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1. DRUG-INDUCED THROMBOCYTOPENIA

The mechanisms underlying drug-induced thrombocytopenia are thought in most cases to be immune, although exceptions exist (such as chemotherapy). Table 14–7 lists medications associated with thrombocytopenia. The typical presentation of drug-induced, antibody-mediated thrombocytopenia is severe thrombocytopenia and mucocutaneous bleeding 5–14 days after exposure to a new drug, although a range of presentations is possible. Discontinuation of the offending agent leads to resolution of thrombocytopenia within 3–7 days in most cases, but recovery kinetics depends on rate of drug clearance, which can be affected by liver and kidney function. Patients with severe thrombocytopenia should be given platelet transfusions with (immune cases only) or without IVIG. The University of Oklahoma Health Sciences center maintains a useful website for drug-induced thrombocytopenia (https://www.ouhsc.edu/platelets/).

Table 14–7.Selected medications causing drug-associated thrombocytopenia.1

2. POSTTRANSFUSION PURPURA

Posttransfusion purpura (PTP) is a rare disorder that features sudden-onset thrombocytopenia in an individual who received transfusion of red cells, platelets, or plasma within 1 week prior to detection of thrombocytopenia. Antibodies against the human platelet antigen PlA1 are detected in most individuals with PTP. Patients with PTP often are either multiparous women or persons who have received transfusions previously. Severe thrombocytopenia and bleeding are typical. Initial treatment consists of administration of IVIG (1 g/kg/day for 2 days), which should be administered as soon as the diagnosis is suspected. Platelets are not indicated unless severe bleeding is present, but if they are to be administered, HLA-matched platelets are preferred. A second course or IVIG, plasma exchange, corticosteroids, TPO-mimetics, or splenectomy may be required in case of refractoriness. PlA1-negative or washed blood products are preferred for subsequent transfusions, but data supporting various treatment options are limited.

3. VON WILLEBRAND DISEASE TYPE 2B

von Willebrand disease (vWD) type 2B leads to chronic, characteristically mild to moderate thrombocytopenia via an abnormal vWF molecule that binds platelets with increased affinity, resulting in aggregation and clearance.

4. PLATELET SEQUESTRATION

One-third of the platelet mass is typically sequestered in the spleen. Splenomegaly, due to a variety of conditions (eTable 14–1), may lead to thrombocytopenia of variable severity. When possible, treatment of the underlying disorder should be pursued, but splenectomy, splenic embolization, or splenic irradiation may be considered in selected cases.

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