From Yvonne Ellis, Hematology Technical Supervisor, IU Health Bedford Laboratory: George, I counseled a physician today about ordering protein C and S on a patient who has a confirmed pulmonary embolism. I told him during a clot was not the time to test for these. He did seem to have a good understanding of the workings of the regulators. He seemed to think though that if someone normally had low levels of these, that the levels would be markedly decreased during a clot process. I told him there is no established evidence of how much prot C and prot S are decreased in a clot formation. It would be different per person and per clot. Was I correct in this? Have there been studies about this subject?
I enjoy the e-mails I receive from the Fritsma Factor. I teach hematology/coag at a 2 year MLT program and use the text you collaborated on with Prof. Rodak. It is a great text. Thank you for any help.
Hi, Yvonne, and thank you for the textbook plug! We’re glad you find it useful. You are absolutely correct, there is nothing to be gained in measuring protein C or protein S activity during active clotting or two weeks after the presumed discontinuance of a deep venous thrombotic event or a pulmonary embolism. Protein C and S are consumed during the event and are likely to be decreased, but the degree of reduction would depend on the patient’s baseline C and S levels, their liver’s ability to produce new C and S, the physical volume of the clot, and the timing of the event. There are no publications supporting this information because DVT or PE patients are immediately put on anticoagulant therapy, usually a combination of heparin and Coumadin, discontinuing the heparin when the INR becomes stable between 2 and 3. The Coumadin, of course, drives down C and S levels, so they cannot be used clinically until two weeks after the drug is discontinued.
I’m glad your physician is aware of the pitfalls of protein C and protein S assays. We possess four years of unpublished data from a local institution in which about 20% of patients who had thrombosis risk profiles performed were shown to be “protein C and S deficient.” Of course, these were all on Coumadin, but occasionally someone writing in to the ASCLS Consumer Web Forum reports they’ve been told they have both congenital C and S deficiency, a combination that has a likelihood of 1 in ten million. These face the risk of being falsely labeled with thrombophilia, which can affect their insurance eligibility and lifestyle.
Jan 28 2014
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Thrombophilia
As an e?ample: Diagnosis of protein C deficiency in a patien
As an e?ample: Diagnosis of protein C deficiency in a patient with fresh thrombosis may be unreliable; in one study, PC was measured within 24 h and prior to anticoagulation of a confirmed unprovoked VTE, and patients with abnormal PC level were retested following completion of anticoagulant therapy. The authors identified low protein C levels in 10 of the 254 patients on initial testing, but six of these patients
had normal protein C on repeat testing, and three had protein C levels of <0.50 U/mL on initial testing (Kovacs et al., 2006). Guidelines for thrombophilia testing state that testing at the time of acute thrombosis is not indicated as the utility and implications of testing need to be considered and that treatment of acute venous thrombosis is not influenced by test results (Baglin et al., 2010) from:
The phenotypic and genetic assessment of protein C deficiency:
http://onlinelibrary.wiley.com/doi/10.1111/j.1751-553X.2012.01401.x/full