21. Relation Of Factor V Leiden Genotype To..., Annals 15 Feb 98 Relation of factor v leiden Genotype to Risk for Acute Deep Venous Thrombosisafter Joint Replacement Surgery. Annals of Internal Medicine 15 Feb 98. http://www.acponline.org/journals/annals/15feb98/ryan.htm

Annals of Internal Medicine Current Issue Past Issues Library for Internists Subscriptions ... Email this page Annals of Internal Medicine Relation of Factor V Leiden Genotype to Risk for Acute Deep Venous Thrombosis after Joint Replacement Surgery Annals of Internal Medicine, 15 February 1998. 128:270-276. Daniel H. Ryan, MD; Mark A. Crowther, MD; Jeffrey S. Ginsberg, MD; and Charles W. Francis, MD Background: A point mutation in coagulation factor V (A1691G) is associated with increased risk for venous thrombosis. However, limited information is available about the prospective risk for deep venous thrombosis in specific high-risk clinical settings. Objective: To determine whether the factor V Leiden mutation is associated with an increased occurrence of deep venous thrombosis in patients undergoing hip or knee replacement surgery. Design: Retrospective analysis of plasma samples obtained during six prospective clinical trials that compared different antithrombotic prophylaxis regimens in patients undergoing hip or knee replacement surgery. Setting: Inpatients at the University of Rochester Medical Center, McMaster University Medical Center, Hamilton Civic Hospitals, and the Genesee Hospital.

22. Kimball Genetics - The Factor V R2 DNA Test factor v leiden is the most common genetic risk factor for venous thrombosis andpulmonary embolism, present in 5% of the Caucasian population and in 2040% of http://www.kimballgenetics.com/tests-factorvfnl.html

The Factor V R2 DNA Test Factor V Leiden is the most common genetic risk factor for venous thrombosis and pulmonary embolism, present in 5% of the Caucasian population and in 20-40% of individuals with a history of venous thromboembolism. Not all individuals who are heterozygous for factor V Leiden will experience a thrombotic event. The presence of the R2 polymorphism in the factor V gene increases the likelihood of thrombosis in factor V Leiden heterozygotes. The R2 polymorphism is very common, occurring in 1 in 10 individuals. This polymorphism is part of the HR2 haplotype, a collection of polymorphisms always inherited together. Factor V Leiden heterozygotes are at a 7-fold increased risk for venous thrombosis. Co-existence of the R2 polymorphism with factor V Leiden increases that risk by an additional 3-fold through a further increase in APC resistance. The average age of the first thrombotic event is six years younger in individuals who are heterozygous for both factor V Leiden and the R2 polymorphism than in those with factor V Leiden alone. Because of this dramatic increase in the risk for a life-threatening event, it is important to identify those factor V Leiden heterozygotes who also have the R2 polymorphism. The R2 polymorphism is identified by PCR amplification and restriction enzyme digestion followed by gel electrophoresis. Within 24 hours of the detection of factor V Leiden, the presence of the additional risk factor, R2, can be determined without an additional blood draw, and an appropriate plan of care can then be initiated.

23. GenID - Factor V-Leiden Risk Factors of Genetic Thrombosis Factor VLeiden and Prothrombin 20210A. Thealtered Factor V gene product is called factor v leiden (FVL). http://www.aid-diagnostika.com/GenID/gen_faktor5_e.htm

Faktor V-Leiden Alpha-1-Antitrypsin HLA-B*27 HLA-DRB1 Shared epitope Risk Factors of Genetic Thrombosis: Factor V-Leiden and Prothrombin 20210A Reverse hybridization kit for the determination of the mutation FV:Q506 in the Factor V gene and the mutation 20210A in the Factor ll gene Factor V-Leiden Thromboses are caused by disorders of the coagulation system. One later complication can be the development of a lung emboly. One of the regulating factors of the coagulation system is Activated Protein C (APC), which is a serin protease influencing the coagulation process together with a cofactor by proteolytic inactivation of Factor Va and VIIIa, two components of the coagulation cascade. Factor Va is derived from the Factor V-Protein by cleavage, which in turn is mediated by Factor IIa. According to current knowledge, the resistance against Activated Protein C (APC) is the most common genetic risk factor for venose coagulation disorders. The cause is a point mutation in the Factor V-gene bringing about a substitution of guanin (G) by adenin (A) at position 1691. In the translated protein this results in the substitution of the amino acid arginin by glutamin at the position 506 (FV:Q ). The altered Factor V gene product is called Factor V Leiden (FVL).

24. Factor V Leiden Genetic Testing distributed. Professor FE Preston, Rutledge Mews 3 Southbourne RoadSheffield S10 2QN, factor v leiden, P20210A, Citrated whole blood. http://www.ukneqas.org.uk/Directory/HAEM/fact5lei.htm

United Kingdom National External Quality Assessment Service "helping to ensure clinical laboratory test results are accurate, reliable and comparable wherever they are produced" Navigation About EQA Directory Scheme Webs ... Webmaste r Office Members Participants Director Address Investigations covered Material distributed Professor FE Preston Rutledge Mews 3 Southbourne Road Sheffield Factor V Leiden, P20210A Citrated whole blood personal email Manager / other staff Year started Recognised UK NEQAS f.e.preston@sheffield.ac.uk talwoods@coageqa. demon.co.uk Mr TAL Woods telephone scheme email CPA(UK) Accreditation Distributions / samples neqas@coageqa.demon.co.uk Awaiting inspection fax scheme web UK public/private labs UK non-clinical labs Performance assessment Information provided Non-UK labs by country Availability The purpose of the scheme is to provide external quality assessment of genetic tests for disorders of haemostasis, in the first instance, the Factor V Leiden mutation In addition to the main function of EQA, the scheme also hopes to offer advisory support in trouble-shooting. Meetings for participants are organised on an annual basis (c.f.), with presentations from authoritative speakers and open discussion on current scheme issues

25. Factor V Leiden Mutation And The Risk Of Venous Thrombolembolism In Pregnant Wom April 17, 2002. factor v leiden Mutation and the Risk of Venous Thrombolembolismin Pregnant Women EJournal Club abstraction form on Tormene D et al. http://www.cdc.gov/genomics/hugenet/ejournal/fvlmutation.htm

April 17, 2002 Factor V Leiden Mutation and the Risk of Venous Thrombolembolism in Pregnant Women E-Journal Club abstraction form on Tormene D et al. Viola Vaccarino, MD, PhD Emory University Past issues The Health Outcome Pregnancy and puerperium are known risk factors for venous thromboembolism (VTE) (1, 2). The incidence of VTE during pregnancy is 1 per 1,000 (1,2) and increases 10 times during the postpartum period (3). These incidence rates are considerably higher than those reported for women of similar age in the general population. A variety of clotting inhibitor deficiencies have been identified as risk factors for VTE in pregnancy, but most of these defects are rare. Factor V Leiden mutation is relatively common: it affects 5% of the southern European population. The Finding The purpose of the study by Tormene et al. (4), therefore, was to assess the relation between factor V Leiden mutation and incidence of pregnancy-related VTE using a case-control design. Study subjects were

26. Case Study: Factor V Leiden And Venous Thrombosis Overview factor v leiden and Venous Thrombosis Case Study, Educational Objectives.After factor v leiden and Venous Thrombosis Overview. Venous http://www.cdc.gov/genomics/hugenet/CaseStudy/FVL/FVLview.htm

Factor V Leiden and Venous Thrombosis Case Study Educational Objectives After reading this case study you should be able to: identify key characteristics of the study population (cases and controls) that should be described when reporting results of gene-disease association studies. summarize gene-disease associations in terms of absolute, relative and attributable risks. discuss possible implications of the findings for researchers, people with Venous Thrombosis, and people with one or more of the newly described Factor V Leiden variants. Factor V Leiden and Venous Thrombosis Overview V enous thrombosis is an important cause of morbidity; incidence is low in young people but increases with age to 1% per year in the elderly. In a small proportion of cases, venous thrombosis leads to pulmonary embolism, which can be fatal. Persons with an initial venous thrombosis are at increased risk for recurrence; however, long-term use of anticoagulant prophylaxis can result in major hemorrhagic complications. This challenging clinical problem has received new attention since the discovery of certain genetic variants that increase susceptibility to venous thrombosis.

27. Factor V Leiden Verhuisd Naar Www.factorvleiden.nl De factor v leiden site heeft een eigen domein! Over 3 seconden linkenwij u automatisch door naar ons nieuwe adres www.factorvleiden http://www.leefwijzer.nl/factor-V-leiden/home.htm

De factor V Leiden site heeft een eigen domein! Over 3 seconden linken wij u automatisch door naar ons nieuwe adres: www.factorvleiden.nl Vergeet niet uw favorieten te wijzigen!!

28. Factor V Leiden Mutation all women, prior to starting postmenopausal estrogen supplementation or oral contraceptives,should have a determination of RAPC/factor v leiden determinations http://www.mdl-labs.com/factorv.htm

Factor V (Leiden) Mutation (Hereditary Thrombotic Predisposition Resistance to Activated Protein C (RAPC) is the most common cause of venous thrombosis. It is mediated by heterozygosity or (more rarely) homozygosity for mutant Factor V (Arg506Glu, AKA, R506Q) Leiden mutation). In the general population, 6% of healthy Caucasian men and women are heterozygous for the mutant Factor V allele. If women are given oral contraceptives or estrogen supplementation, and if they are heterozygous for the mutant allele , their risk of thrombosis is 80 times that of the general population. In order to prevent thrombosis in thrombosis-prone women, we think that all women, prior to starting postmenopausal estrogen supplementation or oral contraceptives, should have a determination of RAPC/Factor V Leiden determinations. The approximately 6% with the mutant factor V Leiden gene should not be given exogenous estrogens, whereas the 94% without the mutant gene should be at very low risk of thrombosis. References: 1. Dahlback, B. (1995) Resistance to activated protein C, the Arg-506 to Gln mutation in the Factor V gene, and venous thrombosis. Thromb. and Haemos. 73:739-42.

29. Clinical Utility Of Factor V Leiden (R506Q) Testing For The Diagnosis And Manage Clinical Utility of factor v leiden (R506Q) Testing for the Diagnosisand Management of Thromboembolic Disorders. Richard D. Press http://www.cap.org/thrombophiliaconference/clinical_utility_of_fvl_testing_press

Clinical Utility of Factor V Leiden (R506Q) Testing for the Diagnosis and Management of Thromboembolic Disorders Richard D. Press MD, PhD Department of Pathology and Medical Genetics Oregon Health and Science University Portland, Oregon, United States Kenneth A. Bauer, MD Department of Medicine Veterans Affairs Boston Healthcare System and Beth Israel Deaconess Medical Center West Roxbury, Massachusetts, United States Jody L. Kujovich, MD Department of Medicine Oregon Health and Science University Portland, Oregon, United States John A. Heit, MD Division of Cardiovascular Diseases, Mayo Clinic Rochester, Minnesota, United States Address correspondence to: Richard D. Press, MD, PhD Dept of Pathology L113 Oregon Health and Science University 3181 SW Sam Jackson Park Rd Portland, OR 97201

30. DNA.com - Clinical Services factor v leiden is associated with the following complications venous thrombosis(blood clots, especially with oral contraceptives); DVT (deep vein thrombosis http://www.dna.com/capabilitiesServices/capabilitiesServices.jsp?site=dna&link=c

31. Member Sign In What are the guidelines for deep vein thrombosis prophylaxis in a patientundergoing surgery with a history of factor v leiden? Focus On http://www.medscape.com/viewarticle/443642

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32. Member Sign In factor v leiden and Activated Protein C Resistance. factor v leiden mutation andthe risks of thromboembolic disease a clinical perspective. Ann Intern Med. http://www.medscape.com/viewarticle/439361_2

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33. Factor V Leiden Deficiency factor v leiden Deficiency PCR for factor v leiden Responsible for 95% ofAPC resistance; Does NOT require that patient be off Anticoagulation. http://www.fpnotebook.com/HEM26.htm

Home About Links Index ... Editor's Choice Paid Advertisement (click above). Please see the privacy statement Hematology and Oncology Coagulopathy Assorted Pages Coagulation Bleeding Disorders Dysfibrinogenemia Hemophilia A Factor IX Deficiency ... Perioperative Anticoagulation Factor V Leiden Deficiency Factor 5 Leiden Deficiency APC Resistance Activated Protein C resistance Book Home Page Cardiovascular Medicine Dental Dermatology Emergency Medicine Endocrinology Gastroenterology General Medicine Geriatric Medicine Gynecology Hematology and Oncology HIV Infectious Disease Jokes Laboratory Neonatology Nephrology Neurology Obstetrics Ophthalmology Orthopedics Otolaryngology Pediatrics Pharmacology Prevention Psychiatry Pulmonology Radiology Rheumatology Sports Medicine Surgery Urology Chapter Hematology and Oncology Index Anemia Cancer Coagulopathy Cardiovascular Medicine Dermatology Endocrinology Otolaryngology Examination Gastroenterology Hematology and Oncology Hemoglobin Hemolysis Histiocytosis HIV Infectious Disease Laboratory Leukemia General Pulmonology Lymph Marrow Neurology Obstetrics Orthopedics Pediatrics Pharmacology Platelet Prevention Procedure Psychiatry Rheumatology Surgery Symptom Evaluation Vascular Page Coagulopathy Index Bleeding Bleeding Dysfibrinogenemia Bleeding Hemophilia A Bleeding Hemophilia B Bleeding Von Willebrands Clotting Pathway Background Clotting Pathway Common Clotting Pathway Extrinsic Clotting Pathway Inhibition Clotting Pathway Intrinsic DIC Hypercoagulable Hypercoagulable Antithrombin III Hypercoagulable APC resistance

34. Factor V Leiden Genetic Testing (DNA Testing) at the Clinical Molecular Diagnostic Laboratory ofthe City of Hope National Medical Center in Duarte, California. factor v leiden. http://www.cityofhope.org/cmdl/factor5.asp

Genetic Testing (DNA Testing) at the Clinical Molecular Diagnostic Laboratory of the City of Hope National ... Center in Duarte, California Factor V Leiden The factor V Leiden mutation, also designated as 1691 G>A or R506Q, is the major heritable risk factor for venous thromboembolism . This mutation in the coagulation factor V gene results in resistance of factor V to inactivation by activated protein C (APC) . Approximately 5% of Caucasians are either heterozygous carriers or homozygous for the factor V Leiden mutation; the prevalences are lower for other ethnic groups To open a printable assay summary in a new window, click the link below. Factor V Leiden Assay Summary (in portable document format (pdf) which requires version 4 or higher to view or print; download latest version free References 1. Voorberg, J. et al. (1994). Lancet 2. Zoller, B. and Dahlback, B. (1994). Lancet 3. Bertina, R. M. et al. (1994). Nature 4. Greengard, J. S. et al. (1994).

35. Gradipore Factor V Leiden Assay Products Gradipore factor v leiden Assay. GradiLeiden V A simple functionalScreening Test for Factor V (Leiden). factor v leiden and APC resistance. http://www.rainbowscientific.com/g-factorvleiden.html

Products Gradipore GradiLeiden V A simple functional Screening Test for Factor V (Leiden) Factor V Leiden and APC resistance The Factor V (Leiden) mutation has been identified as the most important underlying cause of hereditary thrombophilia. This mutation in clotting factor V confers resistance to normal proteolytic cleavage by activated protein C (APC), resulting in impaired function of an important regulatory mechanism in the clotting process. Factor V Leiden has traditionally been first detected by screening tests using addition of exogenous APC to patient plasma in an APTT test, where the clotting time for normal patients is prolonged, while individuals with a mutation in Factor V exhibit shorter clotting time results. However the mutation can also be detected by a Dilute-Russell's Viper Venom Time (DRVVT) based test. The DRVVT method avoids limitations inherent in the APTT based method, which requires a normal baseline APTT and may be affected by high concentrations of Factor VIII, Lupus Anticoagulant and anticoagulant therapy. The use of a DRVVT test also eliminates the requirement to pre-dilute patient samples with Factor V deficient plasma. GradiLeiden V

36. Factor V Leiden Mutation Analysis factor v leiden Mutation Analysis. Note This The factor v leiden mutationcan be diagnosed using a simple PCR genetic assay. Unlike conventional http://www.hpath.com/HPAServices/MolecPath/FactorV.htm

Factor V Leiden Mutation Analysis Note : This section is offered as background information only. If you have particular diagnostic questions relating to you or someone you know, please consult with your local physician or genetic counselor Venous thrombosis is a significant cause of mortality in the U.S., with an annual incidence of 1/1000. It accounts for a half a million hospitalizations and causes over 50,000 deaths annually. Hereditary disorders predisposing to thrombosis include the factor V Leiden genetic mutation, the factor II (prothrombin) gene G to A 20210 mutation, protein C deficiency, protein S deficiency, antithrombin III deficiency, and dysfibrinogenemia. Of these, the factor V Leiden mutation is by far the most common, accounting for up to 40% of all cases, and up to 75% of cases of recurrent thrombosis. It has approximately a 5% prevalence in the general population and is at least 10 times more common than any other known thrombophilic genetic defect. In general, thrombophilic patients are targeted. Clinical criteria for thrombophilia includes venous thrombosis or thromboembolism which occurs before the age of 45 or is recurrent, a family history of venous thrombosis or thromboembolism, or a history of thrombosis in an unusual anatomic location, or recurrent superficial thrombophlebitis.

37. Factor V Leiden, Factor V, V Leiden, Coagulation, Thrombosis, Genetic, Molecular factor v leiden testing by ProADN. For the analysis of factor v genetic mutations,chose ProADN's home factor v leiden tests for canada, montreal, quebec. http://www.proadn.com/en/molecular_factor-v-leiden

Contact us at All secure transactions handled by CLIA ID NUMBER LSPQ PERMIT State of Florida Licence Encryption Certificate Created by For any comment about this site: New Predisposition Factors The Factor V Leiden The factor V gene mutation, known as the factor V Leiden, is present in 3 to 8% of the Caucasian population in the heterozygous state. The prevalence of this gene in the homozygous state is only about 0.1%. While only 8% of the individuals with a heterozygous gene present with a thrombosis, nearly all those with the homozygous gene will have a thrombotic manifestation during their lifetime. Moreover, this mutation has also been identified in significant numbers in women who have had obstetrical complications (preeclampsia, placental detachment, still-born baby, intra-uterine growth retardation, repeated pregnancy losses). For young women with the factor V Leiden mutation, taking birth control pills increases the risk of thrombosis thirty-five (35) times compared with the risk of those who are not carriers of this mutation. Indications for Investigation of Genetic Factors for Thrombophilia Venous thromboembolism (thrombophlebitis, pulmonary embolism)

38. August 1995 - The Factor V Leiden Mutation August, 1995 THE factor v leiden MUTATION. A MAJOR RISK FACTOR FOR INHERITEDTHROMBOSIS. Franklin A. Bontempo, MD, Medical Director, Coagulation Services. http://www.itxm.org/TMU1995/tmu8-95.htm

August, 1995 THE FACTOR V LEIDEN MUTATION A MAJOR RISK FACTOR FOR INHERITED THROMBOSIS Franklin A. Bontempo, M.D., Medical Director, Coagulation Services Andrea Cortese Hassett, Ph.D., Scientific Director, Coagulation Services Introduction Traditional attempts to identify an underlying cause of familial thrombosis by testing for antithrombin III, protein C, and protein S have only rarely provided an explanation for a patient's thrombotic event. Recently, studies have clearly shown that a mutation of clotting factor V is highly associated with thrombosis and may account for as much as 25% of all cases of venous thrombosis of unknown cause. In addition, knowledge that a patient carries this gene may have significant clinical implications. Pathophysiology The factor V mutation, named factor V Leiden after the site of its discovery, is due to a point mutation in the normal factor V molecule. This mutation renders the factor V molecule insensitive to the action of activated protein C, a natural anticoagulant. This in turn appears to shift the patient's overall hemostatic balance toward thrombosis, especially venous thrombosis. Incidence The incidence of the factor V Leiden mutation in both European and American populations has been repeatedly found to be surprisingly high. The best evidence from the United States indicates that 6% of the population carries the gene for the factor V mutation. The reason for its persistence at such a high level is unclear.

39. Hypercoagulability And Thrombosis: Factor V Leiden The factor v leiden mutation is represented by a single adenineto-guanine pointmutation in the gene coding for coagulation factor V. This results in the http://medicine.ucsf.edu/htc/hypernthromb/hypernthromb.fctrvldn.html

The factor V Leiden mutation is represented by a single adenine-to-guanine point mutation in the gene coding for coagulation factor V. This results in the replacement of arginine by glutamine at a key proteolytic site on the activated factor V protein, such that the molecule cannot be cleaved by activated protein C - hence the so-called APC resistance. Factor V clotting activity is normal in coagulation assays. Rather, factor V is resistant to inactivation in vivo. The factor V Leiden mutation is found in 2% - 5% of the asymptomatic caucasian population, and is accountable for approximately 40% of patients presenting with idiopathic venous thromboembolic disease. It has also been associated with increased risks for recurrent venous thromboembolism, for venous thrombosis during use of oral contraceptives and pregnancy, and for thrombosis in the presence of other genetic and acquired abnormalities of anticoagulation, such as protein C and S deficiencies. Homozygous Leiden mutation is estimated to be 1:5,000. The overall thrombotic risk for homozygotes is estimated to be 11-fold higher than for heterozygotes and 80-fold higher than normal individuals. The probability of a thrombotic episode before the age of 33 years in a homozygous Leiden mutation is twice that for a heterozygote (40% versus 20%). Below is a diagram of the inactivation of factor V: Figure: Inactive factor V is activated by thrombin mediated cleavage of the B domain, resulting in the formation of a dimer.

40. JAMA Women's Health Information Center - Factor V Leiden Mutation Annals of Internal Medicine Vol. 128(pt 1), pp. 10001003, June 15, 1998factor v leiden Mutation as a Risk Factor for Recurrent Pregnancy Loss http://www.ama-assn.org/special/womh/library/scan/vol_4/no_21/ridker.htm

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