Risk Factors and Long-term Follow-up of Patients with the Immune Type of Heparin-Induced Thrombocytopenia

Abstract

Dispositional risk factors for developing the immune-type of heparin-induced thrombocytopenia (HIT) are yet unclear. This article presents a long-term follow-up of patients with HIT to define possible risk factors that may increase the risk of HIT. The clinical course of acute HIT was analyzed retrospectively in 52 patients with HIT. Thirteen patients died; 8 due to HIT. A follow-up investigation was performed in 28 of the remaining 39 patients 29 +/- 12 months after the onset of HIT, including genotyping for the factor V G1691A- and the prothrombin G20210A-mutation, measurement of antithrombin, protein C, protein S, factor VIII, and factor XII activity as well as the concentration of antiphospholipid antibodies. The results were compared to an age- and sex-matched control group. New thromboembolic events and re-exposure to heparin were also documented. No difference between patients and controls was observed concerning the factor V Leiden mutation, the prothrombin mutation, factor XII, antithrombin, protein S, or protein C deficiency and antiphospholipid antibodies. Increased factor VIII activity was found in 16 of 21 HIT patients compared to 4 of 21 controls (p=0.0005). New thromboembolic events developed in 5 patients within 9 months after HIT. One patient had been re-exposed to heparin 9 months after acute HIT without any complications. Increased factor VIII activity was frequently observed in patients in whom HIT developed. Thromboembolic complications within the first months after onset of HIT occurred often.

Deep-Vein Thrombosis Prophylaxis in Foot and Ankle Surgery

“…In up to 50% of patients, HIT has been reported to lead to DVT, PE, myocardial infarction, stroke, hemorrhage, amputation, or death. 23,24…”

Current Concepts Review: Venous Thromboembolic Disease in Foot and Ankle Surgery

“…In up to 50% of patients, HIT leads to DVT, PE, myocardial infarction, stroke, organ hemorrhage, systemic and extremity ischemia, amputation, or death. 7,47,52,81,82 Acute symptoms of HIT may include fever, chills, tachycardia, hypertension, pulselessness, diaphoresis, abdominal pain, chest pain, dyspnea, and, less commonly, rash or transient global amnesia. 75,83,84 Once recognized, the hallmark of treatment remains immediate cessation of all forms of heparin or heparin derivative products, followed by the use of a rapidly acting anticoagulant other than heparin or any heparin-derived product to reduce thrombin generation and prevent platelet activation.…”

Current Concepts Review: Heparin-Induced Thrombocytopenia

“…21, 67, 93, 94, 106 Although HIT and its associated risk for paradoxical thrombotic disease, limb amputation, and death, represents an example of one of the most severe complications of VTED chemoprophylaxsis, only 15 papers have been published in the English orthopedic literature focusing on this disease. These case reports discuss less than a total of 30 cases, and do not differentiate between Type I and Type II disease, 4,6,7,9,17,20–22,31,40,42,47,56,57,63–68,70,74a,75,76,93,94,106,108,111,114 Collectively, these clinical accounts provide at best for only Level IV evidence on this issue. A meta-analysis of these scattered orthopaedic publications identified an estimated 22% amputation rate, 11% mortality rate, and 33% major complication rate with HIT.…”

“…Interestingly, there is no increased risk for developing HIT in patients with hypercoagulable conditions such as Factor V Leiden, protein C/antithrombin deficiency, and antiphospholipid antibody syndrome. 57…”