfonamides), quinidine-like drugs, diuretics (e.g., chlorothiazide), and others (e.g., digoxin, propylthiouracil, disulfiram [Antabuse]).




Causes of Platelet Antibody Positive Findings:

As discussed earlier, Positive Results can be caused by:

  • Immune Thrombocytopenia.
  • Idiopathic Thrombocytopenia Purpura.
  • Neonatal Thrombocytopenia.
  • Posttransfusion Purpura.
  • Drug-induced Thrombocytopenia.