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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Extractions: This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Request Permissions PubMed PubMed Citation Articles by Fisher, M. Articles by Griffin, J. H. Stroke. 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.
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Extractions: Vol Page [Advanced] This Article Full Text (PDF) Submit a response Alert me when this article is cited ... Alert me if a correction is posted Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Download to citation manager PubMed PubMed Citation Articles by Pedersen, O. D. Articles by Jespersen, J. 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 =
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Resistance To Activated Protein C A monthly newsletter about evidencebased health care. http://www.jr2.ox.ac.uk/bandolier/bandopubs/keeling.html
Extractions: @import "../styles/advanced.css"; 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.
Extractions: protein C (resistance to activated protein C) Resistance to the anticoagulant effects of activated protein C (APC) (Factor V Leiden heterozygous*) is common (1): 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.
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
Extractions: resistance to activated protein C Resistance to the anticoagulant effects of activated protein C (APC) (Factor V Leiden heterozygous*) is common (1): 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.
Extractions: 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.
Extractions: This Article Full Text Full Text (PDF) P ... Citation Map Services E-mail this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal ... Cited by other online articles PubMed PubMed Citation Articles by Eldridge, J. Articles by Evatt, B. Related Collections Musculoskeletal System PEDIATRICS Vol. 107 No. 6 June 2001, pp. 1329-1334 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
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
Extractions: 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.
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
Extractions: 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:
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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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
Extractions: Add to Personal Archive Add to Citation Manager E-mail When Cited ... PubMed Citation 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
Extractions: Add to Personal Archive Add to Citation Manager ... PubMed Citation 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
