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  1. Activated Protein C Resistance

81. Clinical Chemistry -- Sign In Page
activated protein c resistance in patients with antiß2 glycoprotein I antibodies. Blood Coagul Fibrinolysis 1996;7702-704.ISIMedline Order article
http://www.clinchem.org/cgi/content/full/51/3/545
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-Glycoprotein...
Nojima et al. Clin Chem.
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82. Acquired Activated Protein C Resistance Associated With IgG Antibodies Against {
Acquired activated protein c resistance Associated with IgG Antibodies against ß2Glycoprotein I and Prothrombin as a Strong Risk Factor for Venous
http://www.clinchem.org/cgi/content/abstract/51/3/545
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Clinical Chemistry
51: 545-552, 2005. First published January 6, 2005; 10.1373/clinchem.2004.043414
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clinchem.2004.043414v1

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Hemostasis and Thrombosis
-Glycoprotein I and Prothrombin as a Strong Risk Factor for Venous Thromboembolism
Junzo Nojima ,a Hirohiko Kuratsune Etsuji Suehisa Yoshinori Iwatani and Yuzuru Kanakura
Laboratory for Clinical Investigation, Osaka University Hospital, Osaka, Japan.

83. Activated Protein C Resistance In Ischemic Stroke Not Due To Factor V Arginine50
Background and Purpose Resistance to activated protein C (APC), Cerebral Venous Thrombosis Role of activated protein c resistance and Factor V Gene
http://stroke.ahajournals.org/cgi/content/abstract/27/7/1163
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Articles
Activated Protein C Resistance in Ischemic Stroke Not Due to Factor V Arginine Glutamine Mutation
Mark Fisher, MD Jose A. Fernandez, MD, PhD Sebastian F. Ameriso, MD Dangci Xie, MD, PhD Andras Gruber, MD Annlia Paganini-Hill, PhD John H. Griffin, PhD
Correspondence to Mark Fisher, MD, Department of Neurology, University of Southern California School of Medicine, 1333 San Pablo St, MCH 246, Los Angeles, CA 90033. E-mail mjfisher@hsc.usc.edu. Background and Purpose Resistance to activated protein C (APC), a natural plasma anticoagulant, is the most common identifiable risk factor for venous thromboembolic disease. One point mutation in coagulation factor V that renders it APC-resistant is found the prevalence of APC resistance and of this factor V mutation in stroke, we screened a group of ischemic stroke patients.

84. Cerebral Venous Thrombosis: Role Of Activated Protein C Resistance And Factor V
Medline; Dahlback B. Resistance to activated protein C, the Arg506 to Gln activated protein c resistance in ischemic stroke not due to factor V
http://stroke.ahajournals.org/cgi/content/full/27/10/1719
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Articles
Cerebral Venous Thrombosis
Role of Activated Protein C Resistance and Factor V Gene Mutation
Robin L. Brey, MD Bruce M. Coull, MD
the University of Texas Health Science Center at San Antonio (R.L.B.) and the University of Arizona College of Medicine (Tucson) (B.M.C.). Correspondence to Robin L. Brey, MD, Department of Medicine (Neurology), University of Texas Health Science Center, 7703 Floyd Curl Dr, San Antonio, TX 78284-7883.
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Introduction Top
Introduction
References
The number of well-described familial and acquired conditions that are predisposing factors for thrombosis continues to increase. Although most are uncommon, in 1993 a new condition that has ultimately been recognized as activated protein C resistance (APC-R) was reported.

85. Plasma Resistance To Activated Protein C Regulates The Activation Of Coagulation
There were no associations between the activated protein c resistance ratio and protein C, protein C inhibitor, or plasminogen activator inhibitor type1,
http://heart.bmjjournals.com/cgi/content/abstract/77/2/122

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PAPERS
Plasma resistance to activated protein C regulates the activation of coagulation induced by thrombolysis in patients with ischaemic heart disease
OD Pedersen, J Gram and J Jespersen
Department of Internal Medicine, Ribe County Hospital, Esbjerg, Denmark. OBJECTIVE: To determine whether there was a relation between plasma resistance to activated protein C and the coagulation activation induced during thrombolysis with 100 mg alteplase in 25 patients with acute ischaemic heart disease. METHODS: Blood samples were collected before (t =

86. Inherited Resistance To Activated Protein C Is Corrected By Anticoagulant Cofact
activated protein c resistance and Factor V Leiden Mutation Are Independent Ischemic Stroke in Young Patients With activated protein c resistance A
http://www.pnas.org/cgi/content/abstract/91/4/1396
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ARTICLE
Inherited Resistance to Activated Protein C is Corrected by Anticoagulant Cofactor Activity Found to be a Property of Factor V
B Dahlback and B Hildebrand
This article has been cited by other articles in HighWire Press -hosted journals:
Y.-H. Sun, S. Tran, E. A. Norstrom, and B. Dahlback
Enhanced Rate of Cleavage at Arg-306 and Arg-506 in Coagulation Factor Va by Gla Domain-mutated Human-activated Protein C
J. Biol. Chem., November 12, 2004; 279(46): 47528 - 47535.
[Abstract]
[Full Text] [PDF]
E. Castoldi, J. M. Brugge, G. A. F. Nicolaes, D. Girelli, G. Tans, and J. Rosing
Impaired APC cofactor activity of factor V plays a major role in the APC resistance associated with the factor V Leiden (R506Q) and R2 (H1299R) mutations
Blood, June 1, 2004; 103(11): 4173 - 4179.

87. Resistance To Activated Protein C
A monthly newsletter about evidencebased health care.
http://www.jr2.ox.ac.uk/bandolier/bandopubs/keeling.html
@import "../styles/advanced.css";
Resistance to activated protein C due to Factor V R506Q (Factor V Leiden)
David Keeling BSc MD MRCP MRCPath Consultant Haematologist Oxford Haemophilia Centre, Churchill Hospital, Oxford.
The Discovery of Resistance to Activated Protein C and Identification of the Mechanism.
The phenomenon of resistance to activated protein C (APC) was discovered only three years ago. Dahlback and colleagues identified a middle aged man with a personal and a family history of thrombosis whose APTT did not show the expected prolongation when exogenous APC was added to his plasma [1]. The same phenomenon was found in several of the patient's relatives. The mechanism was unknown but inheritance of a deficiency of a cofactor for APC was hypothesised. This proved not to be the case and one year later the molecular defect was identified as a point mutation in factor V (FV) [2]. The mutation was a G to A substitution at nucleotide position 1,691. This results in the arginine at position 506 (coding triplet CGA) being replaced by a glutamine (coding triplet CAA). Using the single letter amino-acid code the mutant FV can therefore be written as FV R506Q but is more often referred to as FV Leiden (Figure 1).
Figure 1. The G to A point mutation results in the arginine at the protein C cleavage site being replaced by glutamine.

88. Protein C (resistance To Activated Protein C) - General Practice Notebook
protein C (resistance to activated protein C). resistance to the anticoagulant effects of activated protein C (APC) (Factor V Leiden heterozygous*) is
http://www.gpnotebook.co.uk/cache/1711669304.htm
protein C (resistance to activated protein C) Resistance to the anticoagulant effects of activated protein C (APC) (Factor V Leiden heterozygous*) is common (1):
  • 5% of the general population 25-50% of patients with venous thromboembolism 50% of patients with thrombosis who have a family or personal history of thrombosis
APC resistance is usually due to a single point mutation in one or both of the protein C genes. The mutation reduces the susceptibility of factor V to cleavage by APC. There is increasing evidence that individuals with two or more laboratory characterisable thrombophilic abnormalities (or who are homozygous for either factor V Leiden or prothrombin G20210A) are at a greater risk of thrombosis than those in whom there is a single gene abnormality (1). * Factor V Leiden homozygous individuals have an 80x risk of venous thromboembolism Reference: (1) British Heart Foundation (Factfile 2/2002). Thrombophilia (2) Rogier, MB. et al. (1994). Mutation in blood coaulation factor V associated with resistance to activated protein C. Nature, 369, 64-7. (3) Drugs and Therapeutics Bulletin (1995), 33 (1), 6-8.

89. Resistance To Activated Protein C - General Practice Notebook
resistance to activated protein C. resistance to the anticoagulant effects of activated protein C (APC) (Factor V Leiden heterozygous*) is common (1)
http://www.gpnotebook.co.uk/cache/1731526712.htm
resistance to activated protein C Resistance to the anticoagulant effects of activated protein C (APC) (Factor V Leiden heterozygous*) is common (1):
  • 5% of the general population 25-50% of patients with venous thromboembolism 50% of patients with thrombosis who have a family or personal history of thrombosis
APC resistance is usually due to a single point mutation in one or both of the protein C genes. The mutation reduces the susceptibility of factor V to cleavage by APC. There is increasing evidence that individuals with two or more laboratory characterisable thrombophilic abnormalities (or who are homozygous for either factor V Leiden or prothrombin G20210A) are at a greater risk of thrombosis than those in whom there is a single gene abnormality (1). * Factor V Leiden homozygous individuals have an 80x risk of venous thromboembolism Reference: (1) British Heart Foundation (Factfile 2/2002). Thrombophilia (2) Rogier, MB. et al. (1994). Mutation in blood coaulation factor V associated with resistance to activated protein C. Nature, 369, 64-7. (3) Drugs and Therapeutics Bulletin (1995), 33 (1), 6-8.

90. Resistance To Activated Protein C As A Pathogenic Factor Of Thrombophilia
resistance to activated protein C as a pathogenic factor of thrombophilia. ABSTRACT. The proportion of identifiable causes of familial thrombophilia has
http://www.imbiomed.com/Innsz/Nnv48n3/english/Znn63-07.html
Ruiz-Argüelles GJ
Resistencia a la proteína C activada como causa de trombofilia
Rev Invest Clin
Resistance to activated protein C as a pathogenic factor of thrombophilia
ABSTRACT The proportion of identifiable causes of familial thrombophilia has increased from 5 10% to 60 70% since the identification of activated protein C resistance aPCR in February 1993 by Dahlbäck et al. A mutation in the factor V gene G A, 1691 leads to the so called Leiden mutation R 506 Q that produces a mutated factor V resistant to the catalytic action of activated protein C aPC , yet normal in its procoagulant properties. This recently identified aPCR is in Nordic populations the most prevalent and well defined genetic defect associated with disease so far described. Its prevalence in the general population ranges from 0% to up to 15% and suggests that a positive genetic selection pressure has been involved. The aPCR phenotype can be assessed in vitro by measurement of the prolongation of the activated partial thromboplastin time in the presence of aPC, whereas the aPCR genotype is studied using polymerase chain reaction searching for the Arg to Gln mutation in the coagulation factor V gene. Some acquired conditions such as the presence of lupus anticoagulants, antiphospholipid antibodies, pregnancy, liver disease and contraceptives may lead into the aPCR phenotype. The aPCR search must be the initial step in the study of a patient with thrombophilia, either inherited or acquired; aPCR together with protein C, protein S and antithrombin III explain 60 to 70% of cases of familial thrombophilia.

91. The Role Of Protein C, Protein S, And Resistance To Activated Protein C In Legg-
We measured protein C and protein S and resistance to activated protein C (APCR) from plasma. Study Design. Participants were placed into 1 of 3 mutually
http://pediatrics.aappublications.org/cgi/content/abstract/107/6/1329
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PEDIATRICS Vol. 107 No. 6 June 2001, pp. 1329-1334
The Role of Protein C, Protein S, and Resistance to Activated Protein C in Legg-Perthes Disease
Received Apr 13, 2000; accepted Sep 20, 2000. John Eldridge Anne Dilley Harland Austin Muhydine EL-Jamil Lori Wolstein John Doris W. Craig Hooper Peter L. Meehan and Bruce Evatt From the Department of Orthopedics and Pediatrics, University of Louisville School of Medicine, Louisville, Kentucky; Hematologic Diseases Branch, Division of AIDS, STD, and Laboratory Research, National Center for Infectious Diseases, Centers for Disease Control and Prevention, US Department of Health and Human Services, Atlanta, Georgia; Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia; and

92. The Role Of Protein C, Protein S, And Resistance To Activated Protein C In Legg-

http://pediatrics.aappublications.org/cgi/reprint/107/6/1329
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93. Procedure Activated Protein C Resistant FV
activated protein C Resistant FV, Specimen Type. also known as APC Resistant Factor V, protein C resistance Assay, Factor V Leiden, APCFV, Blood
http://health.ucsd.edu/labref/P321.html
CLINICAL LABORATORIES Activated Protein C Resistant FV Specimen Type: also known as APC Resistant Factor V, Protein C Resistance Assay, Factor V Leiden, APCFV Blood SPECIAL COAGULATION LAB specimen requirements: Blue Top normal or reference ranges: Category LOW HIGH UNITS Normal unit of measure: Normal/Abnormal ideal sample: 2.7 mL Whole Blood, blue top tube absolute minimum amount: 2.4 mL Whole Blood The following substances can adversely affect the results: Clots in Specimen, Improper Line Draw request test on form: Hematology Test Request ( 151-204 ) Special Coagulation ( D6115 ) order/entry screen(s): Hematology/Coagulation method: Optical Clot Detection routine turn around time: 10 days For Hillcrest deliver to: SCRAP : Specimen Central Receiving and Processing, room 2-117 For Thornton deliver to: Hematology : Processing Desk, 1st floor, Hospital, room 1-013 Special Instructions: Assay is not affected by heparin, coumadin, or lupus anticoagulant. Results are available on a Chart Copy Results are Qualitative CyberLAB II abbreviation: APCFV CyberLAB II code: This page was updated on 7/27/2005.

94. Summary: Correlation Between Activated Protein C-resistance And Factor V Leiden
Correlation between activated protein Cresistance and factor V Leiden mutation Journal of Clinical and Basic Cardiology 2001; 4 (Issue 1) 73-74
http://www.kup.at/journals/summary/719.html

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Volltext Werbung Abo News Datenbanken Journale ... Impressum Summary Correlation between activated protein C-resistance and factor V Leiden mutation
Journal of Clinical and Basic Cardiology 2001; 4 (Issue 1)

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Keywords: aktivierte Protein C-Resistenz COATEST Faktor V Leiden Venenthrombose ... cybirion.com

95. British Library Direct: Order Details
Order from the British Library Acquired resistance to activated protein C, oral contraceptives and the risk of thromboembolic disease Human Reproduction.
http://direct.bl.uk/research/50/15/RN089533820.html
This is an article from British Library Direct, a new service that allows you to search across 20,000 journals for free and order full text using your credit card. Article details Article title Acquired resistance to activated protein C, oral contraceptives and the risk of thromboembolic disease Author Gris, J.-C. Jamin, C. Benifla, J.-L. Quere, I. Madelenat, P.; Mares, P. Journal title HUMAN REPRODUCTION Bibliographic details 2001, VOL 16; PART 1, pages 3-8 Publisher OXFORD UNIVER PRESS Country of publication Great Britain ISBN ISSN Language English Pricing To buy the full text of this article you pay:
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96. Factor V Leiden
activated protein C (APC) resistance. Can not be anticoagulated when this lab run. PCR for Factor V Leiden. Responsible for 95% of APC resistance
http://www.fpnotebook.com/HEM27.htm
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  • 97. NEJM -- Resistance To Activated Protein C
    Correspondence from The New England Journal of Medicine resistance to activated protein C.
    http://content.nejm.org/cgi/content/short/331/2/129
    HOME SEARCH CURRENT ISSUE PAST ISSUES ... HELP Please sign in for full text and personal services Previous Volume 331:129-130 July 14, 1994 Number 2 Next Resistance to Activated Protein C
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    To the Editor: The article by Svensson and Dahlback on resistance to activated protein C (APC) (Feb. 24 issue) postulates that there is a genetically determined defect in anticoagulation characterized by resistance to APC. The authors subsequently found the anticoagulant cofactor that corrects inherited APC resistance to be identical to unactivated factor V. I believe that these findings could also be due to hyperhomocysteinemia. It has been demonstrated that hyperhomocysteinemia is an independent risk factor for vascular disease . It was previously demonstrated that homocysteine induced a vascular-endothelial-cell activator that led to the activation of factor Full Text of this Article References
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    98. NEJM -- Resistance To Activated Protein C As A Basis For Venous Thrombosis
    Original Article from The New England Journal of Medicine resistance to activated protein C as a Basis for Venous Thrombosis.
    http://content.nejm.org/cgi/content/short/330/8/517
    HOME SEARCH CURRENT ISSUE PAST ISSUES ... HELP Please sign in for full text and personal services Volume 330:517-522 February 24, 1994 Number 8 Next Resistance to Activated Protein C as a Basis for Venous Thrombosis
    Peter J. Svensson, and Bjorn Dahlback
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    ABSTRACT Background In three families with various forms of venous thrombosis, we observed an apparently inherited poor response to the anticoagulant activated protein C (APC). The condition was due to a deficiency in a previously unrecognized anticoagulant factor that functioned as a cofactor to activated protein C. Methods We conducted the present study to determine the prevalence of resistance to APC in patients with venous thrombosis. We compared 104 consecutive patients with venous thrombosis confirmed by objective tests with 130 controls. In addition, 211 members of 34 families of persons with resistance to APC were studied. The anticoagulant response to APC was measured with a modified version of the activated partial-thromboplastin time test; the

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