41. ACTIVATED PROTEIN C RESISTANCE (APC-R), PLASMA activated protein c resistance (APCR), PLASMA Marquette General Health System GeneralInfo Alpha Code. APCR. MGH LIS Test No. 977. Schedule. Monday through Friday. http://www.mgh.org/lab/CATALOG/TESTS/5096.HTM

42. A - Tests CULTURE ACTIVATED PARTIAL THROMBOPLASTIN TIME ACTIVATED PROTEIN C (APC) RESISTANCEMUTATION activated protein c resistance (APCR), PLASMA ACTIVE PROTEIN C (APC http://www.mgh.org/lab/CATALOG/ATESTS.HTM

A(2) HEMOGLOBIN A-1-ANTITRYPSIN A2 HEMOGLOBIN A2 HEMOGLOBIN, COLUMN A(2) HEMOGLOBIN A-1-ANTITRYPSIN A2 HEMOGLOBIN A2 HEMOGLOBIN, COLUMN ... AZT

43. Authors' Response. Swalwell CI, Davis GG . 1999;44(5): 1092. Rulon JJ, Cho CG, Guerra LL, Bux RC, Gulley ML Title activated protein c resistanceis uncommon in sudden death due to pulmonary embolism Keywords activated http://www.astm.org/JOURNALS/FORENSIC/PAGES/3199.htm

Citation Information Stock #: Volume: Issue: Year: Pages: Author(s): Swalwell CI, Davis GG Title: Authors' Response Keywords: forensic science, methamphetamine, toxicologic studies Abstract: *PDF not available Return to Main Page

44. Untitled ANTICOAGULANT PROTEIN DEFICIENCY. activated protein c resistance. ACTIVATED PROTEINC RESISTANCE. activated protein c resistance. PROTEIN C MECHANISM OF ACTION. http://cpmcnet.columbia.edu/dept/ps/2004/Academic/second_year/hematology/html/di

REGULATION OF COAGULATION/DISSEMINATED INTRAVASCULAR COAGULATION REGULATION OF COAGULATIONIntroduction COAGULATION CASCADE COAGULATION INHIBITORS REGULATION OF COAGULATION/DISSEMINATED INTRAVASCULAR COAGULATION REGULATION OF COAGULATIONIntroduction COAGULATION CASCADE COAGULATION INHIBITORS ... LIVER DISEASE

45. Factor V Leiden Deficiency Factor 5 Leiden Deficiency. APC Resistance. activated protein c resistance. LabsActivated Protein C (APC) resistance Can not be anticoagulated when this lab run. 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

46. Biochem. J. (1996) 313, 467-472 - C. Aparicio And B. Dahlba~Dck - Factor V:Q506 Biochem. J. (1996) 313, (467–472) (Printed in Great Britain). Molecularmechanisms of activated protein c resistance Properties http://www.biochemj.org/bj/313/bj3130467.htm

Whole site Author Keywords Title Medline/PubMed Citation Related Articles in PubMed Download to Citation Matcher Biochem. J. (1996) (Printed in Great Britain) Molecular mechanisms of activated protein C resistance Properties of factor V isolated from an individual with homozygosity for the Arg to Gln mutation in the factor V gene Abbreviations used: APC, activated protein C; FV, factor V; FVa, activated factor V; FV:Q , factor V with glutamine (Q) at position 506 ; FV:R , factor V with arginine (R) at position 506; FXa, activated factor X; mAb, monoclonal antibody; HPC4, mAb against protein C; HPS54, mAb against protein S; HFV30, mAb against factor V; EGF, epidermal growth factor; PPACK, D -phenylalanyl- L -prolyl- L -arginine chloromethyl ketone; PEG, polyethylene glycol; APTT, activated partial thromboplastin time. * To whom correspondence should be addressed. Resistance to activated protein C (APC), which is the most prevalent pathogenetic risk factor of thrombosis, is linked to a single point-mutation in the factor V (FV) gene, which predicts replacement of Arg (R) at position 506 with a Gln (Q). This mutation modifies one of three APC-cleavage sites in the heavy chain of activated FV (FVa), suggesting that mutated FVa (FVa:Q ) is at least partially resistant to APC-mediated degradation. To elucidate the molecular mechanisms of APC-resistance and to investigate the functional properties of FV in APC resistance, FV:Q

47. LINEE GUIDA PER LO SCREENING DEI PAZIENTI TROMBOFILICI Koeleman BPC, Reitsma PH, Allaart CF, Bertina RM activated protein c resistanceas an additional risk factor for thrombosis in protein C deficient families. http://www.xxlweb.it/siset/linee/linee17f.htm

48. Activated Protein C Resistance - New Treatments, February 5, 2003 Click here to view. New Treatments for activated protein c resistance. Resistanceto activated protein C is a congenital inherited hypercoagulable disease. http://www.medical-library.org/journals_6a/activated_protein_c.htm

This page has moved. Click here to view. New Treatments for Activated Protein C Resistance Resistance to activated protein C is a congenital inherited hypercoagulable disease. The problem here is that normally protein C with a co-factor of protein S controls the activity, if you will, down the coagulation pathway starting with number 11, then 12, 9, 8 and so on as the cascade moves down. This system here normally protein C co-factor S inactivates number 5 and number 8 coagulation factor proteins. They are kind of keeping a balance here to prevent ongoing conversion of soluble fibrinogen to insoluble fibrin. That’s the whole idea of this system. We see here that here is factor V and normally this undergoes degradation. But in resistance to activated protein C there is at position 506 in the factor V molecule, arginine moiety is replaced by glutamine, and this is what identifies this. The factor V gene also has an abnormality in it at position 1691. The factor V at 506, the factor V molecule, this arginine is replaced by a glutamine, it’s resistant now to the normal degradation of activated protein C, and the factor V gene here at 1691 a glutamine is replaced by an arginine with a single point mutation. This problem is variously reported in different articles and publications to be at a frequency rate in some places of 30, 40, 50, 60% of the populations that are studied. However you and I all know that thrombosis is not in any way shape or form found in that frequency. So one must be somewhat concerned about this and the absolute direct connection that it may have. This may not always really be the answer for this situation, but of the things that you can look for today, it’s certainly going to be high on the list for an etiologic or diagnostic test that can be done. So don’t forget about this population of resistance to activated protein C. The presence of the factor V Leyden molecule, which does not undergo normal degradation as it should, by protein C with a co-factor of protein S.

49. Haematologica/journal Of Hematology - Issue #1, 2000 - Scientific Correspondence Factor V Leiden in absence of activated protein c resistance after orthotopicliver transplantation in a patient without thrombosis but with familial http://www.haematologica.it/abstr/estelles8501.html

Medline reference of this article PDF version Factor V Leiden in absence of activated protein C resistance after orthotopic liver transplantation in a patient without thrombosis but with familial thrombophilia Correspondence E-mail: jaznarl@san.gva.es full text S ir, There are reports that orthotopic liver transplantation may produce phenotypic correction of activated protein C (APC) resistance in patients with FV Leiden. We report the case of a factor V Leiden heterozygote with absence of APC reistance following an orthotopic liver transplantation. The patient suffered not thrombotic episodes prior to or after the transplant despite a strong history of familial thrombophilia. We report a heterozygous FV Leiden individual with absence of activated protein C (APC) resistance following orthotopic liver transplantation. APC resistance is associated with a mutation in factor V gene, named FV Leiden. APC resistance is defined as a poor anticoagulant response of the patient's plasma to APC. Some patients with APC resistance do not have the FV Leiden, and this suggests the existence of an acquired APC resistance phenotype. However, the existence of the FV mutation without APC resistance is a rare cause of discrepancy between the genotypic and phenotypic analyses.

50. Haematologica 1998; Vol. 83, No. 4 Prevalence of phenotypic activated protein c resistance (APCR) invenous thromboembolic patients. Cristina Marzo, Carmen Araguás http://www.haematologica.it/abstr/marzo834.html

Prevalence of phenotypic activated protein C resistance (APCR) in venous thromboembolic patients E-mail: xga@medicina.udl.es Full text Until the discovery of activated protein C resistance (APCR), less than 10% of patients with venous thromboembolism (VT) showed defects in proteins involved in the inhibition of coagulation. APCR is caused by a single point mutation in the factor V gene, and it is accepted that APCR is associated with an increased risk for VT. In this work, we studied the prevalence of APCR in venous thromboembolic patients and found it to be 10.5% compared with 4.5% in controls (p=0.105). We prospectively studied 172 consecutive patients with VT (Table 1). Thrombophilia assay was performed one month after the end of oral anticoagulant therapy. We studied: platelet number, prothrombin, activated-partial-thromboplastin and thrombin time, fibrinogen, antithrombin III, plasminogen, functional C and S proteins, lupus anticoagulant, anticardiolipin antibodies and APCR-test (APCR Coatest, Chromogenix, Sweden). Table 1.

51. Reduced Response To Activated Protein C..., Annals 15 Aug 96 activated protein c resistance as an additional risk factor for thrombosis inprotein Cdeficient families. Blood. 1994;841031-5. 24. Miettinen OS. http://www.acponline.org/journals/annals/15aug96/proteinc.htm

Annals of Internal Medicine Current Issue Past Issues Library for Internists Subscriptions ... Email this page Annals of Internal Medicine Reduced Response to Activated Protein C Is Associated with Increased Risk for Cerebrovascular Disease Annals of Internal Medicine , 15 August 1996. 125:265-269. Johanna G. van der Bom, MD; Michiel L. Bots, MD, PhD; Frits Haverkate, PhD; P. Eline Slagboom, PhD; Piet Meijer, BSc; Paulus T.V.M. de Jong, MD, PhD; Albert Hofman, MD, PhD; Diederick E. Grobbee, MD, PhD; and Cornelis Kluft, PhD Background: Resistance to activated protein C (APC), which results from various factors, including a mutation in the gene for coagulant factor V, has been associated with increased risk for venous thrombosis. However, its relation to arterial disease is still not well defined. Objective: To investigate the association of both response to APC and the factor V Leiden mutation with arterial disease. Design: Population-based case-control study. Setting: A district of Rotterdam, the Netherlands. Participants: 115 patients with a history of myocardial infarction; 112 patients with a history of stroke, transient ischemic attack, or both; and 222 age-matched controls without arterial disease chosen from among 7983 persons in the Rotterdam Study cohort. Patients using anticoagulant drugs were excluded.

52. Clinical Laboratories RIPA); Thrombosis Screen (protein C, protein S, antithrombin III,activated protein c resistance, factor V Leiden); Thrombin Time; http://www-med.stanford.edu/school/clin.labs/coag.html

Coagulation Laboratories Activated Partial Thromboplastin Time (aPTT) Clot retraction D-Dimer DIC Screen ... Medical Center The MedNET Web Project manages this server. Comments are welcomed. This page last changed 10 October 1996.

53. Untitled activated protein c resistance or Factor V Leiden (Factor V is notinhibited so it can make lots and lots of clots); Plasminogen http://www.u.arizona.edu/ic/srl/heme/coaganswers4.html

Coagulation Review - Part 4 FIBRINOLYTIC SYSTEM AND THROMBOSIS FIBRINOLYSIS What are the most important members of the fibrinolytic system? (I know, bad question as they are all important) plasmin, plasminogen, plasminogen activator inhibitors (PAI), tissue plasminogen activators (TPA) Explain why a physician would treat a patient with ATIII rather than use urokinase: ATIII prevents formation of clots while streptokinase/urokinase breaks up clots. Since these are two different problems, the physician would need to determine which situation would be of benefit to the patient's condition. List the activators of the fibrinolytic system: Endogenous: the contact factors XI, XII, PK, and HMWK and tPA Exogenous: Streptokinase, and tPA Does this explain why a deficiency of XII, PK, or HMWK is more likely to cause a thrombosis than a bleed Absolutely. What does tPA do? I don't think anyone knows for sure but it is the most important activator of plasminogen List the inhibitors of the fibrinlytic system: alpha-2-antiplasmin ATIII PAI-1 (plasminogen activator inhibitor) TESTS Most important test to detect activation of the fibrinolytic system is the euglob lysis.

54. ACTIVATED PROTEIN C RESISTANCE activated protein c resistance (0890240). Synonyms APCR. CPT 4 Code85307. Test Order Mnemonic APCR. Applies To A screening assay http://www.utmb.edu/lsg/LabSurvivalGuide/hem/ACTIVATEDproteinC_Resistance.htm

A B C D ... Pathology Clinical Services Home Page ACTIVATED PROTEIN C RESISTANCE (089-0240) Synonyms: APCR CPT 4 Code Test Order Mnemonic: APCR Applies To: A screening assay for the detection of activated protein C resistance (APCR) in patients with a history of recurrent venous thrombosis. Most patients with a positive APCR screening assay have a specific mutation in the coagulant factor V gene (Factor V Leiden mutation). Test Includes: APCV Ratio; Interpretation of result. Request Form: Hematology A Collection: Patient should be at rest for 10-20 minutes prior to collection. Standard venipuncture collection for Coagulation specimens. Discard 1st ml of blood or collect other tubes (EDTA, Serum-separator, etc.) prior to collecting sample in 3.2% citrate (light blue-top) tube. Storage Instructions: Viable for 4 hours at room temperature. If time from draw to delivery is to be greater than 4 hours, centrifuge the sample, separate the plasma from cells, and snap freeze (-70°C) the plasma. Snap frozen plasma is viable for 6 months. Special Instructions: Prior to ordering this test, verify that the APTT is in the normal range

55. Factor V Leiden Polymorphism (FV:R506Q) Related Tests. activated protein c resistance (APC) aPTTBased. Activated ProteinC Resistance (APC) PT-Based. Anticardiolipin Antibodies (IgG, IgM, IgA). http://pathology.mc.duke.edu/coag/fvlflyer2.html

Factor V Leiden Polymorphism (FV Test Overview Resistance to activated protein C (APC) is a frequently identified abnormality in patients with venous thrombosis. In patients presenting with an initial venous thromboembolic event, as many as 21% have APC resistance. Furthermore, in patients with recurrent venous thrombosis, as many as 60% have APC resistance. APC resistance has also been associated with atypical thromboembolic complications, including portal vein thrombosis and cerebral sinus thrombosis. Exposure to certain environmental risk factors, such as surgery, pregnancy, or oral contraceptives, can further increase the risk for a venous thrombotic event. Although APC resistance is a common finding in patients with venous thrombosis, it is seldom identified as a risk factor for arterial thrombosis. Laboratory screening for APC resistance consists of clotting assays that measure the degree of prolongation of the plasma clotting time upon the addition of APC. In more than 90% of cases, APC resistance is linked to a single polymorphism in the factor V gene. This polymorphism, known as Factor V Leiden (Factor V ), involves a single base pair substitution at position 1691 in the factor V gene, resulting in substitution of the arginine (R) at position 506 by glutamine (Q). This substitution blocks an important APC-cleavage site in factor Va after position 506, thereby resulting in a decreased ability of APC to inactivate the procoagulant factor Va. This single polymorphism results in the observed hypercoagulable state that leads to an increased risk for venous thromboembolism.

56. Testing Turn-around Times - DUMC Clinical Coagulation Laboratory Activated Partial Thromboplastin Time (aPTT), daily. activated protein c resistance(aPTTbased), 1/week. activated protein c resistance (Factor V Leiden), 1/week. http://pathology.mc.duke.edu/coag/TAT.htm

Clinical Coagulation Laboratory A division of Duke University Regional Referral Laboratory Services Alert! Beware of falling CLOTS! Images ( Click on the image to see an enlarged version or click on the title for image details. LIS Computer specimen tracking and report generation Central Laboratory Support Services IL ACL 300+ Testing Turn-around-Times Test: Frequency: Activated Partial Thromboplastin Time (aPTT) daily Activated Protein C Resistance (aPTT-based) 1/week Activated Protein C (PT-based) 1/week Activated Protein C Resistance (Factor V Leiden) 1/week ADP Titration Platelet Aggregation Study daily (except weekends) Alpha-2 Plasmin Inhibitor 2/week Anticardiolipin Antibodies (IgG, IgM, IgA) 2/week Antithrombin III-Plasma Activity 2/week Antithrombin III-Plasma Antigen 1/week Automated Blood Count daily Automated Blood Count with Differential daily Bleeding Time daily D-Dimer daily D-Dimer, Titered daily D-Dimer, (ELISA) 1/week daily daily Epinephrine Titration Platelet Aggregation Study daily (except weekends) Euglobulin Clot Lysis Time daily Factor Assays (II, V, VII, VIII, IX, X, XI, XII)

57. Haematologica - February 2003 - 236 activated protein c resistance (APCR), is a biological condition relatedwith venous and to a lesser extent arterial thrombosis. http://www.haematologica.org/2003_02/236.htm

Medline PDF prev index ... next Evaluation of the factor V HR2 haplotype as a risk factor for ischemic cerebrovascular disease Correspondence: Dr. Eduardo Rocha Phone: +34.9.48296397. Fax: +34.9.48296500. The HR2 haplotype of the factor V (FV) gene has been identified as a cause of resistance to activated protein C, specially in the presence of FV Leiden. We studied the prevalence of the HR2 haplotype in 115 patients with a first episode of ischemic cerebrovascular disease (CVD) and 115 age- and sex-matched healthy controls. Our results show that the HR2 haplotype is not associated with an increased risk of CVD. Activated protein C resistance (APCR), is a biological condition related with venous and to a lesser extent arterial thrombosis. A single point mutation in the factor V gene, G1691A, known as FV Leiden, is the most frequent cause of APCR in the Caucasian population. APCR has been associated with an increased risk of CVD, independently of FV Leiden mutation. On the other hand, the contribution of FV Leiden to the risk of CVD seems to be very low, if any.

58. Hematology Center-Education-Information Thrombosis. Antithrombin III Deficiency activated protein c resistance Tests ActivatedProtein C Resistance Factor V Leiden Syndrome Factor V Leiden Mutation http://www.worldoncology.net/hemcenter.htm

Hematology Center Bookstore Home Health Hospice Mental HealthCounselors ... Second Opinion Full Text Articles See Complete Full Text Archive Red Cell Areas Anemia: Approach to Diagnosis Aplastic Anemia Hemoglobinopaties Hemolytic Anemias ... Thalassemia Platelets Corner Adult Chronic Immune Thrombocytopenic Purpura Bernard-Soulier Syndrome Glanzmann Thrombasthenia Hemolytic Uremic Syndrome ... Von Willebrand Disease Hemostasis Molecular Genetics and Blood Coagulation Forum and Resource Center Factor VIII Factor IX ... Vitamin K Deficiency Thrombosis Antithrombin III Deficiency Activated Protein C Resistance Tests Activated Protein C Resistance Factor V Leiden Syndrome ... Protein C Deficiency Bone Marrow Transplant Bone Marrow Transplant Program UNMC/NHS Bone Marrow Transplant Program at Columbia Presbyterian in New York.

59. Journal Of Medical Screening (1998) 5, 1-2 Fortunately, a modification of the activated protein c resistance test, dilutingthe patient's plasma in factor V deficient plasma, results in the sensitivity http://www.medschl.cam.ac.uk/phgu/phgn/Private_documents/Papers/Keeling.asp

60. Descripteur - Activated Protein C Resistance Descripteur MESH Hemic and Lymphatic Diseases Hematologic Diseases Thrombophiliaactivated protein c resistance MESH Congenital, Hereditary, and Neonatal http://alexpub.hospvd.ch/Thesaurus.htm&numrec=051914279919600

A  B  C  D  E  F  G  H  I  J  K  L  M  N  O  P  Q  R  S  T  U  V  W  X  Y  Z

Page 3     41-60 of 87    Back | 1  | 2  | 3  | 4  | 5  | Next 20