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Journal articles on the topic 'Antithrombin III deficiency'

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Published: 4 June 2021
Last updated: 5 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

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.bloodjournal732490.

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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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12

Vikydal, R., C. Korninger, P. A. Kyrle, H. Niessner, I. Pabinger, E. Thaler, and K. Lechner. "The Prevalence of Hereditary Antithrombin-III Deficiency in Patients with a History of Venous Thromboembolism." Thrombosis and Haemostasis 54, no. 04 (1985): 744–45. http://dx.doi.org/10.1055/s-0038-1660123.

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SummaryAntithrombin-III activity was determined in 752 patients with a history of venous thrombosis and/or pulmonary embolism. 54 patients (7.18%) had an antithrombin-III activity below the normal range. Among these were 13 patients (1.73%) with proven hereditary deficiency. 14 patients were judged to have probable hereditary antithrombin-III deficiency, because they had a positive family history, but antithrombin-III deficiency could not be verified in other members of the family. In the 27 remaining patients (most of them with only slight deficiency) hereditary antithrombin-III deficiency was unlikely. The prevalence of hereditary antithrombin-III deficiency was higher in patients with recurrent venous thrombosis.
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13

Emerson, T. E. "Antithrombin III replacement in animal models of acquired antithrombin III deficiency." Blood Coagulation & Fibrinolysis 5, no. 1 (January 1994): S37–46. http://dx.doi.org/10.1097/00001721-199401000-00006.

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14

Knot, E. A. R., J. W. ten Cate, T. Bruin, A. H. C. Iburg, and G. N. J. Tytgat. "Antithrombin III metabolism in two colitis patients with acquired antithrombin III deficiency." Gastroenterology 89, no. 2 (August 1985): 421–25. http://dx.doi.org/10.1016/0016-5085(85)90346-4.

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15

Ernerudh, J., J. E. Olsson, and H. von Schenck. "Antithrombin-III deficiency in ischemic stroke." Stroke 21, no. 6 (June 1990): 967. http://dx.doi.org/10.1161/str.21.6.967a.

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16

Gallus, A. S. "Replacement Therapy in Antithrombin III Deficiency." Transfusion Medicine Reviews 3, no. 4 (October 1989): 253–63. http://dx.doi.org/10.1016/s0887-7963(89)70086-9.

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17

Candrina, R., A. Goppini, A. Salvi, F. Zuccato, and G. Giustina. "Arterial thrombosis in antithrombin III deficiency." Clinical & Laboratory Haematology 8, no. 3 (September 1986): 267–68. http://dx.doi.org/10.1111/j.1365-2257.1986.tb00106.x.

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18

Jackson, Mark R., Stephen B. Olsen, Edward R. Gomez, and Barbara M. Alving. "Use of antithrombin III concentrates to correct antithrombin III deficiency during vascular surgery." Journal of Vascular Surgery 22, no. 6 (December 1995): 804–7. http://dx.doi.org/10.1016/s0741-5214(95)70072-2.

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19

HAMBLEY, H., J. F. DAVIDSON, I. D. WALKER, and T. MENZIES. "Prophylactic use of antithrombin III concentrate following surgery in congenital antithrombin III deficiency." Clinical & Laboratory Haematology 9, no. 1 (March 1987): 27–31. http://dx.doi.org/10.1111/j.1365-2257.1987.tb01379.x.

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20

Lane, D. A., H. Ireland, R. J. Olds, S. L. Thein, D. J. Perry, and M. Aiach. "Antithrombin III: A Database of Mutations." Thrombosis and Haemostasis 66, no. 06 (1991): 657–61. http://dx.doi.org/10.1055/s-0038-1646481.

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SummaryElucidation of the molecular defects reponsible for antithrombin III deficiency is proceeding rapidly. In order that a record is kept of the new and duplicated mutations that are found, we have compiled a database that we plan to update annually. In this, the first report of the database, we list 6 antithrombin III locus sequence polymorphisms and 94 recorded mutations causing functional deficiency of the protein, 38 of which are novel. As is the case with mutations affecting other protein genes, most mutations of antithrombin III involve a CG to TG or CA change.
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21

Jena, Sushanta Kumar, Minakshi Mohanty, Umesh Chandra Patra, and Sanatan Behera. "A study on demographic and clinical profile of children with extra hepatic portal venous obstruction and with special reference to thrombophilic factors." International Journal Of Community Medicine And Public Health 4, no. 3 (February 22, 2017): 640. http://dx.doi.org/10.18203/2394-6040.ijcmph20170468.

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Background: Extra-hepatic portal vein obstruction (EHPVO) due to portal vein thrombosis is an important cause of portal hypertension in several region including India. The cause of thrombosis in these patients remains unclear. Objective of the study was to study the demographic features, etiology, clinical, laboratory findings with special reference to thrombophilic factors like protein C, protein S and antithrombin III deficiency in children with EHPVO.Methods: The prospective analysis of 62 patients of EHPVO (<14 years of age) was done in the Department of Hepatology, SCB medical College, Cuttack. After detailed history, clinical examination, Ultrasound abdomen /color Doppler and Upper GI endoscopy, the subjects were analyzed for any deficiency of thrombophilic factors like protein C, protein S and antithrombin III.Results: A total of 62 patients (37 Male, 25 Female) with mean age of 8.3+3.1 years were studied. Growth retardation was present in the form of wasting (alone) 20.9%, stunting (alone) 25.8% and both wasting and stunting was found in 9.8% cases. History of neonatal, umbilical sepsis and umbilical vein catheterization was found in 15.9% and 10.2% of cases respectively. Haemorrhage from oesophageal varices was prevalent symptoms in 85.9% patients. Splenomegaly was found in 91.9% patients and ascites in 9.4% patients. 47 patients studied for protein C, S and antithromibin III. 14 patients were found to have thrombophilia: protein C deficiency in 9, protein S deficiency in 8, Antithrombin III deficiency in 6.Conclusions: The etiology of EHPVO in the majority of patients remain still unclear. It is commonly associated impaired somatic growth. The risk of EHPVO increases in the presence of thrombophilia, resulting from deficiency of naturally occurring anticoagulant proteins like Protein C, Protein S and Antithrombin III.
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22

Breddin, H. K., C. M. Kirchmaier, N. Bender, M. Schepping, and M. Ziemen. "Substitution of antithrombin III in acquired at-III deficiency." Thrombosis Research 41 (January 1986): 131. http://dx.doi.org/10.1016/0049-3848(86)91606-3.

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23

Loubser, Paul G., John J. McCarthy, and Mohammed Attar. "Coronary thrombosis associated with antithrombin-III deficiency." Journal of Cardiothoracic and Vascular Anesthesia 11, no. 6 (October 1997): 756–59. http://dx.doi.org/10.1016/s1053-0770(97)90171-3.

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24

Piper, B. J., and P. T. Farrell. "Hereditary Antithrombin III Deficiency and Neuraxial Anaesthesia." Anaesthesia and Intensive Care 43, no. 6 (November 2015): 782–85. http://dx.doi.org/10.1177/0310057x1504300618.

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25

Wilson, C., I. D. Walker, J. F. Davidson, and C. W. Imrie. "Mesenteric venous thrombosis and antithrombin III deficiency." Journal of Clinical Pathology 40, no. 8 (August 1, 1987): 906–8. http://dx.doi.org/10.1136/jcp.40.8.906.

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26

Manoharan, A., and B. Hewitt. "Danazol therapy in familial antithrombin III deficiency." Clinical & Laboratory Haematology 12, no. 3 (June 28, 2008): 357–58. http://dx.doi.org/10.1111/j.1365-2257.1990.tb00047.x.

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27

Batra, Munish K., Michael D. Adolph, James C. Thornton, Aspi M. Byramjee, Alan O. Oliver, and Helmut Schreiber. "Antithrombin III Deficiency and White Clot Syndrome." Vascular Surgery 30, no. 1 (January 1996): 37–44. http://dx.doi.org/10.1177/153857449603000107.

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28

Menache, D., BJ Grossman, and CM Jackson. "Antithrombin III: physiology, deficiency, and replacement therapy." Transfusion 32, no. 6 (July 1992): 580–88. http://dx.doi.org/10.1046/j.1537-2995.1992.32692367206.x.

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29

Pitney, W. R., A. Manoharan, and Shirley Dean. "ANTITHROMBIN III DEFICIENCY IN AN AUSTRALIAN FAMILY." British Journal of Haematology 46, no. 1 (July 7, 2008): 147–49. http://dx.doi.org/10.1111/j.1365-2141.1980.tb05947.x.

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30

Nakagawa, Masao. "Antithrombin III deficiency and its molecular analysis." Thrombosis Research 63, no. 2 (July 1991): 263. http://dx.doi.org/10.1016/0049-3848(91)90291-4.

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31

Seguin, John. "Inherited Antithrombin III Deficiency in the Neonate." Archives of Pediatrics & Adolescent Medicine 148, no. 4 (April 1, 1994): 389. http://dx.doi.org/10.1001/archpedi.1994.02170040055009.

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32

Lechner, K., and P. A. Kyrle. "Antithrombin III Concentrates-Are they Clinically Useful?" Thrombosis and Haemostasis 73, no. 03 (1995): 340–48. http://dx.doi.org/10.1055/s-0038-1653778.

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SummaryTreatment with AT III concentrates is a good example for the discrepancy between the optimistic expectations based on theoretical considerations or animal experiments and the result of clinical studies. 15 years after the introduction into clinical practice, a benefit for patients treated with AT III concentrates has not been proven. In hereditary antithrombin III deficiency, randomized clinical trials are completely lacking and only few and small sized randomized studies were performed in patients with acquired AT III deficiency. In none of these trials, a significant clinical benefit with regard to reduction of morbidity or mortality was detectable. Based on the published data, one can state that AT III concentrates may be beneficial in some special clinical situations in patients with hereditary antithrombin III deficiency (such as delivery, acute serious thromboembolic complications and postoperative thromboprophylaxis). In acquired AT III deficiency, there is no proven indication for the use of AT III concentrates.
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33

Tengborn, Lilian, and Thomas Bengtsson. "Antithrombin Iii Concentrate: Thromboprophylaxis During Pregnancy in a Patient with Congenital Antithrombin Iii Deficiency." Acta Obstetricia et Gynecologica Scandinavica 65, no. 4 (January 1986): 375–76. http://dx.doi.org/10.3109/00016348609157365.

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34

Aiach, Martine, Mindy Nora, Jean-Noël Fiessinger, Martine Roncato, Dominique François, and Martine Alhenc Gelas. "A functional abnormal antithrombin III (AT III) deficiency : AT III Charleville." Thrombosis Research 39, no. 5 (September 1985): 559–70. http://dx.doi.org/10.1016/0049-3848(85)90236-1.

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35

Buller, Harry R., and Jan W. Ten Cate. "Acquired antithrombin III deficiency: Laboratory diagnosis, incidence, clinical implications, and treatment with antithrombin III concentrate." American Journal of Medicine 87, no. 3 (September 1989): S44—S48. http://dx.doi.org/10.1016/0002-9343(89)80531-5.

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36

Bock, SC, and EV Prochownik. "Molecular genetic survey of 16 kindreds with hereditary antithrombin III deficiency." Blood 70, no. 5 (November 1, 1987): 1273–78. http://dx.doi.org/10.1182/blood.v70.5.1273.1273.

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Abstract Molecular genetic techniques were utilized to examine antithrombin III (ATIII) gene status in 16 independently ascertained kindreds with hereditary ATIII deficiency. In one of these families antithrombin III deficiency is caused by hemizygosity of the ATIII locus. In the remaining 15 kindreds, two copies of the ATIII gene are present and appear to be grossly normal at the level of whole genome Southern blotting, suggesting that small deletions, insertions or limited nucleotide substitution(s) in the antithrombin III gene, or “trans- acting” defects at other loci involved in the processing, modification, and secretion of biologically active ATIII are responsible for the observed anticoagulant disorders.
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37

Bock, SC, and EV Prochownik. "Molecular genetic survey of 16 kindreds with hereditary antithrombin III deficiency." Blood 70, no. 5 (November 1, 1987): 1273–78. http://dx.doi.org/10.1182/blood.v70.5.1273.bloodjournal7051273.

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Molecular genetic techniques were utilized to examine antithrombin III (ATIII) gene status in 16 independently ascertained kindreds with hereditary ATIII deficiency. In one of these families antithrombin III deficiency is caused by hemizygosity of the ATIII locus. In the remaining 15 kindreds, two copies of the ATIII gene are present and appear to be grossly normal at the level of whole genome Southern blotting, suggesting that small deletions, insertions or limited nucleotide substitution(s) in the antithrombin III gene, or “trans- acting” defects at other loci involved in the processing, modification, and secretion of biologically active ATIII are responsible for the observed anticoagulant disorders.
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38

Finazzi, G., and T. Barbui. "Different Incidence of Venous Thrombosis in Patients with Inherited Deficiencies of Antithrombin III, Protein C and Protein S." Thrombosis and Haemostasis 71, no. 01 (1994): 015–18. http://dx.doi.org/10.1055/s-0038-1642378.

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SummaryA cohort study was undertaken to compare the incidence of thrombosis in patients with inherited deficiency of Antithrombin III (n = 9), Protein C (n = 36) and Protein S (n = 36). The patients were stratified for schedule of antithrombotic prophylaxis and followed for a total period of 160 patient-years. Seven venous thrombosis were observed for a total incidence of 4.3% pts.-ys. The incidence of thrombosis was not significantly different in patients of different age, sex and schedule of prophylaxis, although there was a trend to a lower incidence in young individuals and in those receiving long-term oral anticoagulation. Patients with AT III deficiency had an higher incidence of thrombosis than patients with Protein C or Protein S deficiency (12 vs. 2.8 vs. 3.3% pts.-ys., p <0.05), despite the fact that they were, on average, younger and more prophylaxed. This study suggests that congenital Antithrombin III deficiency constitutes a greater risk of thrombosis than congenital deficiences of Protein C and Protein S.
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39

LEE, M. K., and S. C. NG. "Cerebral venous thrombosis associated with antithrombin III deficiency." Australian and New Zealand Journal of Medicine 21, no. 5 (October 1991): 772–73. http://dx.doi.org/10.1111/j.1445-5994.1991.tb01388.x.

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40

Schmidt, B. K. "Antithrombin III deficiency in neonatal respiratory distress syndrome." Blood Coagulation & Fibrinolysis 5, no. 1 (January 1994): S13–18. http://dx.doi.org/10.1097/00001721-199401000-00003.

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41

Mazza, J. J. "Antithrombin-HI (AT-III) Deficiency Spanning Four Generations." Thrombosis and Haemostasis 66, no. 06 (1991): 737–38. http://dx.doi.org/10.1055/s-0038-1646494.

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42

Creagh, M. D., I. F. Roberts, D. J. Clark, and F. E. Preston. "Familial antithrombin III deficiency and Mycoplasma pneumoniae pneumonia." Journal of Clinical Pathology 44, no. 10 (October 1, 1991): 870–71. http://dx.doi.org/10.1136/jcp.44.10.870.

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43

Yonemitsu, Yoshikazu, Katsuhiko Yanaga, Takashi Matsumata, and Keizo Sugimachi. "Portal Vein Thrombosis Due To Antithrombin III Deficiency." Angiology 46, no. 11 (November 1995): 1043–47. http://dx.doi.org/10.1177/000331979504601111.

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44

Eyster, Elaine, and Mark E. Parker. "Treatment of Familial Antithrombin-III Deficiency with Danazol." Pathophysiology of Haemostasis and Thrombosis 15, no. 2 (1985): 119–25. http://dx.doi.org/10.1159/000215132.

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45

Soutar, R., V. Marzinotto, and M. Andrew. "Overtight nappy precipitating thrombosis in antithrombin III deficiency." Archives of Disease in Childhood 69, no. 5 (November 1, 1993): 599. http://dx.doi.org/10.1136/adc.69.5.599.

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46

Mannucci, P. M., C. Boyer, M. Wolf, A. Tripodi, and M. J. Larrieu. "Treatment of congenital antithrombin III deficiency with concentrates." British Journal of Haematology 50, no. 3 (July 7, 2008): 531–35. http://dx.doi.org/10.1111/j.1365-2141.1982.00479.x-i1.

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47

Duchange, Nathalie, Jean-François Chasse, Georges N. Cohen, and Mario M. Zakin. "Molecular characterization of the antithrombin III tours deficiency." Thrombosis Research 45, no. 1 (January 1987): 115–21. http://dx.doi.org/10.1016/0049-3848(87)90263-5.

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48

Jagtap, Amit, Preeti Shanbag, and Mamta Vaidya. "Budd-chiari syndrome due to antithrombin III deficiency." Indian Journal of Pediatrics 70, no. 12 (December 2003): 1003–5. http://dx.doi.org/10.1007/bf02723831.

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49

Shenaq, S. A., S. Masud, D. H. Yawn, T. J. Greene, R. Sheinbaum, H. J. Safi, P. E. Curling, and M. E. DeBakey. "ACQUIRED ANTITHROMBIN III DEFICIENCY IN CARDIAC SURGERY PATIENTS." Anesthesia & Analgesia 80, Supplement (April 1995): SCA20. http://dx.doi.org/10.1213/00000539-199504001-00020.

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50

Humphries, John E. "Acquired Antithrombin III Deficiency: Replacement with Antithrombin III Concentrates in a Patient with Protein S Deficiency Accelerates Response to Therapy." Acta Haematologica 90, no. 3 (1993): 151–54. http://dx.doi.org/10.1159/000204398.

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