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Factor IX Deficiency

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41. Factor IX (Overview)

Factor IX (Overview) Factor IX Deficiency (Hemophilia B): Practice Essentials, Background, Pathophysiology Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTk5MDg4LW92ZXJ2aWV3 processing > Factor IX Deficiency (...) (Hemophilia B) Updated: Apr 02, 2018 Author: Robert A Schwartz, MD, MPH; Chief Editor: Srikanth Nagalla, MBBS, MS, FACP Share Email Print Feedback Close Sections Sections Factor IX Deficiency (Hemophilia B) Overview Practice Essentials Factor IX (FIX) deficiency or dysfunction, or hemophilia B, is an X-linked inherited bleeding disorder, usually manifested in males and transmitted by females who carry the causative mutation on the X chromosome. Hemophilia B results from a variety of defects in the FIX

2014 eMedicine.com

42. Factor IX (Diagnosis)

Factor IX (Diagnosis) Factor IX Deficiency (Hemophilia B): Practice Essentials, Background, Pathophysiology Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTk5MDg4LW92ZXJ2aWV3 processing > Factor IX Deficiency (...) (Hemophilia B) Updated: Apr 02, 2018 Author: Robert A Schwartz, MD, MPH; Chief Editor: Srikanth Nagalla, MBBS, MS, FACP Share Email Print Feedback Close Sections Sections Factor IX Deficiency (Hemophilia B) Overview Practice Essentials Factor IX (FIX) deficiency or dysfunction, or hemophilia B, is an X-linked inherited bleeding disorder, usually manifested in males and transmitted by females who carry the causative mutation on the X chromosome. Hemophilia B results from a variety of defects in the FIX

2014 eMedicine.com

43. Factor IX (Treatment)

Factor IX (Treatment) Factor IX Deficiency (Hemophilia B) Treatment & Management: Medical Care, Surgical Care, Consultations Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTk5MDg4LXRyZWF0bWVudA== processing (...) > Factor IX Deficiency (Hemophilia B) Treatment & Management Updated: Apr 02, 2018 Author: Robert A Schwartz, MD, MPH; Chief Editor: Srikanth Nagalla, MBBS, MS, FACP Share Email Print Feedback Close Sections Sections Factor IX Deficiency (Hemophilia B) Treatment Medical Care Highly purified factor IX (FIX) concentrates are now available. These include monoclonal antibody–purified plasma-derived FIX (pdFIX; Immunine and Mononine) and recombinant FIX (rFIX). A review of the global experience with pdFIX

2014 eMedicine.com

44. Factor IX (Follow-up)

Factor IX (Follow-up) Factor IX Deficiency (Hemophilia B) Follow-up: Further Outpatient Care, Further Inpatient Care, Inpatient & Outpatient Medications Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache (...) =aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTk5MDg4LWZvbGxvd3Vw processing > Factor IX Deficiency (Hemophilia B) Follow-up Updated: Apr 02, 2018 Author: Robert A Schwartz, MD, MPH; Chief Editor: Srikanth Nagalla, MBBS, MS, FACP Share Email Print Feedback Close Sections Sections Factor IX Deficiency (Hemophilia B) Follow-up Further Outpatient Care Home care programs with self-infusion of FIX concentrate at the earliest sign of bleeding have medical and psychological benefits to the patient. Home care allows prompt care for bleeding, minimizes delays

2014 eMedicine.com

45. Analysis of the factor XI variant Arg184Gly suggests a structural basis for factor IX binding to factor XIa. (PubMed)

Analysis of the factor XI variant Arg184Gly suggests a structural basis for factor IX binding to factor XIa. A patient with factor XI (FXI) deficiency was reported with an Arg184Gly substitution in the FXI A3 domain. The A3 domain contains an exosite required for binding of FIX to activated FXI (FXIa).To test the effects of the Arg184Gly substitution on FIX activation, and to characterize the FIX-binding site on FXIa.Recombinant FXIa and FIX variants were used to identify residues involved

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2013 Journal of Thrombosis and Haemostasis

46. Evidence for factor IX-independent roles for factor XIa in blood coagulation. (PubMed)

Evidence for factor IX-independent roles for factor XIa in blood coagulation. Factor XIa is traditionally assigned a role in FIX activation during coagulation. However, recent evidence suggests this protease may have additional plasma substrates.To determine whether FXIa promotes thrombin generation and coagulation in plasma in the absence of FIX, and to determine whether FXI-deficiency produces an antithrombotic effect in mice independently of FIX.FXIa, FXIa variants and anti-FXIa antibodies (...) were tested for their effects on plasma coagulation and thrombin generation in the absence of FIX, and for their effects on the activation of purified coagulation factors. Mice with combined FIX and FXI deficiency were compared with mice lacking either FIX or FXI in an arterial thrombosis model.In FIX-deficient plasma, FXIa induced thrombin generation, and anti-FXIa antibodies prolonged clotting times. This process involved FXIa-mediated conversion of FX and FV to their active forms. Activation

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2013 Journal of Thrombosis and Haemostasis

47. The economic evaluation of early intervention with Anti-Tumor Necrosis Factor-? treatments in pediatric Crohn's disease

The economic evaluation of early intervention with Anti-Tumor Necrosis Factor-? treatments in pediatric Crohn's disease The Hospital for Sick Children Technology Assessment at SickKids (TASK) FULL REPORT THE ECONOMIC EVALUATION OF EARLY INTERVENTION WITH ANTI-TUMOR NECROSIS FACTOR-a TREATMENTS IN PEDIATRIC CROHN’S DISEASE Authors: Naazish S. Bashir, MSc, MBA, PhD Research Fellow, Child Health Evaluative Sciences, The Hospital for Sick Children, Toronto, Canada Thomas D. Walters, MD, MSc Staff (...) Randomized controlled trial SD Standard Deviation SOC Standard of Care TNF Tumor necrosis factor UC Ulcerative colitis UK United Kingdom USA or US United States of America wPCDAI Weighted Pediatric Crohn’s Disease Activity Index WTP Willingness to pay Table of Contents Executive Summary xx Acknowledgements ii Table of Contents v List of Tables x List of Figures xv List of Appendices xviii List of Abbreviations iii Introduction 1 1.1 Overview 1 1.2 Background Information 6 1.2.1 Crohn’s Disease 6 1.3 Anti

2019 SickKids Reports

48. Extended half-life clotting factor concentrates for treatment of haemophilia A and B

funding through the NBA. MSAC noted that the incidence of haemophilia A (caused by deficiency of factor VIII) is approximately 1 in 10,000, and the incidence of haemophilia B (caused by deficiency of factor IX) is approximately 1 in 50,000. Female carriers of gene mutations for coagulation protein factors may also exhibit symptoms. MSAC noted that there is a high disease burden in patients with moderate and severe haemophilia. Recurrent bleeding can cause arthropathy, intracranial and retroperitoneal (...) funding for extended half-life (EHL) clotting factors VIII and IX products through the national blood arrangements. 2. MSAC’s advice to the Minister After considering the strength of the available evidence in relation to comparative safety, clinical effectiveness and cost effectiveness, MSAC supported the inclusion of extended half- life clotting factor concentrates (factors VIII and IX) in the National Products Price List maintained by the National Blood Authority (NBA). MSAC gave detailed advice

2018 Medical Services Advisory Committee

49. Activation of factor IX by the reaction product of tissue factor and factor VII: additional pathway for initiating blood coagulation. (PubMed)

activated Factor XI, for the activation of Factor IX during hemostasis. It may help to explain the discrepancy between the mild bleeding of hereditary Factor XI deficiency and the severe bleeding of hereditary Factor IX deficiency. (...) Activation of factor IX by the reaction product of tissue factor and factor VII: additional pathway for initiating blood coagulation. A study was carried out on mechanisms, independent of activated Factor XI, capable of activating Factor IX. The reaction product of tissue factor and Factor VII functioned as a potent Factor IX activator in the assay system used. Activated Factor IX itself activated Factor X; thrombin failed to activate Factor IX. Sodium dodecyl sulfate/polyacrylamide gel

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1977 Proceedings of the National Academy of Sciences of the United States of America

50. Activation of Human Factor VII in Plasma and in Purified Systems: ROLES OF ACTIVATED FACTOR IX, KALLIKREIN, AND ACTIVATED FACTOR XII (PubMed)

Activation of Human Factor VII in Plasma and in Purified Systems: ROLES OF ACTIVATED FACTOR IX, KALLIKREIN, AND ACTIVATED FACTOR XII Factor VII can be activated, to a molecule giving shorter clotting times with tissue factor, by incubating plasma with kaolin or by clotting plasma. The mechanisms of activation differ. With kaolin, activated Factor XII (XII(a)) was the apparent principal activator. Thus, Factor VII was not activated in Factor XII-deficient plasma, was partially activated (...) in prekallikrein and high-molecular weight kininogen (HMW kininogen)-deficient plasmas, but was activated in other deficient plasmas. After clotting, activated Factor IX (IX(a)) was the apparent principal activator. Thus, Factor VII was not activated in Factor XII-,HMW kininogen-, XI-, and IX-deficient plasmas, but was activated in Factor VIII-, X-, and V-deficient plasmas. In further studies, purified small-fragment Factor XII(a) (beta-XII(a)), kallikrein, and Factor IX(a) were added to partially purified

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1979 Journal of Clinical Investigation

51. Alloimmunization in Congenital Deficiencies of Platelet Surface Glycoproteins: Focus on Glanzmann's Thrombasthenia and Bernard-Soulier's Syndrome. (PubMed)

Alloimmunization in Congenital Deficiencies of Platelet Surface Glycoproteins: Focus on Glanzmann's Thrombasthenia and Bernard-Soulier's Syndrome. Glanzmann's thrombasthenia (GT) and Bernard-Soulier's syndrome (BSS) are well-understood congenital bleeding disorders, showing defect/deficiency of platelet glycoprotein (GP) IIb/IIIa (integrin αIIbβ3) and GPIb-IX-V complexes respectively, with relevant clinical, laboratory, biochemical, and genetic features. Following platelet transfusion, affected (...) patients may develop antiplatelet antibodies (to human leukocyte antigen [HLA], and/or αIIbβ3 in GT or GPIb-IX in BSS), which may render future platelet transfusion ineffective. Anti-αIIbβ3 and anti-GPIb-IX may also cross the placenta during pregnancy to cause thrombocytopenia and bleeding in the fetus/neonate. This review will focus particularly on the better studied GT to illustrate the natural history and complications of platelet alloimmunization. BSS will be more briefly discussed. Platelet

2018 Seminars In Thrombosis And Hemostasis

52. Everolimus in Castrated Resistant Prostate Cancer(CRPC)Patients With PI3K-AKT-mTOR Signaling Pathway Deficiency

Everolimus in Castrated Resistant Prostate Cancer(CRPC)Patients With PI3K-AKT-mTOR Signaling Pathway Deficiency Everolimus in Castrated Resistant Prostate Cancer(CRPC)Patients With PI3K-AKT-mTOR Signaling Pathway Deficiency - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved (...) studies (100). Please remove one or more studies before adding more. Everolimus in Castrated Resistant Prostate Cancer(CRPC)Patients With PI3K-AKT-mTOR Signaling Pathway Deficiency The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. of clinical studies and talk to your health care provider before participating. Read our for details. ClinicalTrials.gov

2018 Clinical Trials

53. Vitamin K deficiency: a case report and review of current guidelines (PubMed)

Vitamin K deficiency: a case report and review of current guidelines Vitamin K, a fat soluble vitamin, is a necessary cofactor for the activation of coagulation factors II, VII, IX, X, and protein C and S. In neonatal period, vitamin K deficiency may lead to Vitamin K Deficiency Bleeding (VKDB).We present the case of a 2 months and 20 days Caucasian male, presented for bleeding from the injections sites of vaccines. At birth oral vitamin K prophylaxis was administered. Neonatal period (...) was normal. He was exclusively breastfed and received a daily oral supplementation with 25 μg of vitamin K. A late onset vitamin K deficiency bleeding was suspected. Intravenous Vitamin K was administered with complete recovery.Nevertheless the oral prophylaxis, our case developed a VKDB: it is necessary to revise the current guidelines in order to standardize timing and dosage in different clinical conditions.

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2018 Italian journal of pediatrics

54. Recombinant Factor VIIa addition to hemophilic blood perfused over collagen/tissue factor can sufficiently bypass the Factor IXa/VIIIa defect to rescue fibrin generation (PubMed)

Recombinant Factor VIIa addition to hemophilic blood perfused over collagen/tissue factor can sufficiently bypass the Factor IXa/VIIIa defect to rescue fibrin generation Factor VIII (FVIII) or factor IX (FIX)-deficient haemophilic patients display deficits in platelet and fibrin deposition under flow detectable in microfluidics. Compared to fibrin generation, decreased platelet deposition in haemophilic blood flow is more easily rescued with recombinant factor VIIa (rFVIIa), whereas rFVIIa (...) of 100 s-1 .With WB from healthy controls, platelet deposition and fibrin accumulation increased as TF increased. Factor-deficient WB (1-3% of normal) displayed striking deficits in platelet deposition and fibrin formation at either TFlow or TFhigh . In contrast, mildly factor-deficient WB (14-32%) supported fibrin formation under flow on TFhigh /collagen. With either TFlow or TFhigh , exogenously added rFVIIa (20 nm) increased platelet deposition and fibrin accumulation in WB from factor-deficient

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2017 Haemophilia : the official journal of the World Federation of Hemophilia

55. MASAC Statement Regarding Use of Various Clotting Factor Assays to Monitor Factor Replacement Therapy

, magnifying limitations with the assays currently available for monitoring replacement therapy. It has been widely recognized that there is marked variability between factor VIII and factor IX one-stage assays performed in different laboratories, owing to the numerous combinations of aPTT reagents, instruments, calibration standards, and factor- deficient plasmas available. In addition, the variability among the aPTT-based assays is greater when attempting to measure factor levels near the lower limits (...) of the assay range. Moreover, in some test conditions the aPTT may not be sensitive enough to screen for mild factor VIII and factor IX deficiencies, and reliance on the one-stage aPTT assay alone may not allow accurate characterization of some forms of mild hemophilia. These problems are either minimized or not seen when chromogenic assays are performed. Chromogenic assays have become widely utilized in Europe, and the European Pharmacopoeia requires that potency of all factor products be assigned using

2014 National Hemophilia Foundation

56. A Safety, Efficacy and Pharmacokinetics Study of a Recombinant Fusion Protein Linking Coagulation Factor IX With Albumin (rIX-FP) in Children With Hemophilia B

A Safety, Efficacy and Pharmacokinetics Study of a Recombinant Fusion Protein Linking Coagulation Factor IX With Albumin (rIX-FP) in Children With Hemophilia B A Safety, Efficacy and Pharmacokinetics Study of a Recombinant Fusion Protein Linking Coagulation Factor IX With Albumin (rIX-FP) in Children With Hemophilia B - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study (...) Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. A Safety, Efficacy and Pharmacokinetics Study of a Recombinant Fusion Protein Linking Coagulation Factor IX With Albumin (rIX-FP) in Children With Hemophilia B The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S

2012 Clinical Trials

57. Open-Label Single Ascending Dose of Adeno-associated Virus Serotype 8 Factor IX Gene Therapy in Adults With Hemophilia B

Detailed Description: Hemophilia B is a genetic X-linked bleeding disorder caused by a deficiency in blood-clotting Factor IX (FIX) activity. FIX is synthesized in the liver and circulates in the blood as a proenzyme. Current treatment for hemophilia B is based on replacement of the deficient FIX with IV injections of recombinant FIX protein prophylactically or as needed to treat bleeding episodes. This clinical program will test a gene transfer approach involving the use of a gene delivery vector (...) Studies a U.S. FDA-regulated Device Product: No Keywords provided by Shire ( Baxalta now part of Shire ): Hemophilia B factor IX deficiency gene therapy Additional relevant MeSH terms: Layout table for MeSH terms Hemophilia A Hemophilia B Blood Coagulation Disorders, Inherited Blood Coagulation Disorders Hematologic Diseases Coagulation Protein Disorders Hemorrhagic Disorders Genetic Diseases, Inborn Genetic Diseases, X-Linked

2012 Clinical Trials

58. Epac1-deficient mice have bleeding phenotype and thrombocytes with decreased GPIbβ expression (PubMed)

revealed that Epac1-/- mouse platelets (thrombocytes) had unbalanced expression of key components of the glycoprotein Ib-IX-V (GPIb-IX-V) complex, with decrease of GP1bβ and no change of GP1bα. This complex is critical for platelet adhesion under arterial shear conditions. Furthermore, Epac1-/- mice have reduced levels of plasma coagulation factors and fibrinogen, increased size of circulating platelets, increased megakaryocytes (the GP1bβ level was decreased also in Epac1-/- bone marrow) and higher (...) abundance of reticulated platelets. Viscoelastic measurement of clotting function revealed Epac1-/- mice with a dysfunction in the clotting process, which corresponds to reduced plasma levels of coagulation factors like factor XIII and fibrinogen. We propose that the observed platelet phenotype is due to deficient Epac1 activity during megakaryopoiesis and thrombopoiesis, and that the defects in blood clotting for Epac1-/- is connected to secondary hemostasis.

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2017 Scientific reports

59. Acquired Vitamin K Deficiency as Unusual Cause of Bleeding Tendency in Adults: A Case Report of a Nonhospitalized Student Presenting with Severe Menorrhagia (PubMed)

for the patient: factor IX, 24%; factor II, 41%; factor VII, 3%; and factor X, 52%. She had been taking many high-energy drinks and she had inadequate dietary intake for the past 6 months. Given that she had vitamin K deficiency (VKD), a course of vitamin K therapy was started for her in the hospital. This case showed the potential for menorrhagia due to VKD with use of high-energy drinks and the value of a complete and detailed history in early diagnosis. (...) Acquired Vitamin K Deficiency as Unusual Cause of Bleeding Tendency in Adults: A Case Report of a Nonhospitalized Student Presenting with Severe Menorrhagia We report a rare case of acquired vitamin K deficiency presenting with severe menorrhagia and without any gynecological problem. Partial thromboplastin time (59.2 seconds) and prothrombin time (33.1 seconds, INR: 5.97) were considerably prolonged in laboratory evaluations. A complete coagulation factor assay test was performed

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2017 Case reports in obstetrics and gynecology

60. Factor XI Deficiency (Overview)

. Zivelin A, Bauduer F, Ducout L, et al. Factor XI deficiency in French Basques is caused predominantly by an ancestral Cys38Arg mutation in the factor XI gene. Blood . 2002 Apr 1. 99(7):2448-54. . Zivelin A, Ogawa T, Bulvik S, et al. Severe factor XI deficiency caused by a Gly555 to Glu mutation (factor XI-Glu555): a cross-reactive material positive variant defective in factor IX activation. J Thromb Haemost . 2004 Oct. 2(10):1782-9. Media Gallery Factor XI deficiency. Graph depicts factor deficiencies (...) Factor XI Deficiency (Overview) Factor XI Deficiency: Background, Pathophysiology, Epidemiology Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjA5OTg0LW92ZXJ2aWV3 processing > Factor XI Deficiency Updated: May 13

2014 eMedicine.com

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