1. Genomics|Population Research|Health Studies|Protein C And Venous Thrombosis Center for Disease Control s page discussing the background of this disorder including study results, testing, and complications. http://www.cdc.gov/genomics/info/reports/research/protein_c.html

home population research health studies Archived: Aug 1998 Journal Publication This review was published with modifications in Am J Med Sci. 1998 Aug; 316(2): 120-128 The Role of Activated Protein C Resistance in the Pathogenesis of Venous Thrombosis by W. Craig Hooper and Bruce L. Evatt Introduction Pathophysiology APC-R and Factor V Leiden: Clinical Features FV Leiden in Women ... References Introduction Following myocardial infarction and stroke, venous thromboembolism (VTE) is the third most common cardiovascular disease in the United States. The mortality and morbidity of VTE is significant with an annual incidence of approximately 1:1000 individuals and pulmonary embolism is a leading cause of in-patient hospital deaths (1,2). It has been estimated that venous thrombosis is responsible for between 300,000-600,000 hospitalizations and up to 100,000 deaths annually (3,4). The clinical consequences of venous thrombosis such as chronic venous insufficiency with skin ulceration affects up to 500,000 individuals per year. Studies have reported that as many as 90% of patients with venous thrombosis suffer significant disabilities at 2-5 year follow-up intervals (5). The current health costs associated with VTE are significant and are expected to rise as the prevalence of VTE increases in the aging population (6,7). The purpose of this review is to briefly re-acquaint the reader with the pathobiology of the anticoagulant protein system and to review the clinical implications of APC-R.

2. Page Not Found Features articles about blood coagulation disorders including activated protein c resistance, von Willbrand's disease, and hypercoagulability. http://www.beckmancoulter.com/Coulter/Techpubs/coagulation/

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3. FVL Activated Protein C Resistance FVL activated protein c resistance A brief primer for those who are new to the subject of FVL "Factor V Leiden" (FVL) is a description of a http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

4. Activated Protein C Resistance activated protein c resistance (Factor V Leiden) Protein C is a Vitamin Kdependent protease that functions as an anticoagulant by inactivating Factor http://medinfo.ufl.edu/year2/coag/apc.html

Activated Protein C Resistance (Factor V Leiden) I. Review of Protein C and Factor V Factor V is a proenzyme that is activated to Factor Va, whose function is to catalyze the activation of prothrombin to thrombin. Therefore, FVa is a potent procoagulant. Protein C is a Vitamin K-dependent protease that functions as an anticoagulant by inactivating Factor Va. In intact vessels, thrombin binds thrombomodulin (an endothelial cell transmembrane protein). This binding converts thrombin from a procoaglulant to anticoagulant protease which can now cleave and activate Protein C. Activated Protein C in conjunction with a cofactor called Protein S inactivates both Factor Va and VIIIa. II. History Then in 1993 in Holland, Dahlback et al. made a significant discovery. In their experiments to determine the cause of many of these unexplained thrombotic events, they administered exogenous activated protein C (APC) to patients' plasma and then measured the aPTT . In normal healthy men, when exogenous APC was given, the aPTT was substantially prolonged. This was expected given the role of Protein C in inhibiting factors Va and VIIIa. However, when many men with history or family history of unexplained thrombosis were given APC, the aPTT was not prolonged nearly as much. With this novel finding in mind, they proposed mechanisms that could account for this APC resistance. Their hypotheses included: autoantibody against Protein C, antiphospholipid antibodies inhibiting APC function, fast-acting inhibitor of APC, and Protein S Deficiency. They excluded all of these possibilities experimentally, leaving mutation in the genes for Factors V and VIII as possible mechanisms. Through their experiments they eventually found that adding normal Factor V corrected the abnormality and actually prolonged the aPTT to expected levels. This led to studies searching for mutations in the gene for Factor V as the cause for APC resistance.

5. Page Not Found Discusses the thrombotic risks of this inherited disorder, also known as Factor V Leiden. http://www.beckmancoulter.com/Coulter/Techpubs/coagulation/APC.asp

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6. Increased Insulin Receptor Substrate 1 Serine Phosphorylation And 1 Serine Phosphorylation and StressActivated Protein Kinase/c-Jun N-Terminal Kinase Activation Associated With Vascular Insulin Resistance in http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

7. Protein Kinase C And Lipid-Induced Insulin Resistance In Skeletal Protein Kinase C and LipidInduced Insulin Resistance in Skeletal Muscle CARSTEN SCHMITZ-PEIFFER D. LeRoith Peroxisome Proliferator-Activated http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

8. Activated Protein C Resistance The phenomenon of activated protein c resistance (APCr) was first reported by Dahlback (1) et al. in 1993 and refers to the ability to mount an effective http://www.itxm.org/TMU2001/tmu1-2001.htm

January 2001 ACTIVATED PROTEIN C RESISTANCE Andrea Cortese Hassett, Ph.D. Franklin A. Bontempo, M.D. INTRODUCTION The phenomenon of activated protein C resistance (APCr) was first reported by Dahlback (1) et al. in 1993 and refers to the ability to mount an effective anticoagulant response. Clinically this results in an increased risk of thrombosis. Most cases of APC resistance are associated with a single point mutation in the factor V gene (Leiden mutation), which results in the substitution of arginine at position 506 by glutamine. Cleavage of this site by APC is necessary for exposure of the two additional cleavage sites needed for inactivation. The rate of inactivation of factor V Leiden (FVL) is therefore slower than that of normal factor V. In vivo this manifests as an 8 fold increased risk of thrombosis in heterozygotes and a 50 to 100 fold increased risk of thrombosis in homozygotes (2,3). LABORATORY METHODOLOGY The presence of the FVL allele is the major cause of APCr and a well-documented risk factor for venous thrombosis. APC resistance testing is performed on citrated plasma (blue tops) preferably away from the time of the acute event, when the patient is not on treatment with anticoagulants. The first generation, original assay consists of a standard APTT test performed in the absence and presence of commercially available activated protein C.

9. Activated Protein C Resistance/with TIA's activated protein c resistance/with TIA's Click Here to Visit our Sponsor. FREE HealthBoards.com info from vendors! Select Signup http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

10. November1994 - The Activated Protein C Resistance Test The activated protein C (APC) resistance test is a recently described clotting assay that is an important new diagnostic tool to define a cause of http://www.itxm.org/Archive/tmu11-94.htm

November, 1994 THE ACTIVATED PROTEIN C RESISTANCE TEST A New Test for Patients with Thrombosis Franklin A. Bontempo, M.D., Medical Director, Coagulation Services Andrea Cortese Hassett, Ph.D., Scientific Director, Coagulation Services Description The activated protein C (APC) resistance test is a recently described clotting assay that is an important new diagnostic tool to define a cause of hypercoagulability in patients with thrombosis. Defects affecting APC appear to be the most common cause of systemic tendency for excessive clotting. This review will summarize current information as to the incidence and significance of this abnormality. Protein C, in the presence of its cofactor thrombomodulin and thrombin, is enzymatically cleaved to its active form, Activated Protein C. APC is an important natural anticoagulant which functions by inactivating the critical coagulation factors FVa and FVIIIa. The many causes of thrombosis include both hereditary and acquired conditions. Inherited predispositions to thrombosis are perhaps the most disturbing clinically, because they affect patients at a younger age. Currently, only about 5-10% of patients with thrombosis have a definable cause of their thrombotic tendency. In the past year, however, groups working independently in California and Europe have found that failure of the APTT to prolong with the addition of activated protein C occurs in 30-40% of patients with an otherwise unknown cause of thrombosis. Further studies have shown that in 80% of these patients the cause of the APC resistance is a mutant factor V molecule, recently designated factor V Leiden, which is able to clot in the classic coagulation cascade but is resistant to activation by activated protein C.

11. Activated Protein C Resistance And Factor V Leiden Mutation Are activated protein c resistance and Factor V Leiden Mutation Are Independent Risk Factors for Venous Thromboembolism Francesco Rodeghiero, MD http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

12. FVL: Activated Protein C Resistance mutation causes is activated protein c resistance. All people with FVL have activated protein c resistance to one degree or another. However, it http://www.naturalchildbirth.org/natural/resources/prebirth/prebirth31.htm

FVL: Activated Protein C Resistance A brief primer for those who are new to the subject of FVL: "Factor V Leiden" (FVL) is a description of a specific mutation. What that mutation causes is "Activated protein C resistance." All people with FVL have activated protein C resistance to one degree or another. However, it *is* possible to have activated protein C resistance without having FVL. There are probably certain other populations where APCR (Activated Protein C Resistance) is "acquired" through disease or environmental problems. The most common cause of APCR is FVL. Activated Protein C resistance means that when your body forms clots, those clots are more durable than they should be, which means they don't break down as easily as they ought to and they grow faster than they should. One hematologist said he thinks of it as "clot formation not slowing down the way it is supposed to." Activated Protein C is a natural anticoagulant in the blood. There are many, many other causes of thrombophilia (tendency to clot excessively), many of which are genetic. Some people have more than one

13. Hypercoagulability Too Many Tests, Too Much Conflicting Data III).8 In the 1980s, protein C (PC) deficiency and protein S (PS the intermediate phenotype of resistance to activated PC (APC resistance).63 http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

14. UpToDate Activated Protein C Resistance And Factor V Leiden activated protein c resistance and factor V Leiden. Kenneth A Bauer, MD. UpToDate performs a continuous review of over 330 journals and other resources. http://patients.uptodate.com/topic.asp?file=coagulat/4883

15. Isolation And Characterization Of An Antifactor V Antibody Causing Your browser does not support frames. Click here to view the unframed reprint. http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

16. ACTIVATED PROTEIN C RESISTANCE - V LEIDEN Pathology Test - Sinai Hospital Maryla activated protein c resistance V LEIDEN Pathology Test - Sinai Hospital Maryland. http://www.lifebridgehealth.org/22405.cfm

Return to main menu ACTIVATED PROTEIN C RESISTANCE - V LEIDEN Test Name ACTIVATED PROTEIN C RESISTANCE - V LEIDEN Avail Stat? N Specimen Plasma Container Blue 5ml on ice Processing Centrifuge twice, separate, freeze in 2 polystyrene tubes Days Perf. 1X/Week Analytic turn-around time: 1 week. Return to main menu

17. Isolation And Characterization Of An Antifactor V Antibody Causing Isolation and characterization of an antifactor V antibody causing activated protein c resistance from a patient with severe thrombotic http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

18. Activated Protein C Resistance activated protein c resistance, Mail Email this article The APC resistance assay is performed as a screen before ordering the confirmatory factor V http://peir.path.uab.edu/coag/article_19.shtml

Front Page Announcements Contact Us Clinical Conditions ... Test Order Form Search All Categories Front Page Announcements Contact Us Clinical Conditions Guidelines Links Patient Information Test Menu Test Order Form Test Menu Activated protein C resistance Email this article Printer friendly page Primary Name Activated protein C resistance Synonym Screen for factor V Leiden Synonym Contraction APC resistance Contraction APCR Contraction UAB Procedure Number CPT Code Specimen Collect one (1) blue-stopper tube (3.2% sodium citrate), filled to specified volume. Do not underfill or overfill. * If follow-up factor V Leiden mutation test is indicated, collect one (1) lavender-stopper tube (EDTA) whole blood. Specimen Management Centrifuge blue-stopper tube within 1 hour of collection, separate plasma and test or quick-freeze at -70°C. The lavender-stopper tube may be refrigerated up to 72 hours before shipping. Ship overnight at ambient temperature or on wet ice. Specimen Accepted Daily including weekends Times Available Test Performed Twice weekly Available Stat?

19. Dural Puncture And Activated Protein C Resistance Risk Factors Dural puncture and activated protein c resistance risk factors for cerebral venous sinus thrombosis http://tmsyn.wc.ask.com/r?t=an&s=hb&uid=24312681243126812&sid=343126

20. Factor V Leiden / Thrombophilia Support Page - Recently Diagnosed - Activated Pr Factor V Leiden, activated protein c resistance and Protein C Deficiency. by Michael Wosnick As everyone on this list probably knows, the clotting cascade http://www.fvleiden.org/rec_diagnosed/explanations.html

Home Email Forum Programs Resources ... Recently Diagnosed - Factor V Leiden, Activated Protein C Resistance and Protein C Deficiency by Michael Wosnick As everyone on this list probably knows, the clotting "cascade" as they call it is very complex with multiple steps. It is not an A to B kind of thing, but rather and A to B to C to D to .... You can think of this pathway as a road through a series of points, with your ultimate destination being a blood clot at the end of the pathway. But, at each step you can think of having a traffic cop that tells you to speed up (towards clotting) or to slow down (towards not clotting). There are multiple traffic cops and multiple control points. Messing up any of these control points can lead to excess clotting (car is going too fast) or not enough clotting (car is going too slow). Factor V itself is a clotting factor, whose normal role is to help blood to clot when an appropriate trigger is present. However, like all steps in the complex clotting cascade, Factor V is subject to regulation to keep it under control so that clots don't form too easily or too quickly. If you think of normal Factor V as a car on a road, then left to its own devices, it will drive towards the formation of a blood clot. Normally, however, Factor V is not just left to its own devices, but is in fact quite controlled by one of several "traffic cops". The main traffic cop is called Activated Protein C (APC). Another helper traffic cop working with APC is Protein S. Normally, APC interacts with Protein S, and together they make a combo whose job it is to slow down the Factor V so that it does not lead to excessive clotting. To be precise, APC combines with Protein S and functions to inactivate some of the normal Factor V by clipping it into a couple of pieces, rendering the car immobile. Ergo, no clot forms.

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