Prevalence and Clinical Predictors of Heparin Induced Thrombocytopenia

Back Ground: Heparin induced thrombocytopenia (HIT) isthrombocytopenia or thrombosis with one or more positivetests for HIT antibodies. To diagnose HIT, platelet countmonitoring; at least every other day until hospital discharge forday 14 (whichever occurs sooner). A platelet count fall of 50%or greater from baseline or any thrombosis occurs 5 to 10 daysafter heparin starting with exclusion or other causes ofthrombocytopenia are highly suggestive of HIT. Laboratoryconfirming assays are helpful as platelet activations assay.Management of HIT includes discontinuing of any type ofheparin and using an alternative anticoagulant as DTIs(liperudin, argatropan, bivalerudin). Warfarin should be delayedpending substantial recovery of the platelet account.Methods: This study was conducted to 100 patients receivingheparin in a variety of clinical settings to assess the prevalenceof HIT trying to identify clinical predictors of such complication.To all these patients platelet count every other day from baseline to day 14 was done then the 4T score system was appliedto all patients.Results: Only 6 patients developed HIT; 4 of them developedthrombosis and 3 patients died in hospital due to thesethromboembolic events. UFH, surgical treatment and firstheparin exposure were the clinical predictors of HIT.Conclusion: HIT is a serious and life threatening complicationof heparin therapy that should be early diagnosed and properlymanaged to prevent its thromboembolic complications.

Establishing the heparin therapeutic range using aPTT and anti-Xa measurements for monitoring unfractionated heparin therapy

BACKGROUND: Unfractionated heparin (UFH) has unstable pharmacokinetics and requires close monitoring. The activated partial thromboplastin time (aPTT) test has been used to monitor UFH therapy for decades in Korea, but its results can be affected by numerous variables. We established an aPTT heparin therapeutic range (HTR) corresponding to therapeutic anti-Xa levels for continuous intravenous UFH administration, and used appropriate monitoring to determine if an adequate dose of UFH was applied. METHODS: A total of 134 ex vivo samples were obtained from 71 patients with a variety of thromboembolisms. All patients received intravenous UFH therapy and were enrolled from June to September 2015 at Gyeongsang National University Hospital. All laboratory protocols were in accordance with the Clinical and Laboratory Standards Institute guidelines and the College of American Pathologist requirements for aPTT HTR. RESULTS: An aPTT range of 87.1 sec to 128.7 sec corresponded to anti-Xa levels of 0.3 IU/mL to 0.7 IU/mL for HTR under our laboratory conditions. Based on their anti-Xa levels, blood specimen distribution were as follows: less than 0.3 IU/mL, 65.7%; 0.3–0.7 IU/mL (therapeutic range), 33.6%; and more than 0.7 IU/mL, 0.7%. No evidence of recurring thromboembolism was observed. CONCLUSION: Using the conventional aPTT target range may lead to inappropriate dosing of UFH. Transitioning from the aPTT test to the anti-Xa assay is required to avoid the laborious validation of the aPTT HTR test, even though the anti-Xa assay is more expensive.