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Relevant bibliographies by topics / Antithrombin III deficiency

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Journal articles
Dissertations / Theses
Book chapters
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Academic literature on the topic 'Antithrombin III deficiency'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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Journal articles on the topic "Antithrombin III deficiency"

1

Beresford, C. H. "Antithrombin III deficiency." Blood Reviews 2, no. 4 (1988): 239–50. http://dx.doi.org/10.1016/0268-960x(88)90013-6.

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Sakuragawa, Nobuo, Shin-ichi Kondo, Masahiko Katoh, Kaoru Takahashi, and Takehiko Koide. "Antithrombin III microheterogeneity in antithrombin III deficiency and in the antithrombin III abnormality, “antithrombin III toyama”." Thrombosis Research 47, no. 2 (1987): 147–53. http://dx.doi.org/10.1016/0049-3848(87)90371-9.

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Hirsh, Jack, Franco Piovella, and Mario Pini. "Congenital antithrombin III deficiency." American Journal of Medicine 87, no. 3 (1989): S34—S38. http://dx.doi.org/10.1016/0002-9343(89)80529-7.

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Manco-Johnson, Marilyn J. "Neonatal antithrombin III deficiency." American Journal of Medicine 87, no. 3 (1989): S49—S52. http://dx.doi.org/10.1016/0002-9343(89)80532-7.

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Stefano, Valerio De. "Thrombosis in Antithrombin-III Deficiency." Annals of Internal Medicine 117, no. 10 (1992): 875. http://dx.doi.org/10.7326/0003-4819-117-10-875_1.

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Swaim, Laurie S., and Larry C. Gilstrap. "Antithrombin III deficiency in pregnancy." Primary Care Update for OB/GYNS 6, no. 4 (1999): 111–14. http://dx.doi.org/10.1016/s1068-607x(99)00008-6.

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Green, Robert A. "Pathophysiology of Antithrombin III Deficiency." Veterinary Clinics of North America: Small Animal Practice 18, no. 1 (1988): 95–104. http://dx.doi.org/10.1016/s0195-5616(88)50010-4.

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Halfman, Marsha, and David E. Berg. "Venous Thrombosis: Antithrombin III Deficiency." Critical Care Nursing Clinics of North America 5, no. 3 (1993): 499–509. http://dx.doi.org/10.1016/s0899-5885(18)30554-9.

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Sørensen, P. J., J. Dyerberg, E. Stoffersen, and M. Krogh Jensen. "Familial Functional Antithrombin III Deficiency." Scandinavian Journal of Haematology 24, no. 2 (2009): 105–9. http://dx.doi.org/10.1111/j.1600-0609.1980.tb02352.x.

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George, PM, P. Pemberton, IC Bathurst, et al. "Characterization of antithrombins produced by active site mutagenesis of human alpha 1-antitrypsin expressed in yeast." Blood 73, no. 2 (1989): 490–96. http://dx.doi.org/10.1182/blood.v73.2.490.490.

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Abstract Both congenital and acquired antithrombin-III (AT-III) deficiencies are amenable to replacement therapy. We describe two antithrombins produced by recombinant DNA techniques from human alpha 1-antitrypsin (alpha 1AT) cDNA in yeast. Alteration of the alpha 1AT active site, replacing methionine 358 with arginine, results in a thrombin inhibition rate similar to that of heparin-activated AT-III. Alteration of two further residues, to give a five-residue sequence identical to AT-III, does not increase this rate further. Neither antithrombin is activated by heparin; both are unglycosylated

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Dissertations / Theses on the topic "Antithrombin III deficiency"

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Oliveira, André Luiz Malavasi Longo de. "Trombofilias maternas hereditárias com e sem tromboembolismo venoso: resultados maternos e neonatais." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-25082010-112901/.

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O objetivo do presente estudo foi avaliar a diferença de resultados maternos e neonatais em gestações complicadas por trombofilias hereditárias em pacientes com e sem tromboembolismo venoso. Apesar do aumento de evidências, na literatura, sobre a associação de trombofilias congênitas e resultados obstétricos adversos, há ainda dúvida se pacientes trombofílicas com tromboembolismo venoso apresentam resultados maternos e neonatais piores que as pacientes trombofílicas sem tromboembolismo venoso. O estudo analisou 66 gestantes com trombofilias hereditárias, de forma retrospectiva observacional e

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Book chapters on the topic "Antithrombin III deficiency"

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Sheffield, W. P., F. Fernandez-Rachubinski, R. C. Austin, and M. A. Blajchman. "Molecular Defects in Human Antithrombin III Deficiency." In Recombinant Technology in Hemostasis and Thrombosis. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3698-7_9.

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Delphin, Ellise, and Vasanti Tilak. "Antithrombin III Deficiency." In Essence of Anesthesia Practice. Elsevier, 2011. http://dx.doi.org/10.1016/b978-1-4377-1720-4.00021-2.

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Conard, J., M. H. Horellou, and M. Samama. "Congenital Deficiency of Antithrombin III and of Heparin Cofactor II." In Clinical Thrombosis. CRC Press, 2019. http://dx.doi.org/10.1201/9780429261879-20.

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Conference papers on the topic "Antithrombin III deficiency"

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Conard, J., M. H. Horellou, P. Van Dreden, and M. Samama. "PREGNANCY AND CONGENITAL DEFICIENCY IN ANTITHROMBIN III OR PROTEIN C." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642942.

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Pregnancy as well as congenital deficiency in coagulation inhibitors are recognized as predisposing conditions to thrombosis. Thus, in women with a congenital deficiency, the risk of thrombosis associated to pregnancy is expected to be higher than in normal women (incidence of approximately 1°/..). We have investigated this risk in 16 women with congenital Antithrombin III (AT III) deficiency and in 31 with Protein C (PC) deficiency.In the 16 women with AT III deficiency, 30 pregnancies occured 3 of them were interrupted by provoked abortions and a deep vein thrombosis (DVT) or pulmonary embol

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Schwartz, R., E. Kavanagh, K. Bauer, et al. "ANTITHROMBIN III CONCENTRATE (AT-III) FOR PROPHYLAXIS ANDTREATMENT OF CONGENITAL AND ACQUIREDAT-III DEFCIENCY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643678.

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An investigation has been undertakenin 13 patient studies to determine the efficacy of AT-III in prevention and treatment of thrombosis in patients with congenital (cong.) and acquired (acq.) AT-III deficiency. The mean in vivo incremental recovery of 17 infusions of AT-III in 7 patientswith cong. AT-III deficiency (2 kinetic studies, 5 prophylaxis) was 1.4%/U/kg (functional assay) administered. The mean in vivo recovery of 38 infusions in 4 non-bleeding patients(3 cong., 1 acq.) treated for thrombosis or pulmonary embolism (P.E.) with heparin was 1.33%/U/kg which was not significantly differe

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Broekmans, A. W., F. J. M. der Meer, and K. Briët. "TREATMENT OF CONGENITAL THROMBOTIC SYNDROMES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643718.

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Hereditary antithrombin III deficiency,protein C deficiency, and protein S deficiency predispose to the occurrence of venous thrombotic disease at a relatively youngage and often without an apparent cause. These disorders inherit as an autosomal dominant trait. Heterozygotes are at risk fosuperficial thrombophlebitis, thrombosis atnearly every venous site, and pulmonary embolism. Homozygous protein C deficiency may present itself with a purpura fulminans syndrome shortly after birth.In the acute phase of venous thromboembolism heparin is effective for preventing extension of the thrombotic pro

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Lane, D. A., G. DO Lowe, A. Flynn, H. Ireland, E. Thompson, and H. Erdjument. "ANTITHROMBIN III GLASGOW: A VARIANT WITH INCREASED HEPARIN AFFINITY AND REDUCED ABILITY TO INACTIVATE THROMBIN, ASSOCIATED WITH FAMILIAL THROMBOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644369.

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A functional anti thrombin III CAT III) deficiency has been identified in three generations of a family with a high incidence of deep venous thrombosis. The deficiency presented as ~50% reduction in its heparin cofactor activity compared to its antigen concentration. No abnormality was detected by crossed immunoelectrophoresis of plasma in the presence or absence of heparin. Plasma from the propositus was precipitated with dextran sulphate, applied to heparin-Sepharose and the AT III stepwise eluted with NaCl . The AT III had a reduced ability to inactivate thrombin, when this was monitored by

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Jørgensen, M. "HEPARIN INDEPENDENT PURIFICATION OF ANTITHROMBIN III (AT III) BY IMMUNO-AFFINITY CHROMATOGRAPHY RESULTING IN A FUNCTIONALLY INTACT MOLECULE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643682.

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Previous methods for purification of AT III are based on its heparin-binding capacity. However, in congenital AT III deficiency abnormal inhibitor molecules with impaired binding of heparin and/or thrombin has been reported. The aim of the present study was to develop a purification method based on immuno-affinity chromatography, and thus independent of the heparin binding capacity.Rabbits were immunized with human AT III purified by a three-step procedure involving dextran sulphate precipitation, affinity chromatography on heparin-Sepharose and ion-exchange chromatography on DEAE-Sephadex A-5

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Hach-Wunderle, V., R. Walter-Fincke, H. K. Beck, and I. Scharrer. "FAMILY STUDIES OF PATIENTS WITH RECURRENT VENOUS THROMBOSES AND INHERITED DISORDERS OF BLOOD COAGULATION OR FIBRINOLYSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643045.

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Several defects of the coagulation and/or fibrinolytic system have been found to be associated with venous thromboembolism. In young patients with recurrent thromboses or a positive family history, an inherited disorder should be excluded535 young patients with venous thromboses, phlebitis and/or pulmonary embolism were investigated from 1980 until 1986. The first thrombotic event had occurred at an age of less than 45 years.An inborn disorder of the blood coagulation or fibrinolytic system was found in 18 families. Most of them (n=13/18) had a positive family history. In all families either t

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Schoch, U., E. Zanetti, and A. von Felten. "PROPHYLAXIS OF THROMBOEMBOLISM DURING PREGNANCY IN THREE SISTERS WITH CONGENITAL ANTITHROMBIN III (AT m) DEFICIENCY COMBINED WITH REDUCED INDUCIBLE FIBRINOLYTIC ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644363.

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AT III deficiency is associated with a high risk of venous thromboembolism, particularly in pregnancy. As prophylactic treatment it has been recommended to normalize plasma levels of AT in by use of AT III concentrates, besides giving heparin.We report on the prophylactic treatment of three sisters (age 21, 25, 32 years) with congenital AT in deficiency (38-53%, normal: 80-120%) as well as a reduced inducible fibrinolytic activity (1.2, 5.8, 7.9%, normal: >8.5%), who already had suffered from severe thromboembolism. During pregnancy prophylactic measures were taken individually, depending o

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Borg, J. Y., M. C. Owen, C. Soria, J. Caen, and R. W. Carrell. "ANTITHROMBIN ROUEN-I(47 ARG→HIS) AND ROUEN-II (47SER) : TWO NEW VARIANTS WITH DECREASED HEPARIN AFFINITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643679.

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Four families with AT-III variants of decreased heparin affinity have been compared with families with a quantitative deficiency of AT-III. The affinity variants had a lower incidence of thrombosis and, unlike thedefiency variants, had no increase in plasma FDF (defined by anti-D-neo ELISA assay). These results support a major physiological role for the progressive activity of AT-III.The characterisation of the affinity variants provides information onthe heparin-binding site. Variants were isolated from plasma of heterozygotes by NaCl elution gradient from a heparin-Sepharose column. Maps of

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Nakamura, K., K. Iijima, N. Inoue, J. Nishioka, and K. Suzuki. "INHERITED DEFICIENCY OF FUNCTIONAL PROTEIN S IN A JAPANESE FAMILY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644297.

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A family with a history of severe recurrent venous thromboembolic disease in some of the members was studied over three generations. In the propositus, a 36-year-old Japanese man, assays for the coagulation, anticoagulation and fibrinolytic factors including fibrinogen, plasminogen, antithrombin III and protein C associated with inherited venous thrombotic disease were normal. While markedly decreased protein S, a cofactor of activated protein C, was revealed. The functional protein S activity in plasma was lower than 5% of normal. The same laboratory data were shown in his paternal uncle and

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Briët, E., L. Engesser, E. J. P. Brommer, A. W. Broekmans, and R. M. Bertina. "THROMBOPHILIA:ITS CAUSES AND A ROUGH ESTIMATE OF ITS PREVALENCE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642945.

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Idiopathic venous thrombosis and embolism have gained widespread interest since the discovery that, deficiencies of antithrombin III, protein C, and protein S are associated with familial venous thrombophilia. The purpose of our study was to obtain an estimate of the prevalence of this syndrome and to establish the etiology in as many cases as possible.We collaborated with specialists from 37 Dutch hospitals, covering about 10% of the Dutch population. A history as well as blood samples were obtained from 113 unrelated cases with familial thrombophilia and from 90 isolated cases. Assuming that

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