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Editorials |

Lessening the Punch of Heparin-Induced Thrombocytopenia

James P. Maloney, MD
Author and Funding Information

Affiliations: Milwaukee, WI
 ,  Dr. Maloney is Assistant Professor, Division of Pulmonary and Critical Medicine, Medical College of Wisconsin.

Correspondence to: James P. Maloney, MD, Division of Pulmonary and Critical Care Medicine, Medical College of Wisconsin, 9200 W Wisconsin Ave, Milwaukee, WI 53226;



Chest. 2002;122(1):5-6. doi:10.1378/chest.122.1.5
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While bleeding remains the most common serious complication of heparin use, heparin is also a common cause of drug-related thrombocytopenia.1 Heparin-induced thrombocytopenia (HIT) occurs either as an acute, transient, and innocuous phenomenon due to nonimmunologic heparin effects (type I HIT), or as a morbid syndrome that usually occurs after a week of heparin therapy and is associated with platelet activation and a high rate of thromboembolism (type II, commonly termed “HIT”).2 Heparin-associated thrombocytopenia and heparin-associated thrombocytopenia with thrombosis are older classifications now folded into the rubric HIT. Thrombocytopenia usually denotes < 100 × 109 platelets per liter. HIT often is described in the context of antiheparin antibodies in patients with > 100 × 109 platelets per liter, if they have a falling platelet count and/or thrombotic events. A decrease in platelets during illness is usually not due to concomitant heparin therapy.3 Sepsis, disseminated intravascular coagulation, bone marrow suppression by drugs or illness, hypersplenism, or platelet consumption from pulmonary embolism, cardiac bypass, and orthopedic surgery can all decrease platelet counts acutely.4 HIT has a relatively low incidence of 1 to 3% in patients treated with unfractionated heparin (UFH). When do we need to suspect HIT? In this issue of CHEST (see page 37), we are provided with a study that increases our diagnostic accuracy of HIT.

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