In thrombocytopenic patients, sepsis is the leading cause of TP. Bone marrow aspirates may yield significant information on TP mechanisms and contribute to the subsequent management of patients, especially those with absolute TP.
Heparin-induced thrombocytopenia (HIT) is a prothrombotic and potentially devastating complication of heparin therapy. 1,2 Its pathogenesis is complex, but an accepted distinctive feature is the occurrence of antibodies directed against complexes of chemokines and polyanionic macromolecules (such as PF4-heparin complexes) and targeting platelets, which can be strongly activated. Monocytes, neutrophils, and endothelial cells are also targeted. 3 It is crucial to diagnose HIT as early as possible, but also as reliably as possible to enable appropriate management, while avoiding overdiagnosis with the risks associated with the use of alternative anticoagulation regimens. 4 There are often several potential explanations for thrombocytopenia other than HIT in patients receiving heparin.Laboratory testing for HIT, designed to detect HIT antibodies, also has limitations. 5 Immunoassays are highly sensitive, but show insufficient specificity. 6 Platelet activation assays such as heparininduced (washed) platelet activation test and serotonin release assay (SRA) are more specific than immunoassays but are more demanding and time-consuming, and false-positive, false-negative, and undetermined results are possible. [7][8][9] The results of laboratory testing are combined with a clinical estimate of HIT probability.
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