Currently, Percent Cell Volume (PCV) is used. That seems rather primitive compared to our knowledge of clotting pathways and advances in cellular and molecular biology. Wouldn't a specific cell or cell type be better? What would you look for that is compatible with current clinical instrumentation?
You may think about testing for the Factor V Leiden (see link) and prothrombin (Factor II) mutations, which are accepted genetic markers to assess the risk of developing thrombosis. Another marker is activated protein C resistance (APCR). APCR can be done on standard instrumentation in the clinical laboratory, while testing fo the mutations is a standard in molecular genetics.
Dear Oviver, you have mantioned genetic factors of thrombophilia (trombosis predisposition),but we should be aware about enviromental risk factors. Inflammation and injury, they can cause finbrinogen elevationand d-dimer increase. Elevation of fibrinogen is a risk factor for thorombosis, D-dimers are markers of coagulation pathway activatian, thus thay reflect prothrombotic state. Do not forgot about other coagulation inhibitors: antithrombin and protein S. Liver disorders can cause defitiency of AT and can favorize thrombosis.
Factor VII deficiency also increase a risk of thrombosis.
Thanks for your answers. Ewa: What can you recommend that is better than PCV?
It depends what kind of patients you have, which symptoms, other risk factors?
There is no single best clinical measurement for risk of thrombosis due to the fact that a patient can develop thrombosis due to a variety of reasons including all the ones previously stated. Once these and other inherited risk factors have been ruled out, the PCV is probably still the best measure for the situation you described. But if you only use PCV or another single test as a risk factor assessment, you may risk missing another underlying condition that could increase the patient's risk of thrombosis. The best clinical measurement of risk of thrombosis is the one that identifies the risk in the patient, and that can vary from patient to patient.
Again, thank you for your answers. Do any of you know of a study where PCV is affected by ingestion of ~ 100 grams of glucose (as in an energy drink) causing the PCV to go up by osmosis / dehydration? I would think it would peak at about 30 minutes as in a glucose tolerance test.
I believe there is NO SINGLE best clinical method for assessing the risk of thrombosis. One has to rely on a battery of tests - the conventional DNA based tests (FVL, Prothrobin mutation), PAI 1 levels, Lupus A, and modern tests like P selectin, vWF, Factor VIII level and CRP and even Microparticle measures.
As you all answered, DVT depends on a variety of factors. Thus is about 60% of a well known etiology of risk factors and environment. Still we have today unknown (idiopathic) causes. Most of you have mentioned genetic disorders as Leiden and G 202 (PT), Protein deficiency (AT, PC, PS) Some about Coagulation factors (VII?). I would add the unexplained elevation of F VIII, FIX and rarely others, and mostly underlying diseases as LEAD, PA, other Chronic diseases as cancers, Hemopathologies and so on. In the case of PV (Vaquez) JAK2 is very important to be verified if positive
I think this should approached in a stepwise manner, the age of the patient, the recurrence and family history may offer valuable clues, then the presence of acquired risk factors (e.g,? Pregnancy or postpartum , postoperative, immobility etc); then And especially In the younger patients anti phospholipid antibodies need to be checked for. As for genetic causes, this depends on the population in question, since in certain populations factor V Leiden and Prothrombin mutations are important risk factors, while in others they are not. The other issue before embarking on expensive genetic testing, is to determine whether a positive test result would alter management decisions, if not then such testing may not be of value. Genetic testing for thrombotic risk factors, maybe considered particularly in young patients with recurrent thrombosis and family history of thrombosis in young relative.
If you are looking for a clinical estimator tool for the risk of thrombosis in the general population, you can try QRISK2 for arterial thrombosis (http://www.qrisk.org/) and QThrombosis for venous thromboembolism (http://www.qthrombosis.org/). For symptomatic patients there is a lot of clinical tools (eg, the Wells score for DVT and for PE). I discourage the use of any lab test to estimate a generic "thrombosis risk" outside a definite clinical scenario.
There is not a sngle measurement that can predict risk.
For surgical patients we have the Caprini score which combines several factors, The Caprini score has been validated in several studies.
A quantitative D-dimer helps me in judging who is at risk. I have patients who have variably elevated levels but don't show an upward trend. Those that show an upward trend in my experience are the ones that are at most risk for an unprovoked event, either arterial or venous. The ones that run high without an upward trend seem to require a second event such as sepsis to get into trouble.
It is such a simple but useful test. I also use it to judge whether anticoagulation is adequately suppressing thrombosis. I use it to tell if an event is new or remote althouth that is most applicable for venous thrombosis.
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