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Thrombocytopenia is one of the most frequent causes for hematologic consultation in the practice of medicine and may be life threatening. Although the normal platelet count in humans (150–400 × 109/L) far exceeds the minimal level required to avoid pathologic hemorrhage (<50 × 109/L), a number of medical conditions either increasing the destruction of platelets or reducing their production enhance the risk of bleeding. This chapter discusses an approach to the diagnosis of thrombocytopenia, grouping various causes by mechanism of action and describing our current understanding of the pathogenesis, treatment, and prognosis. In the vast majority of patients, a cause of thrombocytopenia can be identified and effective therapy instituted.


Platelets are anucleate blood cells produced in the marrow by polyploid cells termed megakaryocytes and were described in the 19th century after the application of the improved compound microscope allowed these very small cells, 2 μM in diameter, to be identified. Many early investigators are associated with the discovery of blood platelets, including Alfred Donné, Georges Hayem, Guilio Bizzozero, and William Osler, but it was James Homer Wright who in 1906, using his special stain (later called Wright stain), described the morphology of platelets with their central granular area and marginal hyaline zone and established that they were the product of the fragmentation of marrow megakaryocytes. Clot retraction was discovered long before platelets, but Hayem, through a series of studies, showed retraction to be dependent on platelets. During the mid-20th century, the aggregation of platelets, their adherence to collagen of damaged tissues, their acceleration of blood coagulation, and their relationship to the bleeding time and the biochemistry underlying several of these processes were described by scientists, among whom were Paul Owren, Kenneth Brinkhaus, Edwin Chargaff, Ernst Lüsher, Marjorie Zucker, and William Duke.

Platelets circulate in close contact with the endothelium, continually monitoring its integrity. When the vessel wall is damaged, platelets bind to subendothelial proteins, initiating the process of primary hemostasis. At sites of blood loss, the platelets aggregate to form a vessel-sealing plug to halt bleeding. Activated platelets at sites of injury also provide a surface for assembly of coagulation reactions, resulting in the production of fibrin and consolidation of the thrombus. Both qualitative and quantitative deficiencies of the platelets cause bleeding. Platelets also have important functions in inflammation, tissue remodeling, and wound healing.1

Approximately 1 × 1011 platelets are produced per day by an adult human, a number that can be increased 20-fold or more if necessary.2 One-third of the platelets are stored in the spleen, and the remaining two-thirds circulate in blood vessels.3 Disorders that increase splenic volume cause more platelets to be trapped in the spleen, lowering the concentration of circulating platelets, although alone, this redistribution rarely causes a significant bleeding diathesis.

Under normal conditions, human platelets have a mean lifespan ...

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