RT Book, Section A1 Abrams, Charles S. A1 Shattil, Sanford J. A1 Bennett, Joel S. A2 Kaushansky, Kenneth A2 Lichtman, Marshall A. A2 Prchal, Josef T. A2 Levi, Marcel M. A2 Press, Oliver W. A2 Burns, Linda J. A2 Caligiuri, Michael SR Print(0) ID 1121103622 T1 Acquired Qualitative Platelet Disorders T2 Williams Hematology, 9e YR 2015 FD 2015 PB McGraw-Hill Education PP New York, NY SN 9780071833004 LK accessmedicine.mhmedical.com/content.aspx?aid=1121103622 RD 2024/10/04 AB SUMMARYAcquired qualitative platelet disorders are frequent causes of abnormal platelet function measured in vitro, although by themselves are usually associated with little or no clinical bleeding. However, there are important exceptions. Nevertheless, their major clinical impact becomes apparent in the additional presence of thrombocytopenia, or additional acquired or congenital disorders of hemostasis. Acquired disorders of platelet function can be conveniently classified into those that result from drugs, hematologic diseases, and systemic disorders. Drugs are the most frequent cause of acquired qualitative platelet dysfunction. Aspirin is the most notable drug in this regard because of its frequent use, its irreversible effect on platelet prostaglandin synthesis, and its documented effect on hemostatic competency, although this effect is minimal in normal individuals. Other nonsteroidal antiinflammatory drugs reversibly inhibit platelet prostaglandin synthesis and usually have little effect on hemostasis. The antiplatelet effects of a number of drugs have proven useful in preventing arterial thrombosis, but as would be anticipated, excessive bleeding can be a complication of their use. In addition to aspirin, these drugs include the P2Y12 adenosine diphosphate receptor antagonists, clopidogrel, prasugrel and ticagrelor, vorapaxar, an inhibitor of the PAR1 thrombin receptor, and drugs that specifically inhibit adhesive ligand binding to platelet integrin αIIbβ3 (GPIIb/IIIa). Other drugs used to treat thrombosis, such as heparin and fibrinolytic agents, may also impair platelet function in vitro and ex vivo, but the clinical significance of these observations is uncertain. High doses of the β-lactam antibiotics can impair platelet function in vitro, whereas clinically significant bleeding is unusual in the absence of a coexisting hemostatic defect. Similarly, a number of miscellaneous drugs, including a variety of psychotropic, chemotherapeutic and anesthetic agents, as well as a number of foods and food additives, can affect platelet function in vitro, but do not appear to be of clinical significance by themselves. Hematologic diseases associated with abnormal platelet function include marrow processes in which platelets may be intrinsically abnormal such as the myeloproliferative neoplasms, leukemias, and myelodysplastic syndromes; dysproteinemias in which monoclonal immunoglobulins can impair platelet function; and acquired forms of von Willebrand disease. Of the systemic diseases, renal failure is most prominently associated with abnormal platelet function because of the retention in the circulation of platelet inhibitory compounds. Platelet function may also be abnormal in the presence of antiplatelet antibodies, following cardiopulmonary bypass, and in association with liver disease or disseminated intravascular coagulation.