Platelet function testing: aggregometry and lumiaggregometry.

Abstract

1. George A Fritsma, MS MT(ASCP)[⇑][1] 1. is Associate Professor, University of Alabama at Birmingham, Birmingham AL 1. Address for correspondence: George A. Fritsma MS MT (ASCP), Associate Professor, Pathology and Clinical Laboratory Sciences, University of Alabama at Birmingham, 1705 University Boulevard RMSB 448, Birmingham, AL 35294-1212. (205) 934-1348, (205) 975-7302 (fax). fritsmag{at}uab.edu. Upon completion of this article, the reader will be able to: 1. collect blood specimens for platelet aggregometry. 2. prepare platelet rich plasma for optical aggregometry. 3. recount the history and applications of the bleeding time test. 4. illustrate the principle of platelet aggregometry and lumiaggregometry. 5. apply several platelet aggregation agonists and compare results. 6. identify the cause of platelet deficiency-based hemorrhage through analysis of platelet aggregometry and lumiaggregometry. Platelets are central to primary hemostasis, and platelet disorders manifest themselves with mucocutaneous (systemic) bleeding: petechiae, purpura, epistaxis (nosebleed), hematemesis (vomiting blood), and menorrhagia (uncontrolled menses). The accompanying article by Dr. Larry Brace entitled “Thrombocytopenia” describes the most common conditions in which platelet counts fall to hemorrhagic levels. In “Qualitative Platelet Disorders”, Dr. Brace describes hemorrhagic disorders in which platelet count is normal or mildly reduced but function is compromised. This introductory article describes platelet aggregometry and lumiaggregometry, the current laboratory means for diagnosing platelet disorders. These articles are adapted from chapters 43, 44, and 45 of Rodak BF, Fritsma GA, and Doig K, editors. Hematology: Clinical Principles and Applications, 3rd ed. Philadelphia: Saunders; In press. The textbook is due for publication March, 2007. To determine the cause for mucocutaneous bleeding, a platelet count is performed, and the blood film is reviewed before beginning platelet function tests (see “Thrombocytopenia”).1 Functional platelet abnormalities are suspected when bleeding is present but the platelet count exceeds 50,000/μL (see “Qualitative Platelet Disorders”). Acquired platelet defects are associated with liver disease, renal disease, myeloproliferative disorders, myelodysplastic syndromes, myeloma, and drug therapy. Hereditary platelet functional disorders are less common, but provide models for physiological study. Platelet morphology is often a clue; Bernard-Soulier syndrome is associated with mild thrombocytopenia and large, gray platelets. The presence of large platelets with an elevated mean platelet volume often indicates rapid platelet turnover, such as in immune thrombocytopenic purpura or thrombotic thrombocytopenic purpura. Giant or bizarre platelets are seen in myeloproliferative… ABBREVIATIONS: AA = arachidonic acid; ADP = adenosine diphosphate; ATP = adenosine triphosphate; GP = glycoprotein; NSAID = nonsteroidal anti-inflammatory drug; PAR = protease-activatable receptors; PRP = platelet-rich plasma; VWF = von Willebrand factor. Upon completion of this article, the reader will be able to: 1. collect blood specimens for platelet aggregometry. 2. prepare platelet rich plasma for optical aggregometry. 3. recount the history and applications of the bleeding time test. 4. illustrate the principle of platelet aggregometry and lumiaggregometry. 5. apply several platelet aggregation agonists and compare results. 6. identify the cause of platelet deficiency-based hemorrhage through analysis of platelet aggregometry and lumiaggregometry. [1]: #corresp-1