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| | s030406b - Factor VIII Inhibitors - Acquired or Induced |
 | | Abstract: A multicenter prospective study of recombinant activated factor VII (rFVIIa) given by continuous infusion (CI) to treat severe hemorrhages and to handle surgical procedures was carried out. | | | Acquired factor VIII inhibitors in the nonhemophiliac: historical perspectives, and future approaches. | | | Elective surgery on factor VIII inhibitor patients using continuous infusion of recombinant activated factor VII: plasma factor VII activity of 10 IU/ml is associated with an increased incidence of bleeding.[comment]. |
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http://www.emory.edu/WHSCL/grady/amreport/litsrch02/s030406b.html
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| | Dorlands Medical Dictionary |
| | VII proconvertin: a heat- and storage-stable factor participating in the extrinsic pathway of blood coagulation. | | | VIII antihemophilic factor (AHF): a relatively storage-labile factor participating in the intrinsic pathway of blood coagulation, acting (in concert with von Willebrand factor) as a cofactor in the activation of factor X. Deficiency, an X-linked recessive trait, causes hemophilia A (classical hemophilia). | | | X Stuart factor: a storage-stable factor that participates in both the intrinsic and extrinsic pathways of blood coagulation, uniting them to begin the common pathway of coagulation. |
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http://www.mercksource.com/pp/us/cns/cns_hl_dorlands.jspzQzpgzEzzSzppdocszSzuszSzcommonzSzdorlandszSzdorlandzSzdmd_f_02zPzhtm
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| | Oestrogenic repression of human coagulation factor VII expression mediated through an oestrogen response element sequence motif in the promoter region -- Di Bitondo et al. 11 (7): 723 -- Human Molecular Genetics |
| | 20 Humphries,S.E., Lane,A., Green,F.R., Cooper,J. and Miller,G.J. (1994) Factor VII coagulant activity and antigen levels in healthy men are determined by interaction between factor VII genotype and plasma triglyceride concentration. | | | 26 Humphries,S., Temple,A., Lane,A., Green,F., Cooper,J. and Miller,G. (1996) Low plasma levels of factor VIIc and antigen are more strongly associated with the 10 base pair promoter (-323) insertion than the glutamine 353 variant. | | | Promoter activities are expressed relative to the activity of the corresponding construct in the absence of oestrogenic factors. |
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http://hmg.oupjournals.org/cgi/content/full/11/7/723
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| | Clotting Factor Deficiencies |
| | Factor VII deficiency is a rare (1 per 500,000) autosomal recessive deficiency that exhibits little correlation between the bleeding risk and the factor activity. | | | However, considerable controversy surrounding factor use remains, especially with regard to the age of onset of such therapy and the cost. | | | First-generation recombinant products (Bioclate, Helixate, Kogenate, Recombinate) have demonstrated efficacy in clinical trials; however, they continue to carry a theoretic risk of viral transmission because of the added human albumin necessary for factor stabilization. |
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http://www.clevelandclinicmeded.com/diseasemanagement/hematology/clotting/clotting.htm
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| | Clotting Factor Deficiencies |
| | Factor VII deficiency is a rare (1 per 500,000) autosomal recessive deficiency that exhibits little correlation between the bleeding risk and the factor activity. | | | However, considerable controversy surrounding factor use remains, especially with regard to the age of onset of such therapy and the cost. | | | First-generation recombinant products (Bioclate, Helixate, Kogenate, Recombinate) have demonstrated efficacy in clinical trials; however, they continue to carry a theoretic risk of viral transmission because of the added human albumin necessary for factor stabilization. |
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http://www.clevelandclinicmeded.com/diseasemanagement/hematology/clotting/clotting.htm
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| | Hemostatic Mechanism |
| | The extrinsic pathway begins with the interaction of the phospholipid tissue factor with factor VII to activate factor X. Activated factor X is also generated by the intrinsic pathway, which is initiated by contact activation of factor XII (Hageman factor) when it comes in contact with the negatively charged surfaces underlying the endothelium. | | | Factor VII can be activated by a number of different serine proteases, however, it is preferentially, and most effectively, activated by binding to tissue factor. | | | The third newly rediscovered anticoagulant is Tissue Factor Pathway Inhibitor (TFPI). |
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http://www.cariboo.bc.ca/schs/medtech/rice/newcoag.htm
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| | Bleeding Disorders |
| | Inherited factor VII deficiency is a chronic, life-long disorder. | | | For example, some people with low levels of factor VII do not have bleeding problems. | | | Factors I, II, V, VII, VIII, IX, X, XI, XII and XIII are needed for this chain reaction to take place. |
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http://www.accredohealth.net/hhs/bleeding_disorders/other.html
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| | Sly - publications |
| | Enzyme replacement in murine mucopolysaccharidosis type VII: neuronal and glial response to beta-glucuronidase requires early initiation of enzyme replacement therapy. | | | Enzyme replacement therapy improves reproductive performance in mucopolysaccharidosis type VII mice but does not prevent postnatal losses. | | | Murine mucopolysaccharidosis type VII: the impact of therapies on the clinical course and pathology in a murine model of lysosomal storage disease. |
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http://biochemweb.slu.edu/faculty/images/sly_pubs.html
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| | von Willebrand's disease |
| | Von Willebrand's disease should affect factor VII only, so it is should | | | and prothrombin, which are known as the common factors or common pathway. | | | Von Willebrands factor testing is usually done by comparing a pool of |
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http://www.vetinfo.com/dvonwillebrands.html
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| | Bleeding Disorders |
| | Inherited factor VII deficiency is a chronic, life-long disorder. | | | For example, some people with low levels of factor VII do not have bleeding problems. | | | A deficiency in any of these factors can lead to bleeding problems, each with its own symptoms and treatments. |
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http://www.accredohealth.net/hhs/bleeding_disorders/other.html
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| | Bleeding Disorders -2 |
| | c.Exceptions include factor VII inhibitors and some anticardiolipin antibodies | | | b.No hemorrhagic problems in patients lacking this (Hageman) factor | | | g.Does not appear to be a risk factor for cerebrovascular disease or myocardial infarctions |
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http://enotes.tripod.com/bleeding2.htm
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| | MedlinePlus: Hemophilia |
| | Factor VII Deficiency (Proconvertin or Stable Factor) (National Hemophilia Foundation) | | | New Recombinant Antihemophilic Factor Licensed (Food and Drug Administration) | | | Factor XII Deficiency (Hageman Factor) (National Hemophilia Foundation) |
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http://www.nlm.nih.gov/medlineplus/hemophilia.html
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| | cclement5 |
| | Cn3D presentation of thrombin, factors VII, X and IX. | | | WINDOTTER : analysis of factor XI and factor XII. | | | CATH classification of thrombin and other coagulation factors. |
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http://www.geocities.com/cclement_us/outline7.html
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| | Modulation of factor VII levels by intron 7 polymorphisms: population and in vitro studies -- Pinotti et al. 95 (11): 3423 -- Blood |
| | Modulation of factor VII levels by intron 7 polymorphisms: population and in vitro studies -- Pinotti et al. | | | Factor VII coagulant activity and antigen levels in healthy men are determined by interaction between factor VII genotype and plasma triglyceride concentration. | | | Factor VII Arg/Gln353 polymorphism determines factor VII coagulant activity in patients with myocardial infarction (MI) and control subjects in Belfast and in France but is not a strong indicator of MI risk in the ECTIM study. |
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http://www.bloodjournal.org/cgi/content/full/95/11/3423
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| | Faculty-McMaster Department of Pathology and Molecular Medicine |
| | Brothers A, Clarke, B.J., Sheffield, W.P. and Blajchman, M.A. (1993) Cloning and sequencing of rabbit factor VII cDNA. | | | Clarke, B.J., Ofosu, F.A., Sridhara, S., Bona, R.D., Rickles, F.R. and Blajchman, M.A. (1992) The first epidermal growth factor-like domain of human coagulation factor VII is essential for complex formation with tissue factor. | | | Sridhara, S., Clarke, B.J., Ofosu, F.A., High, K.A. and Blajchman, M.A. (1993) The direct binding of factor VII in human plasma to recombinant human tissue factor. |
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http://www.fhs.mcmaster.ca/path/directory/fac/clarke.htm
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| | eMedicine - Factor VII : Article Excerpt by: Jeyanthi Ramanarayanan, MD |
| | This facilitates conversion of factor VII to factor VIIa. | | | Factor VIIa bound to tissue factor in the presence of calcium and phospholipids facilitates the conversion of factor IX to factors IXa and X to factor Xa. | | | In 1951, Alexander and colleagues identified factor VII as the key initiator of coagulation when they reported the first case of factor VII deficiency in a child and called it serum prothrombin conversion accelerator deficiency. |
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http://www.emedicine.com/med/byname/factor-vii.htm
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| | Clotting Factor Deficiencies |
| | Factor VII deficiency is a rare (1 per 500,000) autosomal recessive deficiency that exhibits little correlation between the bleeding risk and the factor activity. | | | Factor IX replacement has traditionally been with prothrombin complex concentrates (PCCs) that contain factors II, VII, and X as well as IX, and were associated with thrombotic risk. | | | Factor X deficiency is a rare (1 per 1 million) autosomal recessive deficiency characterized by asymptomatic heterozygotes and by homozygotes with bleeding symptoms that correlate with factor activity. |
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http://www.clevelandclinicmeded.com/diseasemanagement/hematology/clotting/clotting.htm
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| | Trigger |
| | Trigger is an electronic newsletter for researchers working on the biology of Tissue Factor, Factor VII and Tissue Factor Pathway Inhibitor (TFPI). | | | We call our newsletter "Trigger" because Tissue Factor and Factor VII are the proteins that trigger the blood clotting system in normal hemostasis and most thrombotic diseases. | | | These web pages contain information for biomedical researchers on the biology of Tissue Factor, Factor VII and TFPI. |
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http://tf7.org
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| | Polymorphisms of the Factor VII Gene and Circulating FVII:C Levels in Relation to Acute Cerebrovascular Disease and Poststroke Mortality -- Heywood et al. 28 (4): 816 -- Stroke |
| | Miller GJ, Stirling Y, Esnouf MP, Heinrich J, van de Loo J, Kienast J, Wu KK, Morrissey JH, Meade TW, Martin JC, Cooper JA, Finch A. Factor VII-deficient substrate plasmas depleted of protein C raise the sensitivity of the factor VII bio-assay to activated factor VII: an international study. | | | Heinrich J, Balleisen L, Schulte H, Assmann G, Van de Loo J. Fibrinogen and factor VII in the prediction of coronary risk: results from the PROCAM study in healthy men. | | | Balleisen L, Schulte H, Assman G, Epping PH, Van de Loo J. Coagulation factors and the progress of coronary heart disease. |
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http://stroke.ahajournals.org/cgi/content/full/28/4/816
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| | Morrissey Lab |
| | Factor VIIa/tissue factor generates a form of factor V with unchanged specific activity, resistance to activation by thrombin and increased sensitivity to activated protein C. Biochemistry 38:1829-1837, 1999. | | | Activation of factor VII during alimentary lipaemia occurs in healthy adults and patients with congenital factor XII or factor XI deficiency, but not in patients with factor IX deficiency. | | | The influence exerted by a restricted phospholipid microenvironment on the expression of tissue factor activity at the cell plasma membrane surface. |
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http://tf7.org/pubsthree.htm
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| | MECHANISMS OF THROMBOSIS OF THE ANTIPHOSPHOLIPID ANTIBODIES |
| | Induced tissue factor forms a tissue factor/activated factor VII complex in the presence of phospholipids and activates rapidly factors IX and X. The tissue factor pathway is modulated by the tissue factor pathway inhibitor. | | | Autoantibodies to tissue factor pathway inhibitor in the antiphospholipid syndrome. | | | Induction of endothelial cell tissue factor activity by sera from patients with antiphospholipid syndrome: a possible mechanism of thrombosis. |
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http://www.rheuma21st.com/archives/cutting_edge_22nov2004.html
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| | s030406b - Factor VIII Inhibitors - Acquired or Induced |
| | Elective surgery on factor VIII inhibitor patients using continuous infusion of recombinant activated factor VII: plasma factor VII activity of 10 IU/ml is associated with an increased incidence of bleeding.[comment]. | | | Abstract: A strategy is described for the initial detection, management and elimination of factor VIII inhibitors arising in patients with congenital and acquired haemophilia A. It is suggested that children with severe haemophilia A should be screened every 3 months up to the age of 10 years for inhibitors using the Bethesda method. | | | After that, factor VIII inhibitor was suppressed and the patient's hemostatic defect continued to improve even after the reduction of the steroid dose. |
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http://www.emory.edu/WHSCL/grady/amreport/litsrch02/s030406b.html
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| | Trigger |
| | Trigger is an electronic newsletter for researchers working on the biology of Tissue Factor, Factor VII and Tissue Factor Pathway Inhibitor (TFPI). | | | We call our newsletter "Trigger" because Tissue Factor and Factor VII are the proteins that trigger the blood clotting system in normal hemostasis and most thrombotic diseases. | | | Its purpose is to share information among researchers who are investigating how the blood clotting system is controlled. |
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http://tf7.org
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| | THE MERCK MANUAL, Sec. 11, Ch. 131, Hemostasis And Coagulation Disorders |
| | (Because commercial reagents and instrumentation vary widely, each laboratory should determine its own normal range; 28 to 34 sec is typical.) The PTT is sensitive to deficiencies of 30 to 40% of all clotting factors except factors VII and XIII. | | | Factor X activation requires both routes for normal hemostasis, presumably because the catalytic activity of factor VIIa/tissue factor is inhibited as coagulation proceeds by a factor Xa-dependent mechanism. | | | Factor V Leiden is a genetic mutation (substitution of arginine with glutamine at position 506) that decreases degradation of factor Va by activated protein C. The heterozygous state is extremely common (3 to 15%) in various populations (averaging 7% in the USA) and results in increased incidence of venous thromboembolism. |
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http://www.merck.com/mrkshared/mmanual/section11/chapter131/131b.jsp
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