Abstract
ABSTRACTHeparin resistance can be defined as high doses of unfractionated heparin (UFH), greater than 35,000 IU/day, required to raise the activated partial thromboplastin time (aPTT) and activated coagulation time (ACT) to within therapeutically desired ranges or the impossibility of doing so. The most common pathology responsible is the deficiency of anti-thrombin III (ATIII) deficiency. Other clinically relevant conditions that can present with heparin resistance are congenital deficiencies; use of high doses of heparin during extracorporeal circulation, use of asparaginase therapy and disseminated intravascular coagulation (DIC). Most of these conditions effect the ATIII levels. Patients are typically identified in an acute phase, when determination of the cause of resistance is challenging. We present a case where a patient presented with suspected heparin resistance in an acute phase of sickness, where timely intervention was able to prevent a potentially fatal situation.Abbreviations: Neuroendocrine tumors (NETs), World health Organization (WHO), Radiation therapy (RT)
Highlights
The primary effect of heparin is through its interaction with anti-thrombin III (ATIII) [1]
The most cost-effective and widely used tests to check for therapeutic levels are activated partial thromboplastin time and activated coagulation time (ACT) [3]
It may be more appropriate to check for plasma concentration of heparin instead, especially if there are concerns of supra-therapeutic levels of heparin and bleeding
Summary
The use of heparin over the past few decades has proven to be a life-saving treatment for many. The anticoagulant effect of ATIII is potentiated by a 1000-fold after its transformation when it is bound to heparin molecule [2] This inactivates thrombin, preventing the conversion of fibrin to fibrinogen, and inactivates activated coagulation factors IX, X, XI and XII. This, does not increase the risk of thrombosis but can result in reporting of falsely low ATIII levels during the treatment phase with heparin. Major surgery has been associated with a fall in ATIII levels with the levels reaching a nadir around postoperative day 3 followed by rise back to normal around day 5 This decrease in the levels combined with the rise in the acute reactants in the blood can be a risk factor for thrombus formation and acquired heparin
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