Heparin-induced thrombocytopenia: an update

Heparin is a drug widely used for thromboprophylaxis or treatment in many clinical situations, including cardiovascular surgery and invasive procedures, acute coronary syndromes, venous thromboembolism, atrial fibrillation, peripheral occlusive disease, dialysis and during extracorporeal circulation [1,2]. However, it can cause serious adverse effects, including heparin-induced thrombocytopenia (HIT) which is a common, serious and potentially life-threatening condition [3-6]. Unfortunately, because thrombocytopenia is common in hospitalized patients and can be caused by a variety of factors [7], HIT often remains unrecognized.Heparin-induced thrombocytopenia is defined as a decrease in platelet count during or shortly following exposure to heparin [8]. Two different types of HIT are recognized. The first, HIT type I (also called heparin-associated thrombocytopenia in the past), is a benign form not associated with an increased risk of thrombosis. The mechanism of HIT type I is still unknown but it is likely to be non-immune, probably related to its platelet pro-aggregating effect. This form of HIT affects up to 10% of patients under treatment with heparin and is characterized by a mild and transient asymptomatic thrombocytopenia (rarely less than 100,000 platelets/μL) that develops early (usually within the first two days of starting heparin) and disappears equally quickly once the heparin is withdrawn. The second form of HIT, HIT type II, is immune-mediated and associated with a risk of thrombosis. It has recently been proposed that the term "HIT type I" be changed to "non-immune heparin associated thrombocytopenia" and that the term "HIT type II" be changed to "HIT" to avoid confusion between the two syndromes [9].In this review we briefly analyze the main characteristics of the clinically relevant, immune-mediated, second type of HIT, focusing particularly on the epidemiology, pathophysiology, clinical manifestations and treatment of this syndrome. For simplicity