CHROMOGENIC FACTOR X ASSAYS vs the PT/INR TO MONITOR SUBJECTS ON COUMADIN THERAPY WHEN AN INDIVIDUAL APPROACH IS NECESSARY
Posted on: June 28, 2022
INTRODUCTION
In a previous CLOT CLUB blog post I discussed how chromogenic factor X assays (CFX) were more accurate and less likely to be influenced in certain instances than using the prothrombin time/international ratio assay (PT/INR)1. The PT/INR may be falsely elevated in the presence of lupus anticoagulants (LA), direct thrombin inhibitors (DTI), and dysfibrinogenemia. The PT/INR can give vastly different results between different reagent/instrument combinations from different laboratories.2
Presence of LA can cause a falsely elevated INR depending on the thromboplastin used or whether the instrument is a mechanical or photo-optic coagulation analyzer. The DTIs may falsely elevate the INR as well. Dysfibrinogenemia can also cause inaccurately elevated PT/INR results on a photo-optic system.2
The CFX assay has been proposed as an alternative when PT/INR is unreliable, such as when encountering LAs, DTIs and dysfibrinogenemia in adult subjects. The CFX method is specific for the most stable of the factors influenced by coumadin (FII, FVII, FIX, and FX). Therefore, low levels in other factors could influence the PT/INR. Only FX would be measured and used to monitor subjects on oral anticoagulant therapy (OAT). Interfering substances that would influence the CFX include lipemic, icteric, elevated bilirubin or hemolyzed specimens.
We would like to discuss a specific case where the CFX was imperative in monitoring a pediatric patient on long term coumadin anticoagulation with a mechanical prosthetic mitral valve.3
CASE HISTORY
The anticoagulation of a young child with a mechanical heart valve replacement requires, under current guidelines, oral anticoagulation using coumadin. The direct oral anticoagulants (DOACs) and heparinoids are not currently approved for mechanical heart valve anticoagulant therapy. These subjects require lifelong adjusted anticoagulant medication with constant monitoring. As the pediatric patients age the anticoagulation has to reflect constant changes in all aspects for medical state and dietary intake. They are at constant risk for bleeding and thrombosis. The PT/INR results can be falsely low.
The case we reference experienced acute valvular thrombosis even though the patient was receiving a coumadin dose that should have yielded an INR result that would be in the therapeutic range. Patients with this medical situation that require a replacement of the atrio-ventricular valve (AVV) require a recommended INR range of 2.5-3.5.4 The subject had INR values for two months between 2.0-4.7. The patient started showing symptoms of abdominal pain, distended abdomen, vomiting, and decreased urine output. No indication of infection was present. Most of the INR values were in the therapeutic range with some subtherapeutic and one supratherapeutic level. Bivalirudin, a direct thrombin inhibitor, was administered to try to stabilize the thrombotic issues, the symptoms only worsened.
A coagulation work-up was initiated to determine if a coagulopathy was present. PT and APTT values were elevated, however the Factor V was normal and a liver function problem was ruled out. The CFX level was 47% activity which corresponded to an INR level of 2.2 which was subtherapeutic. To solve this issue and get the subject into the proper dosing regimen, the CFX assay was employed. The Hematology service recommended that the coumadin dosing be adjusted to give a CFX range of 20-30% activity to get an equivalent INR range of 3.0-4.0. After achieving the recommended target range the patient was monitored for 12 months. An echo-cardiography exam displayed excellent AVV function and no incidences of thrombotic issues with no hemorrhaging evident.
DISCUSSION
In this case report it was noted that the health team never discovered the reason for the inability to achieve a therapeutic range for this pediatric patient with the AVV issue using the PT/INR method. This put the patient at risk because they were not properly anticoagulated. After using the CFX method, they were able to achieve a proper level of anticoagulation.
The CFX method cuts out the in vitro pathways that can interfere with the INR causing falsely elevated or in some cases decreased values. Using the CFX method, the coagulation service can overcome the presence of LAs, DTI interference, and dysfibrinogenemia presence. Therefore, the CFX method can be used in individual subjects where the INR is unreliable.
Universal CFX ranges for equivalent INR therapeutic ranges have not yet been established However several excellent studies have been accomplished. Greenmyer et al3 in 2021 used prior suggested ranges for CFX that correlated with therapeutic INR ranges.3 In 2005 Arpino et al predicted the CFX assay to predict the INR in 62 patients who were being switched to coumadin from agatroban. They predicted that a CFX level of 45% or less was a cutoff point for an INR of greater than 2.0.5 In 2008 McGlasson et al conducted a much larger study using 339 specimens to evaluate the CFX vs the INR for monitoring subjects on OAT. Their findings concluded that the therapeutic range of 2.0-3.0 gave a CFX range of 23.5 to 35.5%. A supratherapeutic INR of greater than 3.0 correlated with a CFX level of 20.8%. In the patient described in this paper an INR of 2.2 corresponded to a CFX level of 47% which correlated to the range found in the McGlasson study.6 Their subject required a CFX level of 35% to get an INR of 3.5.
OPINIONS
We have to wonder why do we go to all of the trouble to use the PT/ INR to monitor subjects on OAT? Why doesn’t the laboratory cut out the “middle man” and propose that we use the CFX method much like we use the anti-FXa chromogenic method to monitor subjects on the heparinoids and also the DOACs. The lab can still use the PT/INR to screen subjects who are not on coumadin or for one stage factor assays of the extrinsic system of the coagulation cascade (FII, FV, FVII, FX). The laboratory could theoretically use the CFX much like we do the chromogenic factor assays for FVIII and FIX. Then we don’t have to worry about a number of interfering substances except the pre-analytical variables such as elevated bilirubin, hemolysis and lipemia. The lab could set-up the CFX like the anti-FXa tests and compare to the clotting corresponding method to establish ranges to determine time in range for therapeutic levels. Food for thought.
REFERENCES:
- https://diapharma.com/news-and-events/the-chromogenic-factor-x-assay-cfx/. The Chromogenic Factor X assay.
- McGlasson DL. Laboratory Variables That May Affect Test Results in Prothrombin Times (PT)/International Normalized Ratios (INR). Lab Med Feb 2003(2) 34:124-129.
- Greenmyer JR et al: Chromogenic Factor X Assay for Monitoring Warfarin anticoagulation in a Child with a Prosthetic Mitral Valve. Case Reports Mayo Clin Proc Innov Qual Outcomes 2021.5(5):811-816.https://pubmed.ncbi.nlm.nih.gov/34430797/
- Nishimura Pa et al: American College of Cardiology/American Cardiology/American Heart Association. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Thoroc Cardiovasc Surg 2014;148(1) elel32.
- Arpino PA, Demirijan Z, Van Cott EM. Use of the chromogenic factor X assay to predict the International normalized ratio in patients transitioning from argatroban to warfarin. Pharmacotherapy 2005;25(2):157-64.
- McGlasson DL, Romick BG, Rubal BJ. Comparison of a chromogenic factor X assay with international normalized ratio for monitoring oral anticoagulation therapy. Blood Coagulation and Fibrinolysis 2008, 19:513-517.
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