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Factor IX Deficiency

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141. Factor VII (Follow-up)

manifestations, management, and molecular genetics in congenitalfactor VII deficiency: the International Registry on Congenital Factor VII Deficiency (IRF7). Blood . 2000 Jul 1. 96(1):374. . Roberts HR, Monroe DM, White GC. The use of recombinant factor VIIa in the treatment of bleeding disorders. Blood . 2004 Dec 15. 104(13):3858-64. . Media Gallery Factor VII. Intrinsic and extrinsic pathways of coagulation. Factor VII/tissue factor complex activates factor IX and factor X. Factor IXa along with factor (...) Factor VII (Follow-up) Factor VII Deficiency Follow-up: Further Outpatient Care, Complications, Prognosis 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=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMjA5NTg1LWZvbGxvd3Vw processing > Factor VII Deficiency

2014 eMedicine.com

142. Recurrence of axial malalignment after surgical correction in congenital femoral deficiency and fibular hemimelia (PubMed)

Recurrence of axial malalignment after surgical correction in congenital femoral deficiency and fibular hemimelia Recurrent genu valgum deformity complicates treatment of congenital femoral deficiencies (CFD) and fibular hemimelia (FH). We analysed factors influencing recurrence.Patients who underwent limb lengthening or deformity correction for CFD and/or FH were reviewed. Radiographs after surgery and after a minimum of a further six months were analysed. Change in parameters of mechanical (...)  mm regarding MAD in the first radiograph and patient age. CFD cases Pappas types VII and VIII showed a ∆ MAD/month of 1.6 mm, whereas milder cases of Pappas IX showed a ∆ MAD/month of 0.8. Mild FH (type Ia) showed a mean ∆ MAD/month of 0.39 mm, whereas mean ∆ MAD/month for FH type Ib/II was 0.72 mm. In FH type II cases, mean ∆ MAD/month was 0.79 mm after resection of the fibular anlage compared with 1.98 mm in those without resection.Recurrence in FH and CFD was not dependent on patient age

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2011 International orthopaedics

143. Hereditary disorders of blood coagulation due to defective and deficient synthesis of protein. (PubMed)

Factor VIII 9001-28-9 Factor IX 9001-29-0 Factor X IM Afibrinogenemia genetics Blood Coagulation Disorders etiology genetics Blood Proteins biosynthesis Factor IX metabolism Factor VIII metabolism Factor X metabolism Female Hemophilia A genetics Humans Male Prothrombin metabolism 43 1970 10 26 1970 10 26 0 1 1970 10 26 0 0 ppublish 4934014 PMC2441040 J Clin Invest. 1968 Feb;47(2):360-5 12066779 Fed Proc. 1965 Jul-Aug;24(4):816-21 5829185 Nature. 1965 Oct 9;208(5006):143-5 4956920 Br J Haematol. 1966 (...) Hereditary disorders of blood coagulation due to defective and deficient synthesis of protein. 4934014 1971 09 07 2018 11 13 0065-7778 82 1971 Transactions of the American Clinical and Climatological Association Trans. Am. Clin. Climatol. Assoc. Hereditary disorders of blood coagulation due to defective and deficient synthesis of protein. 114-23 Jackson D P DP eng Journal Article Review United States Trans Am Clin Climatol Assoc 7507559 0065-7778 0 Blood Proteins 9001-26-7 Prothrombin 9001-27-8

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1971 Transactions Of The American Clinical And Climatological Association

144. THE FIRST COMPONENT OF THE KININ-FORMING SYSTEM IN HUMAN AND RABBIT PLASMA : ITS RELATIONSHIP TO CLOTTING FACTOR XII (HAGEMAN FACTOR) (PubMed)

was in precursor form, requiring treatment with kaolin or trypsin to gain activity. Evidence indicated that the protein was Hageman factor (factor XII): it promoted clotting of factor XII-deficient, but not Factor XI- or IX-deficient plasma, and did not convert fibrinogen to fibrin it bound to and was activated by kaolin or other negatively charged particles in the presence of chelating agents; the activation by kaolin could be prevented by pretreating the kaolin with hexadimethrine bromide (H Br (...) ); prekallikrein-activating and clot-promoting activities were identical in their physical properties; and the prekallikrein activator could not be detected in Hageman factor-deficient plasma. Activation of Hageman factor was accompanied by cleavage of the molecule into several fragments, one of which possessed prekallikrein-activating (PKA) and clot-promoting properties. The PKA fragment sedimented at 2.6S and by gel filtration was found to have a molecular weight of 32,000. The PKA possessed only 1/50

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1971 The Journal of experimental medicine

145. Rational Use of Recombinant Factor VIIa in Clinical Practice (PubMed)

Rational Use of Recombinant Factor VIIa in Clinical Practice In the United States, the FDA-approved indications for recombinant factor VIIa is for bypassing inhibitors to factors VIII and IX in patients with hemophilia A and B respectively and for treatment of congenital factor VII deficiency. In European countries, rFVIIa is licensed for the above indications as well as for Glanzmann's thrombasthenia. In absence of high-quality data favoring off-label use of this agent and laboratory test (...) to predict response to this agent, and in view of high cost of rFVIIa, off-label use of recombinant factor VIIa should be restricted to only when hemorrhage has not responded to transfusion or other conventional therapy. It appears, two such conditions where recombinant factor VIIa may be beneficial are traumatic and postpartum hemorrhages.

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2013 Indian Journal of Hematology & Blood Transfusion

146. The effect of repeated freezing and thawing on levels of vitamin K-dependent coagulation factors and fibrinogen in fresh frozen plasma (PubMed)

The effect of repeated freezing and thawing on levels of vitamin K-dependent coagulation factors and fibrinogen in fresh frozen plasma Fresh frozen plasma (FFP) is considered adequate for transfusion immediately after thawing or for up to 24 hours if kept at 1-6°C, and is currently used very often to replace deficient clotting factors. If factor levels in refrozen FFP are within normal limits, then this component can possibly be transfused, thus avoiding wastage of FFP.To study the fate (...) of vitamin K-dependent coagulation factors (F II, F VII, F IX, F X) and fibrinogen activity levels in repeatedly (twice) frozen and thawed FFP.Two hundred FFP units comprising 50 units of each major blood group (A, B, AB, and O) were thawed at 37°C and 10-20 mL of FFP transferred to transfer bags with the help of a sterile connecting device (SCD). The FFP samples were taken into tubes (first sampling), and then the transfer bags were kept for 24 hours at 4°C. After 24 hours, repeat samples were taken

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2013 Asian journal of transfusion science

147. Future of coagulation factor replacement therapy. (PubMed)

Future of coagulation factor replacement therapy. Over a million patients worldwide currently suffer from hemophilia and other congenital clotting factor deficiencies. Patients affected with hemophilia A and B are treated by intravenous replacement therapy of factor VIII and factor IX, respectively. Current hemophilia treatments have favorably supported their efficacy, tolerability, and safety profiles. The onset of alloantibodies inactivating the infused coagulation factor is the main problem (...) in hemophilia patients rendering replacement therapies ineffective; another disadvantage is the short half-life of the infused clotting factors with the need for multiple and frequent infusions to manage a bleeding episode. Now, the challenge in the management of hemophilia treatment is the prolongation of the half-life and reduction in the immunogenicity of recombinant clotting factors. The bioengineering strategies, previously applied successfully to other therapeutic proteins, encourage the current

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2013 Journal of Thrombosis and Haemostasis

148. Coagulation Factors

and IX that occur almost exclusively in men (women are usually who are or have mild bleeding). Other inherited factor deficiencies, not associated with the X chromosome, are found equally in both men and women. The severity of symptoms experienced by a patient with an inherited factor deficiency depends on the factor involved and amount available. Symptoms may vary from episode to episode, from excessive bleeding after dental procedures to severe recurrent bleeding into joints or muscles. Patients (...) with a modest reduction in coagulation factor level may experience few symptoms and may discover their deficiency as an adult - after a surgical procedure or trauma or during screening that includes a or . Those with severe factor deficiencies may have their first bleeding episode very early; for example, a male infant with a deficiency of Factor VIII, IX, or XIII may bleed excessively after circumcision. Acquired deficiencies may be due to diseases, such as or cancer; to an condition such as , which uses

2012 Lab Tests Online UK

149. Hereditary combined deficiency of the vitamin K-dependent clotting factors (PubMed)

Hereditary combined deficiency of the vitamin K-dependent clotting factors Hereditary combined vitamin K-dependent clotting factors deficiency (VKCFD) is a rare congenital bleeding disorder resulting from variably decreased levels of coagulation factors II, VII, IX and X as well as natural anticoagulants protein C, protein S and protein Z. The spectrum of bleeding symptoms ranges from mild to severe with onset in the neonatal period in severe cases. The bleeding symptoms are often life

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2010 Orphanet journal of rare diseases

150. Factor deficiencies in venom-induced consumption coagulopathy resulting from Australian elapid envenomation: Australian Snakebite Project (ASP-10). (PubMed)

Factor deficiencies in venom-induced consumption coagulopathy resulting from Australian elapid envenomation: Australian Snakebite Project (ASP-10). Limited information exists on the dynamics of hemostasis in patients with venom-induced consumption coagulopathy (VICC) from snake envenomation.The aim of the present study was to investigate specific factor deficiencies and their time course in Australasian elapid envenomation.We measured coagulation parameters and factor concentrations in patients (...) recruited to the Australian Snakebite Project, an observational cohort study. There were 112 patients with complete VICC, defined as an international normalized ratio (INR) > 3, and 18 with partial VICC. Serial citrated plasma samples were collected from 0.5 to 60 h post-bite. INR, activated partial thromboplastin time (aPTT), coagulation factors (F)I, II, V, VII, VIII, IX, X, von Willebrand factor antigen (VWF:Ag) and D-dimer concentrations were measured.Complete VICC was characterized by near/total

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2010 Journal of Thrombosis and Haemostasis

151. A central role of GPIb-IX in the procoagulant function of platelets that is independent of the 45-kDa GPIbalpha N-terminal extracellular domain. (PubMed)

A central role of GPIb-IX in the procoagulant function of platelets that is independent of the 45-kDa GPIbalpha N-terminal extracellular domain. Activated platelets become procoagulant and efficiently promote the conversion of prothrombin to thrombin. A role of the GPIb-V-IX complex has long been postulated in view of the decreased prothrombin consumption in Bernard-Soulier patients. We evaluated the impact of GPIb-V-IX deficiency and the requirement for the GPIbalpha extracellular domain (...) . In GPIbbeta(-/-) mice, thrombin generation was profoundly decreased in tissue factor- or collagen-related peptide (CRP)-activated platelet-rich plasma and in washed platelets supplemented with normal plasma or with FVa, FXa, and prothrombin. Phosphatidylserine (PS) exposure was similarly decreased in response to thrombin, CRP, or CRP + PAR4 peptide despite a normal platelet phospholipid composition. The hypothesis that these defects originate from lack of the GPIbalpha N-terminal domain was evaluated

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2010 Blood

152. Von Willebrand Factor

Factor Aka: Von Willebrand Factor , VWF , Von Willebrand Factor Antigen , Von Willebrand Factor Ristocetin Cofactor Activity , VWF:Ag , VWF:RCo From Related Chapters II. Physiology Von Willebrand Factor synthesis Vascular endothelium s Von Willebrand Factor release Platelet activation Endothelial cells Von Willebrand Factor activity Binds factor VIII in circulation (prolongs Factor VIII half-life) Releases factor VIII in response to bleeding Factor VIII in turn is a or in the conversion of Factor IX (...) to IXa in the initrinsic to form thrombin Bridges exposed collagen and platelets when vascular injury occurs Von Willebrand Factor mediates platelet adhesion Von Willebrand Factor is a large protein that binds damaged vasculature and traps, binds platelets to form a platelet plug Analogous to 6-pack plastic ring holder that traps wildlife Von Willebrand Factor deficiency Results in delayed platelet plug formation Results in mucocutaneous bleeding III. Labs Normal VWF range: 50-200 IU/dl IV. Causes

2015 FP Notebook

153. Thromboembolism Risk Factors

) increase after acute therapy completed (2.2) Persistent risk factors - see above (2) Idiopathic VTE (2) Protein C,Protein S and deficiency (1.8) Prothrombin mutation - G20210A (1.7) for (1.6) Second VTE (1.5) Mild (0.9) Distal VTE (0.5) Transient risk factors (0.5) VII. Risk Factors: Venous Stasis Prolonged immobility Long leg or other limb immobilization Paralysis (CVA) Spinal cord injury s High risk for DVT in surgery without Cardiac Disease VIII. Risk Factors: Hypercoagulable state See Inherited (...) cause found in up to one third of DVT cases Prior (DVT) Medications Increased or Pregnancy (Nolvadex) Phenothiazines Major Recent Surgery (e.g. ) Cancer Consider evaluation for occult cancer in DVT Polycythemia History of thromboembolic disease Deep Venous Thrombosis Type A Blood IX. Risk Factors: Intimal damage Local Surgery (Especially ral and Orthopedic Surgery) ral anesthesia is an independent risk factor Consider Penetrating vessel injury Especially femoral X. References Images: Related links

2015 FP Notebook

154. Gla-domainless factor Xa: molecular bait to bypass a blocked tenase complex. (PubMed)

Gla-domainless factor Xa: molecular bait to bypass a blocked tenase complex. Hemophilia is caused by deficiencies in coagulation factor VIII or IX, resulting in direct blockade of the intrinsic tenase complex and indirect blockade of the extrinsic tenase complex which is rapidly inhibited upon binding of factor Xa to tissue factor pathway inhibitor. We evaluated the ability of Gla-domainless factor Xa, a truncated form of factor Xa devoid of procoagulant properties, to bind to tissue factor (...) pathway inhibitor and to alleviate the physiological inhibition of the extrinsic tenase.Using a thrombin generation assay triggered by a low concentration of tissue factor, we evaluated the ability of Gla-domainless factor Xa to restore blood coagulation in plasma from hemophilia A and B patients without and with inhibitors. We then compared its efficacy to generate thrombin to depletion of antithrombin or tissue factor pathway inhibitor by specific antibodies. Finally, we compared the kinetics

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2012 Haematologica

155. Protein C Deficiency

SOCIAL MEDIA Add to Any Platform Loading , MD, Baylor College of Medicine Click here for Patient Education NOTE: This is the Professional Version. CONSUMERS: Because activated protein C degrades coagulation factors Va and VIIIa, deficiency of protein C predisposes to venous thrombosis. (See also .) Protein C is a vitamin K–dependent protein, as are coagulation factors VII, IX, and X; prothrombin; and proteins S and Z. Because activated protein C (APC) degrades factors Va and VIIIa, APC is a natural (...) Protein C Deficiency Protein C Deficiency - Hematology and Oncology - MSD Manual Professional Edition Brought to you by The trusted provider of medical information since 1899 SEARCH SEARCH MEDICAL TOPICS Common Health Topics Resources QUIZZES & CASES Quizzes Cases The trusted provider of medical information since 1899 SEARCH SEARCH MEDICAL TOPICS Common Health Topics Resources QUIZZES & CASES Quizzes Cases / / / / IN THIS TOPIC OTHER TOPICS IN THIS CHAPTER Test your knowledge Multiple Myeloma

2013 Merck Manual (19th Edition)

156. Vitamin Deficiency, Dependency, and Toxicity - Vitamin K

K, containing about 2.5 mcg/L (cow’s milk contains 5000 mcg/L). The neonatal gut is sterile during the first few days of life. In adults , vitamin K deficiency can result from Fat malabsorption (eg, due to , , , or resection of the small intestine) Use of coumarin anticoagulants Coumarin anticoagulants interfere with the synthesis of vitamin–K dependent coagulation proteins (factors II, VII, IX, and X) in the liver. Certain antibiotics (particularly some cephalosporins and other broad-spectrum (...) supplemental vitamin K. Vitamin K 2 refers to a group of compounds (menaquinones) synthesized by bacteria in the intestinal tract; the amount synthesized does not satisfy the vitamin K requirement. Vitamin K controls the formation of coagulation factors II (prothrombin), VII, IX, and X in the liver (see Table: ). Other coagulation factors dependent on vitamin K are protein C, protein S, and protein Z; proteins C and S are anticoagulants. Metabolic pathways conserve vitamin K. Once vitamin K has

2013 Merck Manual (19th Edition)

157. Coagulation factors in chronic liver disease (PubMed)

Coagulation factors in chronic liver disease Coagulation studies were carried out on 30 patients with chronic liver disease. The clotting defect was complex and involved factors V, VII, IX (Christmas factor), and prothrombin. Some patients showed a significant depression of factor IX in the presence of a normal one-stage prothrombin time. Thrombotest was found to be a good indicator of factor IX deficiency in this group of patients and may be of use as an additional liver function test (...) . The screening of patients with liver disease for surgery or liver biopsy should assess the coagulation factors involved in both intrinsic and extrinsic thromboplastin generation.

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1969 Journal of Clinical Pathology

158. Coagulation factor concentrate in the treatment of the haemorrhagic diathesis of fulminant hepatic failure. (PubMed)

patients, fell subsequently, particularly in those given concentrate alone. There was some improvement in the prothrombin ratio in both groups of patients but not complete correction, and serial assays of clotting factors showed that although factor II rose to high levels during treatment, factors IX and X showed little response. Thus, the use of concentrate of factor IX in this trial, as well as potentiating intravascular coagulation, was inadequate as replacement for the clotting factor deficiencies. (...) Coagulation factor concentrate in the treatment of the haemorrhagic diathesis of fulminant hepatic failure. To assess the value of clotting factor concentrate infusions in fulminant hepatic failure, a controlled trial was performed in which nine patients were randomly allocated to treatment with either concentrate alone or concentrate plus heparin. The five patients receiving concentrate alone all died, with major bleeding as the direct cause of death in three, whereas in the four receiving

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1974 Gut

159. Public health guidance on prevention and control of blood-borne viruses in prison settings

treatment in prison settings 27 Table 11. Evidence for the effectiveness of interventions to prevent BBVs post-release 29 Table 12. Evidence for the effectiveness of interventions to increase linkage to care post-release 30 Public health guidance on prevention and control of blood-borne viruses in prison settings SCIENTIFIC ADVICE iv Abbreviations AIDS Acquired immune deficiency syndrome ALT Alanine aminotransferase ART Antiretroviral therapy BBV Blood-borne virus CD4 Cluster of differentiation 4 DAAs (...) . transmission of infectious diseases) associated with drug use disorders Jail Locally-operated, short term facilities that hold adults awaiting trial or sentencing or both, and people sentenced mostly to a term of less than one year Mandatory testing Testing which is offered to all eligible individuals, and the person is obliged to be tested Opt-in Testing which is voluntary and offered to all eligible individuals, often on the basis of identified risk factors, and the person chooses whether or not to have

2019 European Centre for Disease Prevention and Control - Public Health Guidance

160. Critical Assessment of Diabetes Guidelines

. It interferes with vitamin K reductase, inhibiting vitamin K cycle and activation of vitamin K-dependent coagulation factors II (fibrinogen), VII, IX, and X, and works as an anticoagulant. Note2:An enzyme which hydrolyzes ester. There are various kinds of esterase. Hemorrhage could be predicted based on the results of animal tests: The package insert explains that mechanism of onset and risk factors of hemorrhage due to interaction with warfarin are unknown [3,8]. However, at least vitamin K deficiency (...) K, which activates factors II, VII, IX and X, and prolongs PT and skin. It should be noted that there are cases in which bleeding occurred on the day of the treatment (cases 3 and 4) and those in which bleeding occurred and abnormality in coagulation factors was detected several days after the treatment (cases 1 and 2). In the latter, PT and PT-INR were immeasurable and there were increased potential risks of irreversible hemorrhage and death. Xofluza is metabolized by esterase (Note 2

2019 Med Check - The Informed Prescriber

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