- Last Update On : 2013-01-28
Many antigen systems are present on platelet membranes, including ABO, HLA, and PLA1. Antibodies to platelets may be directed to any of these antigens and may be either alloantibodies or autoimmune antibodies. Alloantibodies are antibodies that a person makes against foreign antigens, usually after transfusion or pregnancy. Autoantibodies are formed against a person's own platelets. This can occur as a primary disorder, such as idiopathic thrombocytopenic purpura (ITP) or secondary to other diseases, such as lymphoma. Both allo and autoantibodies can cause thrombocytopenia. Tests for platelet antibodies are useful in the following clinical situations:
- Platelet refractoriness after multiple transfusions
- Post-transfusion purpura
- Neonatal isoimmune purpura
- Drug induced platelet antibodies
- Idiopathic thrombocytopenic purpura (ITP)
Multiply transfused patients, who become refractory to random donor platelet transfusions, usually have platelet alloantibodies. This can be confirmed by testing their serum for platelet antibodies. If antibody is demonstrated, crossmatch compatible single donor platelets should be considered for future platelet transfusions.
Post-transfusion purpura is a rare cause of thrombocytopenia that occurs approximately one week after a blood transfusion. It is due to the formation of platelet specific alloantibodies, which destroy the transfused platelets as well as the patient's own platelets. The platelet antibody can be detected in the patient's serum.
Neonatal isoimmune thrombocytopenia arises in the neonate as a result of the transplacental passage of maternal alloantibodies directed to paternal platelet antigens carried by the platelets of the fetus. This disorder causes thrombocytopenia in about 1 in 10,000 neonates. Platelet antibody can be detected in the serum of both the mother and neonate. It can also be detected in fetal blood obtained by periumbilical blood sampling. The antibody reacts against paternal platelets, neonatal or fetal platelets, and 90% of random donor platelets. It does not react with maternal platelets.
Many drugs can also cause an immune thrombocytopenia. The two most common drugs are heparin and quinidine. Drug induced platelet antibodies can be confirmed by demonstrating that patient's serum contains antibody that reacts with platelets in the presence, but not the absence, of the offending drug.
In recent years, the diagnosis of ITP has been based on history, physical examination, CBC, peripheral smear exam, and exclusion of other causes of thrombocytopenia. This approach has been recommended by the American Society of Hematology, which stated that other diagnostic tests (including platelet antibody assays) are generally unnecessary, unless atypical findings are present suggesting other etiologies. Several studies have indicated that platelet antibody testing is useful in the diagnosis of ITP, and may be associated with disease severity, nonetheless the clinical utility of platelet antibody tests has remained controversial.
A recent prospective study analyzed the association between the presence or absence of platelet antibodies and the clinical course of ITP (Blood, 2004;103:4562). Fifty consecutive adult patients with ITP (both acute and chronic) were tested, using a modified ELISA assay for detection of serum autoantibodies against specific platelet glycoproteins (GP IIb/IIIa, GP Ib/IX, and GPIa/IIa). Fifty percent of the patients had detectable antibody and the other 50% did not. Patients were followed clinically for at least 6 months, and monitored for evidence of clinical worsening, defined as the need for starting or modifying therapy because of platelet counts lower than 10,000/uL, or admission for bleeding.
Antibody-negative patients had a significantly lower incidence of clinical worsening (32%) compared with antibody-positive patients (72%). The degree of thrombocytopenia and duration of disease also affect the outcome in ITP, however the relationship of detectable platelet antibody to incidence of clinical worsening also existed for patients with moderate to severe ITP (platelet count < 50 X 103 /uL), and duration of disease greater than 6 months (chronic ITP). The median time to clinical worsening was 2.1 months for antibody-positive and 27.7 months for antibody-negative patients. Specificity of antibodies did not correlate with clinical outcome. In conclusion, this study provides evidence that the presence of platelet antibodies in patients with ITP may be a useful prognostic indicator.
Results are reported as negative or positive. The reference value is negative.
Specimen requirement for serum platelet antibody testing is one plain red top tube of clotted blood. Two yellow top (ACD) tubes or two lavender top (EDTA) tubes of blood are required for platelet associated IgG testing. If drug induced platelet antibodies, a sample of the suspected drug should accompany the specimen.