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Factor IX Deficiency

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1201. Effects of coagulation factor deficiency on plasma coagulation kinetics determined via thrombelastography: critical roles of fibrinogen and factors II, VII, X and XII. (PubMed)

, VIII, IX, X, XI, XII, or XIII activated with celite (0.28 mg ml(-1)) or tissue factor (TF, 0.1%) (n = 6 per condition). Additional fibrinogen concentration activity (75-345 mg dl(-1)) and Factor II, VII, X and XII activity-response relationships (1%, 6.25%, 12.5%, 25%, 50% and 100% activity) were obtained (n = 8 per condition). Thrombelastography parameters included reaction time (R), angle (alpha), and clot strength (A, amplitude; G, elastic modulus).Celite activation of FXII-deficient plasma, TF (...) Effects of coagulation factor deficiency on plasma coagulation kinetics determined via thrombelastography: critical roles of fibrinogen and factors II, VII, X and XII. Thrombelastography (TEG) is used to assess coagulopathy. However, a comprehensive characterization of the effects of specific coagulation factor deficiencies and mode of activation on TEG data does not exist.Thrombelastography was performed for 15 min with control plasma and plasmas deficient (<1% activity) in Factors II, V, VII

2005 Acta Anaesthesiologica Scandinavica

1202. Association of congenital deficiency of multiple vitamin K-dependent coagulation factors and the phenotype of the warfarin embryopathy: clues to the mechanism of teratogenicity of coumarin derivatives. (PubMed)

Association of congenital deficiency of multiple vitamin K-dependent coagulation factors and the phenotype of the warfarin embryopathy: clues to the mechanism of teratogenicity of coumarin derivatives. We have evaluated a boy who had excessive bleeding and bruising from birth and showed markedly prolonged prothrombin times, partially correctable by oral vitamin K administration. Additional laboratory studies demonstrated decreased activities of plasma factors II, VII, IX, and X; near normal (...) levels of immunologically detected and calcium binding-independent prothrombin; undercarboxylation of prothrombin; excess circulating vitamin K epoxide; decreased excretion of carboxylated glutamic acid residues; and abnormal circulating osteocalcin. These results all are consistent with effects resulting from decreased posttranslational carboxylation secondary to an inborn deficiency of vitamin K epoxide reductase. This individual also had nasal hypoplasia, distal digital hypoplasia, and epiphyseal

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1987 American Journal of Human Genetics

1203. Acquired Antibody to Factor XI in a Patient with Congenital Factor XI Deficiency (PubMed)

as that of patients with severe Factor VIII or IX deficiency. This suggests that physiologic activation of Factors XI and IX does not occur exclusively in series because deficiency of factors XII, XI, VIII, and IX should then have similar hemostatic consequences. We propose that independent mechanisms for bypass of Factors XII and XI are important in physiologic activation of coagulation. (...) Acquired Antibody to Factor XI in a Patient with Congenital Factor XI Deficiency The results of studies in a patient with congenital deficiency of Factor XI who developed an inhibitor are presented. The patient presented with a severe, apparently spontaneous bleed into the thigh, which progressed despite infusion of fresh frozen plasma, but which responded promptly to activated prothrombin complex. During therapy with plasma his clotting time and Factor XI level were unresponsive and a Factor

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1982 Journal of Clinical Investigation

1204. Regional localization on the human X chromosome and polymorphism of the coagulation factor IX gene (hemophilia B locus). (PubMed)

Regional localization on the human X chromosome and polymorphism of the coagulation factor IX gene (hemophilia B locus). Hemophilia B is an X-linked disease caused by a functional deficiency in coagulation factor IX. A cDNA clone corresponding to factor IX has been used to detect homologous sequences in the human genome. All DNA fragments hybridizing to the probe, under medium- or high-stringency conditions, are X-linked, and the patterns obtained suggest that a single large (greater than

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1984 Proceedings of the National Academy of Sciences of the United States of America

1205. Molecular basis of hemophilia B: a defective enzyme due to an unprocessed propeptide is caused by a point mutation in the factor IX precursor. (PubMed)

of the factor IX, indicating the importance of the leader sequence in substrate recognition by the vitamin K-dependent carboxylase. This represents an example of an enzyme defect due to the presence of a point mutation in a precursor protein (preproenzyme) that is the cause of a human hereditary disease. This defect will serve as a prototype for understanding the molecular basis of some forms of hemophilia and other hereditary enzyme deficiencies. (...) Molecular basis of hemophilia B: a defective enzyme due to an unprocessed propeptide is caused by a point mutation in the factor IX precursor. A mutant factor IX, designated factor IXCambridge, was isolated from a patient with hemophilia B. This protein includes an 18-residue propeptide attached to the NH2 terminus of factor IX. A point mutation at residue -1, from an arginine to a serine, precludes cleavage of the propeptide by a processing protease and interferes with gamma-carboxylation

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1986 Proceedings of the National Academy of Sciences of the United States of America

1206. An intragenic deletion of the factor IX gene in a family with hemophilia B. (PubMed)

. The deletion included two exons (exons V and VI) coding for the amino acid sequence from number 85 to 195 of the factor IX protein. The deleted portion of the gene contained the entire factor IX activation peptide. The length of the deletion was estimated to be 10 +/- 0.3 kilobase pairs. This specific gene has been named FIXSeattle. In this family both the deletion and a Taq 1 restriction fragment length polymorphism can be used as a useful marker for accurate detection of female carriers of the deficient (...) An intragenic deletion of the factor IX gene in a family with hemophilia B. A family of seven patients severely afflicted with hemophilia B has been studied for their factor IX genes through the use of factor IX cDNA and genomic DNA probes. The patients had detectable (less than 10% of normal) factor IX antigen in urine and no detectable inhibitors in sera to factor IX protein. Based on the DNA hybridization analysis, these patients showed a partial intragenic deletion in their factor IX gene

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1985 Journal of Clinical Investigation

1207. Ulnar artery pseudoaneurysm in a patient with factor IX deficiency (hemophilia B) (PubMed)

Ulnar artery pseudoaneurysm in a patient with factor IX deficiency (hemophilia B) The hypothenar hammer syndrome describes a constellation of symptoms resulting from repetitive trauma to the hypothenar eminence, often due to the use of the hand as a hammer. Sequelae of this syndrome include both true and false aneurysms, as well as thrombosis of the ulnar artery due to its vulnerability to blunt trauma as it exits Guyon's canal. Although this is a relatively well-documented phenomenon (...) , an extensive review of the literature revealed that no cases have been described involving a patient with hemophilia. The present case describes a 46-year-old farmer with factor IX deficiency (hemophilia B) presenting with a 5 cm x 7 cm pseudoaneurysm of the ulnar artery of the right hand.

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2007 The Canadian Journal of Plastic Surgery

1208. Prophylaxis in factor IX deficiency product and patient variation. (PubMed)

Prophylaxis in factor IX deficiency product and patient variation. To determine the dosing needed to maintain a prophylactic level of factor IX (FIX) >/=2%, 15 non-inhibitor severe (deficient subjects participated in a double-blind, two-period crossover study to assess the pharmacokinetics of two FIX concentrates, Mononine (pd-FIX), an ultra-high-purity plasma-derived concentrate, and BeneFix (r-FIX), a recombinant product. The median recovery in the pd-FIX group was 1.67 IU dL(-1

2003 Haemophilia : the official journal of the World Federation of Hemophilia

1209. A simple technique to reduce epistaxis and nasopharyngeal trauma during nasotracheal intubation in a child with factor IX deficiency having dental restoration. (PubMed)

A simple technique to reduce epistaxis and nasopharyngeal trauma during nasotracheal intubation in a child with factor IX deficiency having dental restoration. Epistaxis and airway trauma are often associated with nasotracheal intubation. We describe a patient with Factor IX deficiency who required nasotracheal intubation. An inexpensive, nonproprietary, rapid technique was used to reduce the trauma of intubation.

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2004 Anesthesia and Analgesia

1210. Acute hepatitis in a patient with mild factor IX deficiency after anesthesia with isoflurane. (PubMed)

Acute hepatitis in a patient with mild factor IX deficiency after anesthesia with isoflurane. 3756695 1986 10 30 2018 11 13 0820-3946 135 6 1986 Sep 15 CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne CMAJ Acute hepatitis in a patient with mild factor IX deficiency after anesthesia with isoflurane. 645-6 Grégoire S S Smiley R K RK eng Case Reports Journal Article Canada CMAJ 9711805 0820-3946 CYS9AKD70P Isoflurane AIM IM Adult Anesthesia, General

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1986 CMAJ: Canadian Medical Association Journal

1211. Phase I/II Study of Monoclonal Factor IX Concentrate for Factor IX Deficiency

Phase I/II Study of Monoclonal Factor IX Concentrate for Factor IX Deficiency Phase I/II Study of Monoclonal Factor IX Concentrate for Factor IX 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 (...) . Phase I/II Study of Monoclonal Factor IX Concentrate for Factor IX 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. Read our for details. ClinicalTrials.gov Identifier: NCT00004801 Recruitment Status : Completed First Posted : February 25, 2000 Last Update Posted : June 24, 2005 Sponsor: National Center for Research Resources (NCRR) Collaborator

2000 Clinical Trials

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