Platelet Antibodies

General

Synonym/Acronym:
antiplatelet antibody.

Rationale
To assess for the presence of platelet antibodies to assist in diagnosing thrombocytopenia related to autoimmune conditions and platelet transfusion compatibility issues.

Patient Preparation
There are no food, fluid, activity, or medication restrictions unless by medical direction.

Normal Findings
(Method: Enzyme-linked immunoassay) No platelet antibodies detected.

Critical Findings and Potential Interventions
N/A

Overview

(Study type: Blood collected in a red-top tube for indirect immunoglobulin G [IgG] antibody; related body system: Circulatory/hematopoietic and immune systems.)

Platelet autoantibodies are immunoglobulins of autoimmune origin (i.e., immunoglobulin G [IgG]), and they are present in various autoimmune disorders, including thrombocytopenias. Platelet antibodies can be formed by primary (idiopathic) or secondary (related to an underlying condition) responses. Drug interactions are an example of a primary immune response where a person develops autoantibodies against their own platelets. Although many medications are associated with development of platelet antibodies, heparin is at the top of the list, along with quinine and sulfa drugs. There are two types of heparin-induced thrombocytopenia (HIT): type I and type II. For additional information regarding HIT, refer to the study titled “Platelet Count and Tests of Platelet Function.”

Platelet alloantibodies are another example of a primary immune response. In one type of situation, the immune reaction develops in recipients of transfusion who become sensitized to donor platelet antigens in transfused blood products. As a result, destruction of both donor and recipient platelets occurs in the transfusion recipient. Alloantibodies can also form in response to an incompatibility between fetal and biological mother’s platelets. The patient develops alloantibodies to fetal platelets, when the patient’s antibodies cross the placenta, the immune response results in a potentially life-threatening fetal or neonatal thrombocytopenia.

The relationship between underlying diseases and thrombocytopenia is complex, and the exact mechanisms are not completely understood. Examples of testing for secondary immune responses associated with development of platelet antibodies include direct and indirect testing. The indirect immunoassay is a screening tool that detects both autoantibodies and alloantibodies but does not specifically identify either type. Testing for fetal alloantibodies should be performed on a blood sample from the biological mother due to the immaturity of the fetal immune system that may produce false-negative findings. Direct platelet antibody test methods have been developed and are performed in specialty reference laboratories (e.g., the American Red Cross National Reference Laboratory for Platelet Serology, Versiti Blood Centers) to perform platelet typing (which makes it possible to identify compatible platelets for treatment of conditions such as aplastic anemia, cancer, or platelet transfusion refractiveness) and to diagnose specific primary immune response conditions.

Indications

  • Assist in the detection of platelet alloimmune disorders.
  • Determine platelet type for refractory patients.

Interfering Factors

  • There are many drugs and other substances that may induce immune thrombocytopenia (production of antibodies that destroy platelets in response to the drugs). The most common include acetaminophen, gold salts, heparin (type II HIT), oral diabetic medications, penicillin, quinidine, quinine, salicylates, sulfonamides, and sulfonylurea.
  • There are many drugs and other substances that may induce nonimmune thrombocytopenia (effect of the drug includes bone marrow suppression or nonimmune platelet destruction). The most common include anticancer medications (e.g., bleomycin), ethanol, heparin (type I HIT), procarbazine, protamine, ristocetin, thiazide, and valproic acid.

Other Considerations:

  • Hemolyzed or clotted specimens will affect results.

Potential Medical Diagnosis: Clinical Significance of Results

Increased in

Development of platelet antibodies associated with autoimmune conditions and medications.

Idiopathic (primary) causes of increased antibody-associated platelet destruction

  • Drug-induced thrombocytopenia provoked by medications (listed under Interfering Substances)
  • Idiopathic thrombocytopenic purpura (ITP) (related to development of platelet-associated IgG antibodies)
  • Neonatal immune thrombocytopenia (alloimmune thrombocytopenia related to patient’s platelet–associated antibodies directed against fetal platelets)
  • Posttransfusion purpura (alloimmune thrombocytopenia related in most cases to sensitization to PLA1 antigens on donor red blood cells that will stimulate formation of antiplatelet antibodies)
  • Multiple platelet transfusions where refractoriness to further treatment develops (related to development of antibodies against human leukocyte antigen [HLA] and/or platelet alloantigens; requiring platelet typing for further treatment)

Secondary causes of increased antibody-associated platelet destruction related to an underlying disease

  • Immune complex diseases (e.g., rheumatoid arthritis, systemic lupus erythematosus (related to vascular injury and inflammation caused by the antigen–antibody complexes and in some cases is related to medications used therapeutically)
  • Lymphoproliferative diseases (e.g., leukemias, lymphomas, multiple myeloma)
  • Paroxysmal hemoglobinuria (severe) (related to bone marrow dysfunction that results in pancytopenia)
  • Viral infections (e.g., thrombocytopenia associated cytomegalovirus, Epstein-Barr virus, hantavirus, hepatitis B virus, herpes viruses, HIV, varicella zoster, severe acute respiratory syndrome, and coronavirus) (immune viral response is multifactorial and generally increases consumption of platelets; in some cases, a decrease in platelet count is related to medications used therapeutically)

Decreased in

N/A

Nursing Implications, Nursing Process, Clinical Judgement

Before the Study: Planning and Implementation


Teaching the Patient What to Expect

  • Explain that a blood sample is needed for the test.
  • Discuss how this test can assist in evaluating for platelet transfusion compatibility or immune-related causes of decreased platelet counts.

Potential Nursing Actions

  • Observe for symptoms of altered coagulation such as bruising, bleeding gums, or blood in urine, sputum, or stool. Discuss transfusion reaction symptoms: fever, chills, itching, wheezing, lung injury with difficulty breathing, edema.

Safety Considerations

  • Bleeding precautions may be necessary if there is a known or suspected coagulation problem.

After the Study: Implementation & Evaluation Potential Nursing Actions


Treatment Considerations

  • Interventions/actions include the following: Note patient response to ordered platelet transfusions. Explain to those with a bleeding disorder the importance of taking precautions against bruising and bleeding. Emphasize reporting severe bruising or bleeding from any areas of the skin or mucous membranes. Provide education for bleeding precautions, including the use of a soft-bristle toothbrush and electric razor, and avoidance of constipation, intramuscular injections, and acetylsalicylic acid (and similar products).

Clinical Judgement

  • Consider ways to provide education that will decrease concerns regarding the negative effects of blood and blood product transfusion.

Followup Evaluation and Desired Outcomes

  • Acknowledges that depending on the results of this procedure, additional testing may be performed to evaluate or monitor progression of the disease process and determine the need for a change in therapy including referral to another health-care provider.

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