Relevant bibliographies by topics / Antithrombin III deficiency

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

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"

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Beresford, C. H. "Antithrombin III deficiency." Blood Reviews 2, no. 4 (December 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 (July 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 (September 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 (September 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 (November 15, 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 (July 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 (January 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 (September 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 (April 24, 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, RW Carrell, HL Gibson, S. Rosenberg, RA Hallewell, and PJ Barr. "Characterization of antithrombins produced by active site mutagenesis of human alpha 1-antitrypsin expressed in yeast." Blood 73, no. 2 (February 1, 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 and have shorter in vivo half-lives (t1/2) than human alpha 1AT. These antithrombins should be suitable for therapeutic replacement of AT-III in cases of congenital deficiency and in conditions associated with acquired AT-III deficiency, such as disseminated intravascular coagulation.
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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 comparativa, das quais 33 apresentavam tromboembolismo venoso e 36 o não apresentavam. Os principais desfechos relacionados a resultados maternos e neonatais adversos foram: pré-eclâmpsia grave, descolamento prematuro de placenta, restrição de crescimento fetal, natimortalidade, prematuridade e complicações hemorrágicas maternas. As trombofilias congênitas incluídas no estudo foram o fator V de Leiden (FVL), mutação da protrombina G20210A, mutação C677T do gene da 5,10-metilenotetrahidrofolato redutase (MTHFR), deficiência de proteína S, deficiência de proteína C e deficiência de antitrombina. Ambos os grupos apresentaram características populacionais similares. A ocorrência de complicações maternas e fetais/neonatais foi similar nos dois grupos: pré-eclâmpsia grave (P=0,097), descolamento prematuro de placenta (P=0,478), restrição de crescimento fetal (P=0,868), natimortalidade (P=0,359), prematuridade (P=0,441) e complicações hemorrágicas maternas (P=0,478). Este estudo concluiu que a presença de tromboembolismo venoso em gestantes com trombofilia hereditária apresenta resultados maternos e neonatais semelhantes àquelas com trombofilias hereditárias sem tromboembolismo venoso.
The aim of this study was to evaluate differences in maternal and neonatal outcomes in pregnancies complicated by inherited thrombophilias between patients with and without venous thromboembolism. Despite increasing evidence in the literature indicating an association between inherited thrombophilias and adverse obstetric outcomes, doubts remain whether thrombophilic patients with venous thromboembolism present poorer maternal and neonatal outcomes than thrombophilic patients without venous thromboembolism. In this retrospective, observational and comparative study, 66 pregnant women with inherited thrombophilias, including 33 with venous thromboembolism and 36 without thromboembolism, were investigated. The main end-points analyzed were severe pre-eclampsia, placental abruption, fetal growth restriction, stillbirth, preterm delivery, and maternal hemorrhagic complications. The congenital thrombophilias included in this study were factor V Leiden (FVL), prothrombin G20210A mutation, C677T mutation in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene, protein S deficiency, protein C deficiency, and antithrombin deficiency. The two groups were similar in terms of population characteristics. The frequency of maternal and fetal/neonatal complications was similar in the two groups: severe pre-eclampsia (P=0.097), placental abruption (P=0.478), fetal growth restriction (P=0.868), stillbirth (P=0.359), preterm delivery (P=0.441), and maternal hemorrhagic complications (P=0.478). This study concluded that venous thromboembolism in thrombophilic patients does not worsen maternal or neonatal outcomes when compared to thrombophilic patients without venous thromboembolism.
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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, 133–46. Boston, MA: 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, 27. 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, 235–42. 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 embolism were observed in 2 patients after abortion. Of the 27 other pregnancies, in the absence of any anticoagulant treatment, 17 were complicated by thrombosis (62 %), either during pregnancy (n = 8) or in the post-partun period (n = 9).In the group of 31 women with PC deficiency, 82 pregnancies occured : 16 ended with a provoked abortion, followed by a DVT in one case. Out of the 66 other pregnancies, 17 (25 %) were associated with thrombosis, during pregnancy (n = 5) or in the post-partum (n = 12).Thus, pregnancy is a situation at high risk of thrombosis in PC deficient women, and even higher in AT III deficient ones. No standardized anticoagulant prophylaxis being available, various anticoagulant treatments (mainly SC heparin) were given at various doses, started at different moments of pregnancy to 6 AT III and 3 PC deficient women : 3 and O thrombosis occured respectively.In the post-partum, a thrombosis was observed in 1 of 4 AT III and 2 of 4 PC deficient women who received a treatment. Consequently, an efficient treatment remains to be determined.If a pregnancy is unwanted, estroprogestogens are contra-indicated but progestogen only treatments with chlormadinone acetate, levonorgestrel or low dose of norethisterone were given to 4 AT III and 6 PC deficient women who were simultaneously receiving AVK : no recurrence of thrombosis was observed afer 1 to 3 years of treatment.
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Schwartz, R., E. Kavanagh, K. Bauer, R. Rosenberg, J. Ballard, J. Latino, V. Strother, M. Mosesson, W. Haire, and M. DeLeo. "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 different. The half-life determined in an earlier study exceeded 2.5 days. All patients treated prophylactically or therapeutically received a loading dose to increase plasma AT-III to 120%, and then received maintenance doses, generally every 24 hours, to maintain plasma AT-III levels in the general range 80-120%. AT-III levels were monitored every 12 hours initially and doses and intervals modified accordingly. None of 5 patients with cong. deficiency treated prophylactically for high risk situations (surgery, delivery, catheterization) developed a thrombotic complication. Six patients (3 cong., 2 acq., 1 probably acq.) were treated for thrombosis/P.E., two of whom were pregnant. Heparin resistance was reversed in two, both pregnant. One patient with superior mesenteric-portal vein thrombosis (cong. deficiency) and another with superior mesenteric artery-aortic occlusion (acq. deficiency) survived without further progression of thrombosis. DIC resolved in one patient treated with AT-III and benefit was observed in a 2nd patient as well. AT-III was well tolerated, with but a single mild reaction in 176 infusions. We conclude AT-III may be beneficialas prophylaxis in patients with cong.AT-III deficiency during high thrombotic risk situations, as well as anadjunct to heparin in treatment for thrombotic complications in congenital and acquired AT-III deficiency.
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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 process, and pulmonary embolism. In patients with antithrombin III deficiency the concomittant useof antithrombin III concentrate is controversial, although some patients may requirehigher doses of heparin.Substitution therapy is only indicated in homozygous protein C deficient patientswith purpura fulminans. Fresh frozen plasma i.v. is the treatment of choice, in a dosage of 10 ml/kg once or twice daily. The current prothrombin complex concentrates may induce new skin lesions and disseminated intravascular coagulation. After the lesions have been healed(mostly in 4 to6 weeks)coumarin therapy may effectively prevent new episodes of purpura fulminans, provided the prothrombin time is kept within 2,5 - 4,0 INR. Heparin is ineffective for preventing purpura fulminans due to homozygous protein C deficiency.The thrombotic manifestations in heterozygotes are effectively prevented by coumarin therapy. This is supported by the observation that patients may remain free of thrombosis during long-term treatment and may have recurrences shortly after the withdrawal of the coumarin drug. The therapeutic range for the prothrombin time should be within 2,0 - 4,0 INR, target value 3,0 INR. In the initial phase of oral anticoagulant therapy protein C deficient patients are prone to the development of coumarin induced hemorrhagic skin (tissue) necrosis.In the patients studied in Leiden, it occurred in about 3% of the treated patients. Heparin appears to be ineffective for the prevention of coumarin-induced skin necrosis; high loading doses of coumarin should be avoided and the prothrombin timeshouldbe checked dialy during the initial phase of oral anticoagulant treatment. Tissue necrosis may contribute to bleeding complications after fibrinolytic therapy, ashas been observed in two protein C deficient patients.In clinical situations with an increased risk for thrombosis such as surgery and pregnancy, heparin (in-low-doses) alone orin combination with coumarins have been used succesfully for the prevention of thrombosis. The need for antithrombin III concentrates in patients with hereditary antithrombin III deficiency in such situations is not substantiated.Although anabolic steroids are capable to increase the plasma concentrations of antithrombin III and of protein C in the respective deficiency states, its efficacy in preventing thrombotic episodes remains to be established.An optimal strategy for preventing thrombosis in congenital thrombotic syndromes is to identify still asymptomatic patients. In case of antithrombin III, protein C, and protein S deficiency this search is feasible. During risk situations for thrombosis patients are to be protected against the development of thrombosis.In Leiden pregnant women with one of the deficiencies are treated from the 14th week of pregnancy, initially with a shortacting coumarin drug, after the 34th week withheparin s.c. b.i.d. at therapeutic dosages,and after delivery coumarin therapy is reTnstituted during 6 weeks. The use of oralcontraceptives should be avoided, unlesspatients are under coumarin treatment. As long as deficient patients remain asymptomatic no antithrombotic treatment is indicated. After the first documented thromboticincident patients are treated indefinitelywith oral anticoagulants.
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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 substrate hydrolysis or by SDS PA gel e1ectrophoresis. Its mobility was normal when examined by the latter technique on 10-20X gels under reducing and non-reducing conditions. Patient AT III was reapplied to heparin-Sepharose and eluted with a NaCl gradient. A minor active pool eluted in the same concentration range, 0.5-1.2M, used to purify normal AT III, while predominantly inactive AT III eluted at higher NaCl concentrations, 1.2-2.0M. Further purification of variant AT III was achieved by passage of heparin-Sepharose eluates through a thrombin-Sepharose column and structural studies are being undertaken on this material. It is concluded that AT III Glasgow has increased affinity for heparin but reduced ability to inactivate thrombin. It can be differentiated from two other AT III variants that bind heparin with high affinity, Milano and Northwick Park, but has similar features to those of AT III Chicago.
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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-50. Rabbit immunoglobulins against human AT III were isolated by affinity chromatography using purified human AT III coupled to CNBr-activated Sepharose 4B. Trace amounts of immunoglobulin against human albumin, IgG and IgM were removed by solid phase immunoadsorption. The highly purified immunoglobulins against human AT III were coupled to CNBr-activated Sepharose 4B. This anti-AT III-Sepharose was used for single-step purification of AT III from plasma. Elution was performed by Na-citrate buffer at pH 3.0 and the eluted fractions immediately neutralized. The recovery was more than 60%.The purified AT III appeared as a single protein band in SDS-poly-acrylamide gel electrophoresis with or without reduction. Affinity purified AT III and AT III purified by the three-step procedure were indistinguishable when analyzed by crossed immunoelectrophoresis in the absence and the presence of heparin isoelectrical focusing in polyacrylamid gel at a pH 4-6.5 gradient, and SDS-polyacrylamide gel electrophoresis. AT III antigen concentration was determined by electroimmunoassay and the reactive site concentration determined by titration with purified human thrombin using Phe-Pip-Arg-Nan (S-2238) as substrate. The ratio (active site conc.)/(antigen conc.) was identical in the two AT III preparations. It is concluded that this single-step immuno-affinity chromatography gives a high recovery from plasma of a highly purified functionally intact AT III molecule. The purification method is independent of the heparin binding capacity of AT III. This is of particular importance for the purification and characterization of abnormal AT III molecules with impaired heparin-binding site.
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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 thromboses had occurred in at least one member (n=12/18) and/or the defect could be detected in one of them (n=12/18)Most often we found a deficiency of antithfombin III (n=6). A deficiency of protein C (type I) was detected in 3 and a deficiency of protein S in 5 families. In one patient a combined deficiency of anti thrombin III, protein C and protein S was found. Extensive family studies revealed a deficiency of antithrombin III in the grandmother of the patient, who suffered from arterial thrombosis. A deficiency of plasminogen and an abnormal plasminogen molecule were detected in 2 other families. Defective release of t-PA could be demonstrated in 3 members of one investigated family up to nowSeme family members with either defects of protein C, protein S or plasminogen as well as a defective release of t-PA lack thrombotic events. Furthermore thromboses of mesenteric veins occurred in 2 of 6 patients with anti thrombin III deficiency and in 1 of 5 patients with protein S deficiency. Superficial vein thromboses were mainly found in patients with protein C- or protein S-deficiency
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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 on the plasma level of 3-throm-boglobulin (BTG) determined every 2-3 weeks. At the time of the first increase of BTG (around 10th week of gestation) prophylaxis with s. c.heparin 2x7'500IU/d was started, leading to normalization of BTG. When BTG was again elevated, the dose of heparin was successively increased up to 2x15'000IU/d; thereby, functional AT IH levels remained in the range of 28-50%. Two patients received only heparin throughout the pregnancy. However, in one patient BTG levels could not be normalized by heparin alone (60-130ng/ml, normal: <43ng/ml). Injections of AT in concentrate, 11000IU, led to reduction of BTG within 2 hrs (60 → 42, 220 → 61 ng/ml). Therefore, AT m was given from the 25th week of gestation in increasing amounts up to 5'000IU/week (funct. AT m in plasma: 51 -72%) in addition to heparin (2x12'500IU/d), resulting in BTG levels of 33-51 ng/ml. From the onset of labour, all patients received AT IU concentrates (two patients l'OOOIU every second day, one patient 1'0001U daily) together with i. v. heparin 20'000-27'500IU/d, until the oral anticoagulant treatment started after delivery had reached therapeutic levels. The amount of AT m concentrate totally administered was 5'000IU in two patients and 66'000IU in one patient. None of the patients showed ever signs of venous thrombosis.Our observations demonstrate that instead of an AT in substitution with the aim to normalize its plasma level, an effective thrombosis prophylaxis - monitored by plasma levels of BTG - may be achieved with heparin alone or combined with low amounts of AT in concentrate.
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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 tryptic and SA V8 peptides were compared on TLC and HPLC with analysis of aberrant peptides. Confirmation was by gas-phase automated sequencing.Two variants were unequivocally identified.1) Rouen-I (47Arg→His) wasfoundin a heterozygote with a history of a single cerebral occlusion.2) Rouen-II (47Arg→Ser) was in a forty years old heterozygote with an acute myocardial infarction but no other history of thrombosis.Three mutations of Arg47 are known: Cys(Toyama), His(Rouen-I) and Se(Rouen-II) all with decreased heparinaffinity.Functional and structural modelling studies are reported indicating apositive heparin-binding site formedby the A and D helices centred on Arg47 (A2). The mutation in Rouen-IIcreates an unutilised oligosaccharide attachment Asn⋆-Arg-Ser suggesting facultative glycosylation. This would, as an incidental observation, support a translational (pre-secretory) origin of the high affinity AT-III beta.
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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 two sisters who had recurrent thrombotic episodes, and his asymptomatic father as well. The mean protein S antigen was 38%(range 22-52%) by the conventional Laurell rocket immunoelectrophoresis. But by the crossed immunoelectrophoresis and the Laurell rocket electrophoresis using the PEG 8000 precipitation method, the free form protein S was undetectable in their plasma(Table). Thus, a significant coincidence between the antigenic free protein S levels and the functional protein S activities was clarified.It is suggested that the recurrent, thrombotic disease family is due to an inherited deficiency of protein S, larly of free form and functional protein S.
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10

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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Abstract:
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 each proband in a family with thrombophilia has an average of four affected relatives, a rough estimate of the prevalence of familial thrombophilia in The Netherlands is 40 cases per 100.000. The prevalence of non-familial thrombophilia is probably lower.In 35 out of the 113 familial cases we established a diagnosis of hereditary antithrombin III deficiency (n=5), protein C deficiency (type I: n=9; type II: n=4), protein S deficiency (n=15) and dysfibrinogenemia (n=2). In 36 cases we found no abnormality at all and in the remaining 42 cases abnormalities were found in one or more of the following: heparin cofactor II, factor V, factor VII, factor VIII, von Willebrand factor, plasminogen, tissue plasminogen activator, plasminogen activator inhibitor, alpha 2 antiplasmin and histidine rich glycoprotein. In most of these cases, however, the hereditary nature of the abnormalities could not be demonstrated and the causal relationships remain to be established.In the 90 isolated cases, we diagnosed hereditary deficiencies of anti thrombin III, protein C and protein S each in one case and a lupus anticoagulant in two cases. In 54 cases no abnormality was found and in the remaining 31 cases various abnormalities were found in one or more of the proteins mentioned above.We conclude that the syndrome of thrombophilia is not rare but its true prevalence needs to be established by more rigorous means. An etiological diagnosis can be made with confidence in only one third of the familial cases and in less than 10 percent of the isolated cases.
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