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Factor IX Deficiency

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101. Purine Nucleoside Phosphorylase Deficiency (Follow-up)

Purine Nucleoside Phosphorylase Deficiency (Follow-up) Purine Nucleoside Phosphorylase Deficiency Follow-up: Further Outpatient Care, Further Inpatient Care, 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 (...) =aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvODg3ODIzLWZvbGxvd3Vw processing > Purine Nucleoside Phosphorylase Deficiency Follow-up Updated: Dec 11, 2018 Author: Alan P Knutsen, MD; Chief Editor: Harumi Jyonouchi, MD Share Email Print Feedback Close Sections Sections Purine Nucleoside Phosphorylase Deficiency Follow-up Further Outpatient Care See the list below: Intravenous immunoglobulin (IVIG) therapy is typically continued for 6-12 months after bone marrow transplantation. Reimmunization of the patient begins approximately 1 year after transplantation

2014 eMedicine Pediatrics

102. Glucuronyl Transferase Deficiency (Diagnosis)

Glucuronyl Transferase Deficiency (Diagnosis) Unconjugated Hyperbilirubinemia: 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=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTc4ODQxLW92ZXJ2aWV3 processing (...) % is derived from the hepatic turnover of heme proteins, such as myoglobin, cytochromes, and catalase. A small portion of daily bilirubin is derived from the destruction of young or developing erythroid cells. Bilirubin is poorly soluble in water at physiologic pH because of internal hydrogen bonding that engages all polar groups and gives the molecule an involuted structure. The fully hydrogen-bonded structure of bilirubin is designated bilirubin IX-alpha-ZZ. The intramolecular hydrogen bonding shields

2014 eMedicine Pediatrics

103. Proximal Femoral Focal Deficiency (Overview)

knee arthroscopy to identify changes in cruciate ligaments and their relation to the different types of PFFD in patients with Pappas type III, IV, VII, VIII, or IX deficiency, Chomiak et al found variable changes of the cruciate ligaments in all but one patient. Although these changes were not clinically relevant in most of the patients and were not related to the Pappas classification, the authors recommended imaging of cruciate ligaments before lengthening of the extremity in order to avoid knee (...) age, whereas others will be more inclined to attempt to preserve the natural limb no matter what. Treatment must be individualized on the basis of the following factors [ ] : Limb-length discrepancy Presence of associated malformations Adequacy of musculature Proximal joint stability Previous References Oppenheim WL, Setoguchi Y, Fowler E. Overview and comparison of Syme's amputation and knee fusion with the van Nes rotationplasty procedure in proximal femoral focal deficiency. Herring JA, Birch J

2014 eMedicine Surgery

104. Proximal Femoral Focal Deficiency (Diagnosis)

knee arthroscopy to identify changes in cruciate ligaments and their relation to the different types of PFFD in patients with Pappas type III, IV, VII, VIII, or IX deficiency, Chomiak et al found variable changes of the cruciate ligaments in all but one patient. Although these changes were not clinically relevant in most of the patients and were not related to the Pappas classification, the authors recommended imaging of cruciate ligaments before lengthening of the extremity in order to avoid knee (...) age, whereas others will be more inclined to attempt to preserve the natural limb no matter what. Treatment must be individualized on the basis of the following factors [ ] : Limb-length discrepancy Presence of associated malformations Adequacy of musculature Proximal joint stability Previous References Oppenheim WL, Setoguchi Y, Fowler E. Overview and comparison of Syme's amputation and knee fusion with the van Nes rotationplasty procedure in proximal femoral focal deficiency. Herring JA, Birch J

2014 eMedicine Surgery

105. Vitamin K Deficiency (Diagnosis)

functions as cofactor with the carboxylase is not fully understood. Vitamin K is required in the synthesis of 4 clotting factors in the liver: factors II,VII, IX, and X. It is also essential in the production of protein C and S, which are anticoagulant proteins. [ ] Bone matrix proteins, specifically osteocalcin, undergo gamma carboxylation with calcium much the way coagulation factors do; this process also requires VK. Previous Next: Etiology In infants, the low transmission of vitamin K (VK) across (...) Infectious diarrhea Cholestatic disease Parenchymal liver disease Cystic fibrosis Inflammatory bowel disease Drugs - Antibiotics (cephalosporin), cholestyramines, warfarin, salicylates, anticonvulsants, and certain sulfa drugs) are some of the common causes of VK deficiency Massive transfusion Disseminated intravascular coagulation (DIC) - Severe Chronic kidney disease/hemodialysis [ ] The synthesis of VK-dependent factors are decreased by parenchymal liver diseases, such as cirrhosis secondary to viral

2014 eMedicine.com

106. Vitamin K Deficiency (Overview)

with the carboxylase is not fully understood. Vitamin K is required in the synthesis of 4 clotting factors in the liver: factors II,VII, IX, and X. It is also essential in the production of protein C and S, which are anticoagulant proteins. [ ] Bone matrix proteins, specifically osteocalcin, undergo gamma carboxylation with calcium much the way coagulation factors do; this process also requires VK. Previous Next: Etiology In infants, the low transmission of vitamin K (VK) across the placenta, liver prematurity (...) Parenchymal liver disease Cystic fibrosis Inflammatory bowel disease Drugs - Antibiotics (cephalosporin), cholestyramines, warfarin, salicylates, anticonvulsants, and certain sulfa drugs) are some of the common causes of VK deficiency Massive transfusion Disseminated intravascular coagulation (DIC) - Severe Chronic kidney disease/hemodialysis [ ] The synthesis of VK-dependent factors are decreased by parenchymal liver diseases, such as cirrhosis secondary to viral hepatitis, alcohol intake, and other

2014 eMedicine.com

107. Purine Nucleoside Phosphorylase Deficiency (Overview)

Purine Nucleoside Phosphorylase Deficiency (Overview) Purine Nucleoside Phosphorylase Deficiency: 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 (...) =aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvODg3ODIzLW92ZXJ2aWV3 processing > Purine Nucleoside Phosphorylase Deficiency Updated: Dec 11, 2018 Author: Alan P Knutsen, MD; Chief Editor: Harumi Jyonouchi, MD Share Email Print Feedback Close Sections Sections Purine Nucleoside Phosphorylase Deficiency Overview Practice Essentials Purine nueoside phosphorylase (PNP) deficiency causes a form of severe combined immunodeficiency (SCID) characterized by profound T cell deficiency, failure to thrive (FTT), recurrent deep seeded infection, developmental delay

2014 eMedicine Pediatrics

108. IgA and IgG Subclass Deficiencies (Diagnosis)

vaccine in children with recurrent infections who are unresponsive to the polysaccharide vaccine. Pediatr Infect Dis J . 1998 Aug. 17(8):685-91. . Meyts I, Bossuyt X, Proesmans M, De B. Isolated IgG3 deficiency in children: to treat or not to treat? Case presentation and review of the literature. Pediatr Allergy Immunol . 2006 Nov. 17(7):544-50. . Garcia-Lloret M, McGhee S, Chatila TA. Immunoglobulin replacement therapy in children. Immunol Allergy Clin North Am . 2008 Nov. 28(4):833-49, ix (...) IgA and IgG Subclass Deficiencies (Diagnosis) IgA and IgG Subclass Deficiencies: Background, Pathophysiology, Epidemiology 50% of cases) involves deficient antibody production." /> 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

2014 eMedicine Pediatrics

109. Purine Nucleoside Phosphorylase Deficiency (Diagnosis)

Purine Nucleoside Phosphorylase Deficiency (Diagnosis) Purine Nucleoside Phosphorylase Deficiency: 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 (...) =aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvODg3ODIzLW92ZXJ2aWV3 processing > Purine Nucleoside Phosphorylase Deficiency Updated: Dec 11, 2018 Author: Alan P Knutsen, MD; Chief Editor: Harumi Jyonouchi, MD Share Email Print Feedback Close Sections Sections Purine Nucleoside Phosphorylase Deficiency Overview Practice Essentials Purine nueoside phosphorylase (PNP) deficiency causes a form of severe combined immunodeficiency (SCID) characterized by profound T cell deficiency, failure to thrive (FTT), recurrent deep seeded infection, developmental delay

2014 eMedicine Pediatrics

110. IgA and IgG Subclass Deficiencies (Treatment)

acute-onset neuropsychiatric syndrome. Pediatr Therapeut . 2012. 2:2. Murphy TK, Storch EA, Lewin AB et al. (2012). Clinical factors associated with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. J Pediatr . 2012. 160:314-9. Schaffer FM. Clinical assessment and management of abnormal IgA levels. Ann Allergy Asthma Immunol . 2008 Mar. 100(3):280-2. . Browning MJ. Specific polysaccharide antibody deficiency in chromosome 18p deletion syndrome (...) deficiency in children: to treat or not to treat? Case presentation and review of the literature. Pediatr Allergy Immunol . 2006 Nov. 17(7):544-50. . Garcia-Lloret M, McGhee S, Chatila TA. Immunoglobulin replacement therapy in children. Immunol Allergy Clin North Am . 2008 Nov. 28(4):833-49, ix. . . Karaca NE, Gulez N, Aksu G, Azarsiz E, Kutukculer N. Does OM-85 BV prophylaxis trigger autoimmunity in IgA deficient children?. Int Immunopharmacol . 2011 Nov. 11(11):1747-51. . Borte S, Pan-Hammarstrom Q

2014 eMedicine Pediatrics

111. IgA and IgG Subclass Deficiencies (Overview)

vaccine in children with recurrent infections who are unresponsive to the polysaccharide vaccine. Pediatr Infect Dis J . 1998 Aug. 17(8):685-91. . Meyts I, Bossuyt X, Proesmans M, De B. Isolated IgG3 deficiency in children: to treat or not to treat? Case presentation and review of the literature. Pediatr Allergy Immunol . 2006 Nov. 17(7):544-50. . Garcia-Lloret M, McGhee S, Chatila TA. Immunoglobulin replacement therapy in children. Immunol Allergy Clin North Am . 2008 Nov. 28(4):833-49, ix (...) IgA and IgG Subclass Deficiencies (Overview) IgA and IgG Subclass Deficiencies: Background, Pathophysiology, Epidemiology 50% of cases) involves deficient antibody production." /> 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

2014 eMedicine Pediatrics

112. Glucuronyl Transferase Deficiency (Overview)

Glucuronyl Transferase Deficiency (Overview) Unconjugated Hyperbilirubinemia: 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=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTc4ODQxLW92ZXJ2aWV3 processing (...) % is derived from the hepatic turnover of heme proteins, such as myoglobin, cytochromes, and catalase. A small portion of daily bilirubin is derived from the destruction of young or developing erythroid cells. Bilirubin is poorly soluble in water at physiologic pH because of internal hydrogen bonding that engages all polar groups and gives the molecule an involuted structure. The fully hydrogen-bonded structure of bilirubin is designated bilirubin IX-alpha-ZZ. The intramolecular hydrogen bonding shields

2014 eMedicine Pediatrics

113. IgA and IgG Subclass Deficiencies (Follow-up)

vaccine in children with recurrent infections who are unresponsive to the polysaccharide vaccine. Pediatr Infect Dis J . 1998 Aug. 17(8):685-91. . Meyts I, Bossuyt X, Proesmans M, De B. Isolated IgG3 deficiency in children: to treat or not to treat? Case presentation and review of the literature. Pediatr Allergy Immunol . 2006 Nov. 17(7):544-50. . Garcia-Lloret M, McGhee S, Chatila TA. Immunoglobulin replacement therapy in children. Immunol Allergy Clin North Am . 2008 Nov. 28(4):833-49, ix (...) IgA and IgG Subclass Deficiencies (Follow-up) IgA and IgG Subclass Deficiencies Follow-up: Further Outpatient Care, Complications, Prognosis 50% of cases) involves deficient antibody production." /> 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

2014 eMedicine Pediatrics

114. Antithrombin III Deficiency (Treatment)

of vitamin K–dependent procoagulant factors (II, VII, IX, X) is reduced adequately for anticoagulation. The duration of warfarin therapy in children with acquired or heterozygous congenital antithrombin III deficiency experiencing their first clot is controversial, but therapy is generally continued for at least 3-6 months before cessation of anticoagulation. If the underlying triggering event cannot be removed, indefinite anticoagulation should be considered. Antithrombin III–deficient patients (...) . Previous References Gaman AM, Gaman GD. Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature. Curr Health Sci J . 2014 Apr-Jun. 40 (2):141-3. . . Yilmaz S, Gunaydin S. Inherited risk factors in low-risk venous thromboembolism in patients under 45 years. Interact Cardiovasc Thorac Surg . 2015 Jan. 20 (1):21-3. . Beauchamp NJ, Pike RN, Daly M, et al. Antithrombins Wibble and Wobble (T85M/K): archetypal conformational diseases with in vivo latent-transition, thrombosis

2014 eMedicine Pediatrics

115. Voncento - human coagulation factor VIII / human von willebrand factor

. VWF and FVIII are two distinct glycoproteins that circulate in plasma in the form of a non-covalently bound complex. Both factors are essential for normal haemostasis in humans. Deficiencies in FVIII or VWF lead to two distinct hereditary coagulation disorders: haemophilia A and von Willebrand disease (VWD). Voncento belongs to the pharmacological class of hemostatic agents. The product is administered by intravenous infusion to raise FVIII and VWF levels in patients with corresponding (...) Voncento - human coagulation factor VIII / human von willebrand factor 11 June 2013 EMA/404213/2013 Committee for Medicinal Products for Human Use (CHMP) Assessment report Voncento HUMAN COAGULATION FACTOR VIII / VON WILLEBRAND FACTOR Procedure No. EMEA/H/C/002493/0000 Note Assessment report as adopted by the CHMP with all information of a commercially confidential nature deleted. 7 Westferry Circus ? Canary Wharf ? London E14 4HB ? United Kingdom An agency of the European Union Telephone +44

2013 European Medicines Agency - EPARs

116. Safety and Pharmacokinetic Study of a Recombinant Coagulation Factor IX Albumin Fusion Protein in Subjects With Hemophilia B

Safety and Pharmacokinetic Study of a Recombinant Coagulation Factor IX Albumin Fusion Protein in Subjects With Hemophilia B Safety and Pharmacokinetic Study of a Recombinant Coagulation Factor IX Albumin Fusion Protein in Subjects 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. Safety and Pharmacokinetic Study of a Recombinant Coagulation Factor IX Albumin Fusion Protein in Subjects 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. Federal Government. Read our for details. ClinicalTrials.gov Identifier: NCT01233440 Recruitment Status

2010 Clinical Trials

117. Use of prophylactic factor VIII concentrate in children and adults with severe haemophilia A (Full text)

bleeding. This group reported a trend in improving orthopaedic and radiological joint scores over a 20‐year review period ( ). The last two cohorts of nine and six patients (each of which included one patient with haemophilia B) started treatment at the age (range) of 1·3 years (1–2) and 1·2 years (1–1·5) respectively; annual consumption of factor VIII/IX concentrate/kg body weight (range) was 5741 iu (4730–7817) for the older of the two groups and 6354 iu (5305–8915) for the younger group (...) . , Beek, F.J.A. , Roosendaal, G. , Van Der Bom, J.G. & Nieuwenhuis, H.K. ( 2001 ) Long‐term outcome of individualized prophylactic treatment of children with severe haemophilia . British Journal of Haematology , 112 , 561 . Bjorkman, S. ( 2003 ) Prophylactic dosing of factor VIII and factor IX from a clinical pharmacokinetic perspective . Haemophilia , 9 ( Suppl. 1 ), 101 – 110 . Bjorkman, S. & Berntorp, E. ( 2001 ) Pharmacokinetics of coagulation factors: clinical relevance for patients

2010 British Committee for Standards in Haematology PubMed

118. Tissue Factor Pathway Inhibitor (TFPI) and Haemorrhagic Manifestations in Haemophilia A and B Patients

to a factor VIII (FVIII) deficiency and Haemophilia B (15 % of cases) due to factor IX (FIX) deficiency. According to the intensity of the defect, there are three forms of haemophilia: severe (FVIII or FIX lower than 1 %), moderate (factor level between 1 and 5 %), minor (factor level between 5 and 40 %). For a same level of factor VIII or IX, hemorrhagic manifestations are variable from one patient to the other. Moreover, several studies showed that haemophilic B patients bleed less and consume fewer (...) by the amplification pathway being strongly altered because of factor VIII or IX deficiency, thrombin generation (via Xa) comes exclusively from TFPI regulated tissue factor pathway. We can thus say that if haemophilic patients bleed, it is also because of the presence of TFPI that inhibits at the same time Xa and the complex TF-VIIa as soon as factor Xa is generated. Condition or disease Intervention/treatment Hemophilia Other: blood specimen Study Design Go to Layout table for study information Study Type

2015 Clinical Trials

119. Clotting Factor Product Administration and Same-Day Occurrence of Thrombotic Events, as Recorded in Large Healthcare Database During 2008-2013. (Full text)

products were identified by procedure codes, and TEs were ascertained via diagnosis codes. Crude same-day TE rates (per 1000 persons exposed) were estimated overall and by congenital factor deficiency (CFD) status, CF products, age and gender. Multivariable logistic regression analyses were used to control for confounding. Laboratory analysis was used to compare the procoagulant activities of FIX products.Of 3801 individuals exposed to CFs, 117 (30.8 per 1000) had same-day TEs recorded. The crude same (...) -day TE rate was higher for CF users without CFD, 70.2 (102 of 1452), as compared with those with CFD, 6.4 (15 of 2349) (RR, 11.0; 95% CI, 6.4-18.9). For individuals without CFD, a significantly increased same-day TE risk was identified for factor IX complex (OR, 6.92; 95% CI, 3.11-15.40), factor VIIa (OR, 9.42; 95% CI, 4.99-17.78) and other products when compared with fibrin sealant. An increased risk of a TE was found with older age (≥ 45 years), history of TEs and underlying health conditions

2015 Journal of Thrombosis and Haemostasis PubMed

120. A Study Comparing Factor Level and Inhibitor Titer Testing Results Drawn From Central Venous Lines and Venipuncture

line (CVL) instead of from a peripheral stick. Condition or disease Intervention/treatment Hemophilia A Factor VIII Deficiency Hemophilia Hemophilia B Factor IX Deficiency Procedure: Peripheral Vein Blood draw Detailed Description: Patients with hemophilia A and B sometimes require the placement of a central venous line (CVL). A CVL is a medical device that is placed into a vein that gives easier access to a vein either for a blood draw or to give factor replacement product. Patients (...) A Study Comparing Factor Level and Inhibitor Titer Testing Results Drawn From Central Venous Lines and Venipuncture A Study Comparing Factor Level and Inhibitor Titer Testing Results Drawn From Central Venous Lines and Venipuncture - 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

2015 Clinical Trials

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