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5 - Hereditary and acquired thrombophilia in pregnancy

Published online by Cambridge University Press:  01 February 2010

Rodger L. Bick M.D., Ph.D., F.A.C.P.
Affiliation:
Professor of Medicine and Pathology, University of Texas Southwestern Medical Center; Director: Dallas Thrombosis Clinical Center, Dallas, Texas; Director: Pacific Thrombosis Clinical Center, Southern California, USA
William F. Baker Jr., M.D., F.A.C.P.
Affiliation:
Associate Clinical Professor of Medicine, Center for Health Sciences, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, CA, USA, Thrombosis, Hemostasis, and Special Hematology Clinic, Kern Medical Center, Bakersfield; California Clinical Thrombosis Center, Bakersfield, California, USA
Rodger L. Bick
Affiliation:
University of Texas Southwestern Medical Center, Dallas
Eugene P. Frenkel
Affiliation:
University of Texas Southwestern Medical Center, Dallas
William F. Baker
Affiliation:
University of California, Los Angeles
Ravi Sarode
Affiliation:
University of Texas Southwestern Medical Center, Dallas
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Summary

Introduction

Thrombophilia in pregnancy represents a challenging problem for obstetricians, reproductive medicine specialists and hematologists. Normal pregnancy is known to be associated with an enhanced risk of deep vein thrombosis (DVT) and pulmonary embolus (PE). When combined with a thrombophilic disorder, this risk is significantly enhanced, usually considered to about 5–8-fold elevated in normal pregnant women, and addition of a thrombophilia, or other clinically significant risk factor, requires particular attention to avoid unnecessary fetal loss and maternal morbidity and mortality. Thrombophilia in obstetrics and pregnancy is known to be associated with not only enhanced risks of DVT and PE, but also recurrent miscarriage syndrome, infertility, stillborn births, eclampsia intrauterine growth retardation, pre-eclampsia, frank eclampsia, HELLP syndrome and abruption, with the additional usual thrombohemorrhagic complications, such as disseminated intravascular coagulation. Indeed many women with undiagnosed thrombophilia will experience their first clinical manifestation when pregnant – usually miscarriage or DVT with or without PE. In addition, many pregnancy patients who have had a prior DVT/PE harbor an undiagnosed thrombophilic disorder, thus emphasizing the importance of adequate investigation when a suggestive personal or family history warrants. This chapter summarizes (1) antithrombotic approaches to pregnant women with thrombophilia and other risk factors, and (2) the particular thrombophilias of concern to the obstetrician, reproductive medicine specialist and hematologist. In addition, treatment discussions and recommendations will be discussed in general and then, when necessary, for any particular disorder. It must be appreciated the clinical course of thrombophilic patients, particularly during pregnancy, is highly dynamic.

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Publisher: Cambridge University Press
Print publication year: 2006

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References

Brandenburg, V. M., Frank, R. D., Heintz, B., et al. HELLP syndrome, multifactorial thrombophilia and postpartum myocardial infarction. J. Perinat. Med., 32: 181, 2004.CrossRefGoogle ScholarPubMed
Bick, R. L. Disseminated intravascular coagulation: current concepts of etiology, pathophysiology, diagnosis and management. (Chapter 8) In Hematology Oncology Clinics North America, 17: 149, 2003.
Colman-Brochu, S.Deep vein thrombosis in pregnancy. Am. J. Maternal Child. Nursing, 29: 186, 2004.CrossRefGoogle ScholarPubMed
Anteby, E. Y., Musalam, B., Milwidsky, A.Fetal inherited thrombophilias influence the severity of preeclampsia, IUGR and placental abruption. Eur. J. Obstet Gynecol. Reprod. Biol., 113: 31, 2004.CrossRefGoogle ScholarPubMed
Bick, R. L.Disseminated intravascular coagulation: objective criteria for clinical and laboratory diagnosis and assessment of therapeutic response. Clinical & Applied Thrombosis Hemostasis, 1: 3, 1995.CrossRefGoogle Scholar
Bick, R. L. and Haas, S. Thromboprophylaxis and thrombosis in medical, surgical, trauma and obstetric/gynecologic patients. (Chapter 11) In Hematology Oncology Clinics North America, 17: 217, 2003.
Stefano, V., Rossi, E. and Leone, G.Inherited thrombophilia, pregnancy, and oral contraceptive use: clinical implications. Semin. Vasc. Med., 3: 47, 2003.CrossRefGoogle ScholarPubMed
Ducloy-Bouthors, A. S. and Trillot, N.Risk factors of thromboembolism associated with pregnancy and the puerperium. Role of inherited and acquired thrombophilia. Ann. Med. Interne, (Paris) 154: 295, 2003.Google ScholarPubMed
Belt, A. G. M., Prins, M., Huisman, M. H., et al. Familial thrombophilia: a review analysis. Clin. Appl. Thromb. Hemostas., 2: 227, 1996.CrossRefGoogle Scholar
Laposata, M., Green, D., Cott, E. M., et al. The clinical use and laboratory monitoring of low-molecular-weight heparin, danaparoid, hirudin and related compounds, and argatroban. College of American Pathologists Conference XXXI on laboratory monitoring of anticoagulant therapy. Arch. Path. Lab. Med., 122: 799, 1998.Google ScholarPubMed
Douiketis, I. J. D., Johnson, J. A. and Turpie, A. G.Low molecular weight heparin as bridging anticoagulation during interruption of warfarin. Archives Internal Medicine, 164: 1319, 2004.CrossRefGoogle Scholar
FDA MEDWATCH ADVERSE REACTION ALERT, JANUARY, 2002: LOVENOX (enoxaparin sodium) injection: Pregnancy and heart valves. http://www.fda.gov/medwatch/SAFETY/2002/jan02.htm#lovenox.
Bick, R. L.Heparin therapy and monitoring: Guidelines and practice parameters for clinical and laboratory approaches. Clin. Appl. Thrombosis Hemostas., 2: 12, 1996.Google Scholar
Bick, R. L.Recurrent miscarriage syndrome and infertility caused by blood coagulation protein or platelet defects. Hematology Oncology Clinics North America, 14: 1131, 2000.CrossRefGoogle ScholarPubMed
Thomas, D. P.Heparin prophylaxis and treatment of venous thromboembolism. Semin. Hematol., 15: 1, 1978.Google ScholarPubMed
Yett, H. S., Skillman, J. J. and Salzman, E. W.The hazards of aspirin plus heparin. N. Engl. J. Med., 298: 1092, 1978.Google ScholarPubMed
Warkentin, T. E., Soutar, R. L. and Panju, A.Acute systemic reactions to intravenous bolus heparin therapy: characterization and relationship to heparin induced thrombocytopenia. Blood, 80: 160 (Abst). 1992.Google Scholar
Jaffe, M. D. and Willis, P. W.Multiple fractures associated with long-term sodium heparin therapy. JAMA, 193: 152, 1965.CrossRefGoogle ScholarPubMed
Levine, M.Non-hemorrhagic complications of anticoagulant therapy. Semin. Thromb. Hemost., 12: 63, 1986.CrossRefGoogle Scholar
Howell, R., Fidler, J., Letsky, E., et al. The risks of antenatal subcutaneous heparin prophylaxis: a controlled trial. Br. J. Obstet. Gynaecol., 90: 1124, 1983.CrossRefGoogle ScholarPubMed
Monreal, M., Lafoz, E., Olive, A., et al. Comparison of subcutaneous unfractionated heparin with low molecular weight heparin (fragmin) in patients with venous thromboembolism and contraindications. Thrombosis Haemostasis, 71: 7, 1994.Google ScholarPubMed
Morabia, A.Heparin doses and major bleedings. Lancet, 1: 1278, 1986.CrossRefGoogle ScholarPubMed
Bick, R. L. and Frenkel, E. P.Clinical aspects of heparin-induced thrombocytopenia and thrombosis and other side effects of heparin therapy. J. Clin. Appl. Thrombosis Hemostasis, 5 (Suppl 1): 7, 1999.CrossRefGoogle ScholarPubMed
Warkentin, T. E., Soutar, R. L. and Panju, A.Acute systemic reactions to intravenous bolus heparin therapy: characterization and relationship to heparin induced thrombocytopenia. Blood, 80: 160 (Abst). 1992.Google Scholar
Bick, R. L. Four cases of anaphylaxis with first or second dose of low-molecular-weight heparin therapy. FDA: Adverse Reaction Report – on file.
Jaffe, M. D. and Willis, P. W.Multiple fractures associated with long-term sodium heparin therapy. JAMA, 193: 152, 1965.CrossRefGoogle ScholarPubMed
Levine, M.Non-hemorrhagic complications of anticoagulant therapy. Semin. Thromb. Hemost., 12: 63, 1986.CrossRefGoogle Scholar
Hirsh, J., Raschke, R., Warkentin, T. E., et al. Heparin: mechanism of action, pharmacokinetics, dosing considerations, monitoring, efficacy, and safety. Chest, 108: 259S, 1995.CrossRefGoogle ScholarPubMed
Howell, R., Fidler, J., Letsky, E., et al. The risks of antenatal subcutaneous heparin prophylaxis: a controlled trial. Br. J. Obstet. Gynaecol., 90: 1124, 1983.CrossRefGoogle ScholarPubMed
Monreal, M., Lafoz, E., Olive, A., et al. Comparison of subcutaneous unfractionated heparin with a low molecular weight heparin (fragmin) in patients with venous thromboembolism and contraindications to coumarin. Thromb. Haemost., 71: 7, 1994.Google ScholarPubMed
Barbour, L. A., Kick, S. D., Steiner, J. F., et al. A prospective study of heparin-induced osteoporosis in pregnancy using bone densitometry. Am. J. Obst. Gyn., 170: 862, 1994.CrossRefGoogle ScholarPubMed
Dahlman, T. C.Osteoporotic fractures and the recurrence of thromboembolism during pregnancy and the puerperium in 184 women undergoing thromboprophylaxis with heparinAm. J. Obst. Gyn., 168: 1265, 1993.CrossRefGoogle ScholarPubMed
Hunt, B. J., Doughty, H., Majumdar, G., et al. Thromboprophylaxis with low molecular weight heparin (Fragmin) in high risk pregnancies. Thromb. Haemost., 77: 39, 1997.Google Scholar
Douketis, J., Ginsberg, J. S., Burrows, R. F., et al. The effects of long-term heparin therapy during pregnancy on bone density. A prospective matched cohort study. Thromb. Haemost., 75: 254, 1996.Google Scholar
Walenga, J. M. and Bick, R. L.Heparin-induced thrombocytopenia, paradoxical thromboembolism, and other side effects of heparin therapy. Med. Clin. North. Am., 82: 635, 1998.CrossRefGoogle ScholarPubMed
Walenga, J. M. and Bick, R. L.Heparin-induced thrombocytopenia, paradoxical thromboembolism, and other side effects of heparin therapy. Card Clinics: Annual Drug Therapy, 2: 123, 1998.Google Scholar
Muir, J. M., Andrew, M., Hirsh, J., et al. Histomorphometric analysis of the effects of standard heparin on trabecular bone in vivo. Blood, 88: 1314, 1996.Google ScholarPubMed
Muir, J. M., Hirsh, J., Weitz, J. I., et al. A histomorphometric comparison of the effects of heparin and low-molecular-weight heparin on cancellous bone in rats. Blood, 89: 3236, 1997.Google ScholarPubMed
Panagakos, F. S., Jandinski, J. J., Feder, L., et al. Heparin fails to potentiate the effects of IL-1 beta-mediated bone resorption of fetal rat long bones in vitro. Biochimie, 77: 915, 1995.CrossRefGoogle ScholarPubMed
Shaughnesy, S. G., Young, E., Deschamps, , et al. The effects of low molecular weight and standard heparin on calcium loss from fetal rat calvoria. Blood, 86: 1368, 1995.Google Scholar
Murray, W. J., Clinical pesentations of heparin induced thrombocytopenia. Seminars Hematology, 35 (Suppl) 9, 1998.Google Scholar
Bick, R. L. Heparin and low molecular weight heparins. (Chapter 17) In Disorders of Thrombosis and Hemostasis, Bick, R. L., ed. Philadelphia, PA; Lippincott, Williams and Wilkins, 2002, p. 359.Google Scholar
Warkentin, T. E.Heparin-induced skin lesions. Br. J. Haematol., 92: 494, 1996.CrossRefGoogle ScholarPubMed
Hall, J. C., McConahay, D., Gibson, D., et al. Heparin necrosis and anticoagulation syndrome. JAMA, 244: 1831, 1980.CrossRefGoogle ScholarPubMed
Hill, J., Caprini, J. A. and Robbins, J. L.An unusual complication of minidose heparin therapy. Clin. Orthop., 118: 130, 1976.Google Scholar
White, P. W., Sadd, J. R. and Wensel, R. E.Thrombotic complications of heparin therapy. Ann. Surg., 190: 595, 1979.CrossRefGoogle ScholarPubMed
Levine, L. E., Bernstein, J. E. and Soltani, K.Heparin-induced cutaneous necrosis unrelated to injection sites. Arch. Derm., 119: 400, 1983.CrossRefGoogle ScholarPubMed
Bircher, A. J., Itin, P. H. and Buchner, S. A.Skin lesions, hypereosinophilia and subcutaneous heparin. N. Engl. J. Med., 343: 861 (letter), 1994.Google ScholarPubMed
Aull, L., Chao, H. and Coy, K.Heparin-induced hyperkalemia. Ann. Pharmacotherapy, 24: 244, 1990.Google ScholarPubMed
Bick, R. L.Introduction to thrombosis: proficient and cost-effective approaches to thrombosis. Hematology Oncology Clinics North America, 17: 1, 2003.CrossRefGoogle ScholarPubMed
Krabbendam, I. and Dekker, G.Pregnancy outcome in patients with a history of recurrent spontaneous miscarriages and documented thrombophilias. Obstet. Gynecol. Surv., 59: 651, 2004.CrossRefGoogle Scholar
Rees, D. S., Cox, M. and Clegg, J. B.World distribution of factor V Leiden. Lancet, 346: 1133, 1995.CrossRefGoogle ScholarPubMed
Svensson, P. and Dahlback, B.Resistance to activated protein C as a basis for venous thrombosis. N. Engl. J. Med., 330: 517, 1994.CrossRefGoogle ScholarPubMed
Koster, T., Rosendaal, F. R., Ronde, H., et al. Venous thrombosis due to poor anticoagulant response to activated protein C: Leiden Thrombophilia Study. Lancet, 342: 1503, 1993.CrossRefGoogle ScholarPubMed
Dahlback, B., Carlsson, M. and Svensson, P. J.Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C. Proc. Natl. Acad. Sci. USA, 90: 1004, 1993.CrossRefGoogle ScholarPubMed
Bertina, R. M.Factor V Leiden and other coagulation factor mutations affecting thrombotic risk. Clin. Chem., 43: 1678, 1997.Google ScholarPubMed
Bertina, R. M., Reitsma, P. H., Rosendaal, F. R., et al. Resistance to activated protein C and factor V Leiden as risk factors for venous thrombosis. Thromb. Haemostas., 74: 449, 1995.Google ScholarPubMed
Greengard, J. S., Fisher, C. L., Villoutreix, B., et al. Structural basis for type I and type II deficiencies of antithrombotic plasma protein C: patterns revealed by three-dimensional molecular modeling of mutations of the protease domain. Proteins, 18: 367, 1994.CrossRefGoogle Scholar
Voorberg, J., Roelse, J., Koopman, R., et al. Association of idiopathic venous thromboembolism with single-point mutation at Arg506 of factor V. Lancet, 343: 1535, 1994.CrossRefGoogle ScholarPubMed
Zoller, B., Hillarp, A., Berntorp, E.Activated protein C resistance due to a common factor V gene mutation is a major risk factor for venous thrombosis. Annu. Rev. Med., 48: 45, 1997.CrossRefGoogle ScholarPubMed
Laffan, M. A. and Manning, T.The influence of factor VIII on measurement of activated protein C resistance. Blood Coag. Fibrinol., 7: 761, 1996.CrossRefGoogle ScholarPubMed
Bontempo, F. A.The factor V Leiden mutation: spectrum of thrombotic events and laboratory evaluation. J. Vasc. Surg., 2: 271, 1997.CrossRefGoogle Scholar
Simioni, P., Scalia, D., Tormene, D., et al. Intra-arterial thrombosis and homozygous factor V Leiden mutation. Clin. Appl. Thromb. Hemostas., 3: 215, 1997.CrossRefGoogle Scholar
Vefring, H., Lie, R., Odegard, R., et al. Maternal and fetal variants of genetic thrombophilias and the risk of preeclampsia. Epidemiology, 15: 317, 2004.CrossRefGoogle ScholarPubMed
Samama, M. M., Simon, D., Horellou, M. H., et al. Diagnosis and clinical characteristics of inherited activated protein C resistance. Haemostasis, 26, Suppl 4: 315, 1996.Google ScholarPubMed
Hile, E. T., Westendorp, R. G., Vandenbroucke, J. P., et al. Mortality and causes of death in families with the factor V Leiden mutation (resistance to activated protein C). Blood, 89: 1963, 1997.Google Scholar
Middeldorp, S., Henkens, C. M., Koopman, M. M., et al. The incidence of venous thromboembolism in family members of patients with factor V Leiden mutation and venous thrombosis. Ann. Int. Med., 128: 15, 1998.CrossRefGoogle ScholarPubMed
Bick, R. L. Syndromes of thrombosis and hypercoagulability. In Cullen, J. H., (ed.): Current Concepts of Thrombosis, vol. 82. Philadelphia, PA; W. B. Saunders Co., 1998, p. 409.Google Scholar
Prandoni, P., Lensing, A. W., Cogo, A., et al. The long-term clinical course of acute deep venous thrombosis. Ann. Int. Med., 125: 1, 1996.CrossRefGoogle ScholarPubMed
Miletich, J. P., Stampfer, M. J., Goldhaber, S. Z., et al. Factor V Leiden and recurrent idiopathic venous thromboembolism. Circulation, 92: 2800, 1995.Google Scholar
Simioni, P., Prandoni, P., Lensing, A. W., et al. The risk of recurrent venous thromboembolism in patients with an Arg506 → Gln mutation in the gene for factor V (factor V Leiden). N. Engl. J. Med., 336: 399, 1997.CrossRefGoogle Scholar
Rintelen, C., Pabinger, I., Knobl, P., et al. Probability of recurrence of thrombosis in patients with and without factor V Leiden. Thromb. Haemostas., 75: 229, 1996.Google ScholarPubMed
Levine, M. N., Hirsh, J., Gent, M., et al. Optimal duration of oral anticoagulant therapy: a randomized trial comparing four weeks with three months of warfarin in patients with proximal deep vein thrombosis. Thromb. Haemostas., 74: 606, 1995.Google ScholarPubMed
Vandenbroucke, J. P., Koster, T., Briet, E., et al. Increased risk of venous thrombosis in oral-contraceprive users who are carriers of factor V Leiden mutation. Lancet, 344: 1453, 1994.CrossRefGoogle ScholarPubMed
Bloemenkamp, K. W., Rosendaal, F. R., Helmerhorst, F. M., et al. Enhancement by factor V Leiden mutation of risk of deep-vein thrombosis associated with oral contraceptives containing a third-generation progestagen. Lancet, 346: 1593, 1995.CrossRefGoogle ScholarPubMed
Rintelen, C., Mannhalter, C., Ireland, H., et al. Oral contraceptives enhance the risk of clinical manifestation of venous thrombosis at a young age in females homozygous for factor V Leiden. Br. J. Haematol., 93: 487, 1996.CrossRefGoogle Scholar
Gandrille, S., Greengard, J. S., Alhenc-Gelac, M., et al. Incidence of activated protein C resistance caused by the ARG 506 GLN mutation in factor V in 113 unrelated symptomatic protein C-deficient patients. The French Network on the behalf of INSERM. Blood, 86: 219, 1995.Google ScholarPubMed
Zoller, B., Berntsdotter, A., Garcia de Frutos, P., et al. Resistance to activated protein C as an additional genetic risk factor in hereditary deficiency of protein S. Blood, 85: 3518, 1955.Google Scholar
Ridker, P. M., Hennekens, C. H., Selhub, J., et al. Interrelation of hyperhomocyst(e)inemia, factor V Leiden, and risks of future venous thromboembolism. Circulation, 95, 1777, 1997.CrossRefGoogle Scholar
Bick, R. L., Laughlin, H. R., Cohen, B., et al. Fetal wastage syndrome due to blood protein/platelet defects: results of prevalence studies and treatment outcome with low-dose heparin and low-dose aspirin. Clin. Appl. Thromb. Hemostas., 1: 286, 1995.CrossRefGoogle Scholar
Bick, R. L. and Hoppensteadt, D.Thrombohemorrhagic defects and recurrent miscarriage syndrome. Blood, 104: 712A, 2004.Google Scholar
Dudding, T. and Attia, J.The asociation between adverse pregnancy outcomes and maternal factor V Leiden genotype: a meta-analysis. Thromb. Haemostasis., 91: 700, 2004.Google Scholar
Gebhardt, G. and Hall, D.Inherited and acquired thrombophilias and poor pregnancy outcome: should we be treating with heparin? Curr. Opinion Obstet. Gynecol., 15: 501, 2003.CrossRefGoogle ScholarPubMed
Sonmezer, M., Aytac, R., Demirel, L., et al. Mesenteric vein thrombosis in a pregnant patient heterozygous for the factor VG (1691 G to A) Leiden mutation. European J. Obstet. Gynaecol. Reproductive Bio., 114: 234, 2004.Google Scholar
Camilleri, R., Peebles, D., Portmann, C., et al. 455G/A beta fibrinogen gene polymorphism factor V Leiden, prothrombin G 20210 A mutation and MTHFR C677T, and placental vascular complications. Blood Coagulation Fibrinolysis, 15: 139, 2004.CrossRefGoogle Scholar
Kovalevsky, G., Gracia, C., Berlin, J., et al. Evaluation of the asociation between hereditary thrombophilias and recurrent miscarriage loss: a meta-analysis. Arch. Int. Med., 164: 558, 2004.CrossRefGoogle Scholar
Yilmazer, M., Kurtay, G., Sonmezer, M., et al. Factor V Leiden and prothrombin G20210A G-A mutations in controls and in patients with thromboembolic events during pregnancy or the puerperium. Arch. Gynecol. Obstet., 268: 304, 2003.CrossRefGoogle ScholarPubMed
Bokarewa, M. I., Bremme, K. and Blomback, M.Arg506-Gln mutation in factor V and risk of thrombosis during pregnancy. Br. J. Haematol., 92: 473, 1996.CrossRefGoogle ScholarPubMed
Kibbe, M. R. and Rhee, R. Y.Heparin-induced thrombocytopenia: pathophysiology. Semin. Vasc. Surg., 9: 284, 1996.Google ScholarPubMed
Wallis, D. E., Lewis, B. E., Messmore, H., et al. Heparin-induced thrombocytopenia and thrombosis syndrome. Clin. Appl. Thromb. Hemostas., 4: 160, 1998.CrossRefGoogle Scholar
Williamson, D., Brown, K., Luddingtonm, R., et al. Factor V Cambridge: a new mutation (Arg306→Thr) associated with resistance to activated protein C. Blood, 91: 1140, 1998.Google Scholar
Chan, W. P., Lee, C. K., Kwong, Y. L., et al. A novel mutation of Arg306 of factor V gene in Hong Kong Chinese. Blood, 91: 1135, 1998.Google ScholarPubMed
Poort, S. R., Rosendaal, F. R., Reitsma, P. H., et al. A common genetic variation in the 3′-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood, 88: 3698, 1996.Google ScholarPubMed
Arruda, V. R., Annichino-Bizacchi, J. M., Goncalves, M. S., et al. Prevalence of the prothrombin gene variant (nt20201A) in venous thrombosis and arterial disease. Thromb. Haemostas., 78: 1430, 1997.Google Scholar
Ferraresi, P., Marchetti, G., Legnani, C., et al. The heterozygous 20210 G/A prothrombin genotype is associated with early venous thrombosis in inherited thrombophilias and is not increased in frequency in artery disease. Arterioscler. Thromb. Vasc. Biol., 17: 2418, 1997.CrossRefGoogle Scholar
Makris, M., Preston, F. E., Beauchamp, N. J., et al. Co-inheritance of the 20210 A allele of the prothrombin gene increases the risk of thrombosis in subjects with familial thrombophilia. Thromb. Haemost., 78: 1426, 1997.Google Scholar
Bloem, B. R., Putten, M. J., Meer, J. M., et al. Superior saggital sinus thrombosis in a patient heterozygous for the novel 20210 A allele of the prothrombin gene. Thromb. Haemostas., 79: 235, 1997.Google Scholar
Martinelli, I., Sacchi, E., Landi, G., et al. High risk of cerebral-vein thrombosis in carriers of a prothrombin-gene mutation and in users of oral contraceptives. NEJM, 338: 1793, 1998.CrossRefGoogle ScholarPubMed
Gould, J., Deam, S. and Dolan, G.Prothrombin 20210: A polymorphism and third generation oral conraceptives – a case report of coeliac axis thrombosis and splenic infarction. Thromb. Haemostas., 79: 1214, 1998.Google Scholar
Poort, S. R., Rosendaal, F. R., Reitsma, P. H., et al. A common genetic variation in the 3′-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood, 88: 3698, 1996.Google ScholarPubMed
Ratnoff, O. D. and Colopy, J. E.A familial hemorrhagic trait associated with a deficiency of clot-promoting fraction of plasma. J. Clin. Invest., 34: 602, 1955.CrossRefGoogle ScholarPubMed
Seegers, W. H.Factor X (autoprothrombin III). Semin. Thromb. Hemostas., 7: 233, 1981.Google Scholar
Bick, R.Disorders of Thrombosis and Hemostasis: Clinical and Laboratory Practice. Chicago, IL, ASCP Press, 1992, p. 109.Google Scholar
Mcpherson, R. A.Thromboembolism in Hageman trait. Am. J. Clin. Pathol., 68: 240, 1977.CrossRefGoogle ScholarPubMed
Baker, W. F. Jr. and Bick, R. L.Deep vein thrombosis: diagnosis and management. Med. Clin. N. Am., 78: 685, 1994.CrossRefGoogle ScholarPubMed
Hoak, J. C., Swanson, L. W., Warner, E. D., et al. Myocardial infarction associated with severe factor XI deficiency. Lancet, 2: 884, 1966.CrossRefGoogle Scholar
Ratnoff, O. D., Busse, R. J. and Sheon, R. P.The demise of John Hageman. N. Engl. J. Med., 279: 760, 1968.CrossRefGoogle Scholar
Goodnough, L. T., Saito, H. and Ratnoff, O.Thrombosis or myocardial infarction in congenital clotting factor abnormalities and chronic thrombocytopenias: a report of 21 patients and a review of 50 previously reported cases. Medicine, 62: 248, 1983.CrossRefGoogle ScholarPubMed
Di Imperato, D. and Dettori, A. G.Ipofibrinogenemia congenita con fibrinoastenia. Helvitica Pediatrica Acta, 13: 380, 1958.Google Scholar
Bithell, T. C.Hereditary dysfibrinogenemia. Clin. Chem., 31: 509, 1985.Google ScholarPubMed
Mammen, E. F.Fibrinogen abnormalities. Semin. Hemostas. Thromb., 9: 1, 1983.CrossRefGoogle Scholar
Al Mondhiry, H. and Galanakis, D.Dysfibrinogenemia and lupus anticoagulant in a patient with recurrent thrombosis. J. Lab. Clin. Med., 110: 726, 1987.Google Scholar
Lijnen, H. R., Soria, J. and Soria, C.Dysfibrinogenemia (Fibrinogen Dusard) associated with impaired fibrin-enhanced plasminogen activation. Thromb. Haemostas., 51: 108, 1984.Google ScholarPubMed
Reber, P., Furlan, M. and Henschen, A.Three abnormal fibrinogen variants with the same amino acid substitution (gamma-275 Arg-His): Fibrinogens Bergamo II, Essen and Perugia. Thromb. Haemostas., 56: 401, 1986.Google ScholarPubMed
Welch, G. N. and Loscalzo, J.Homocysteine and atherothrombosis. N. Engl. J. Med., 338: 1042, 1998.CrossRefGoogle ScholarPubMed
Carson, N. A. J. and Neill, D. W.Metabolic abnormalities detected in a survey of mentally backward individuals in Northern Ireland. Arch. Dis. Child, 37: 505, 1962.CrossRefGoogle Scholar
Mudd, S. H., Finkelstein, J. D., Irreverre, F., et al. Homocystinuria: an enzymatic defect. Science, 143: 1443, 1964.CrossRefGoogle Scholar
Valle, D., Pai, G. S., Thomas, G. H., et al. Homocystinuria due to cystathione beta-synthetase deficiency: clinical manifestations and therapy. Johns Hopkins Med. J., 146: 110, 1980.Google Scholar
McCully, K. S.Vascular pathology of homocysteinemia: implications for the pathogenesis of arteriosclerosis. Am. J. Pathol., 56: 111, 1969.Google ScholarPubMed
Carey, M. C., Donovan, D. E., Fitzgerald, O., et al. Homocystinuria, I: a clinical and pathologic study of nine subjects in six families. Am. J. Med., 45: 17, 1968.Google Scholar
Goyette, P., Sumner, J. S., Milos, R., et al. Human methylenetetrahydrofolate reductase: isolation of cDNA, mapping and mutation identification. Natural Genetics, 7: 195, 1994.CrossRefGoogle ScholarPubMed
Frosst, P., Blom, H. J., Milos, R., et al. A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydrofolate reductase. Natural Genetics, 10: 111, 1995.CrossRefGoogle ScholarPubMed
Put, N. M. J., Steegers-Theunissen, R. P. M., Frosst, P., et al. Mutated methylenetetrahydrofolate reductase as a risk factor for spina bifida. Lancet, 346: 1070, 1995.Google ScholarPubMed
Jacques, P. F., Bostom, A. G., Williams, R. R., et al. Relation between folate status, a common mutation in methylenetetrahydrofolate reductase, and plasma homocysteine concentrations. Circulation, 93: 7, 1996.CrossRefGoogle ScholarPubMed
Rozen, R.Molecular genetic aspects of hyperhomocysteinemia and its relation to folic acid. Clin. Investig. Med., 19: 171, 1996.Google ScholarPubMed
Kang, S. S., Wong, P. W. and Malinow, M. R.Hyperhomocyst(e)inemia as a risk factor for occlusive vascular disease. Ann. Rev. Nutr., 12: 279, 1992.CrossRefGoogle Scholar
Stampfer, M. J., Malinow, M. R., Wilett, W. C., et al. A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians. JAMA, 268: 877, 1992.CrossRefGoogle Scholar
Kang, S. S., Wong, P. W. K., Susmano, A., et al. Thermolabile methylenetetrahydrofolate reductase: an inherited risk factor for coronary artery disease. Am. J. Hum. Genetics, 48: 536, 1991.Google ScholarPubMed
Malinow, M. R.Hyperhomocyst(e)inemia: a common and easily reversible risk factor for occlusive atherosclerosis. Circulation, 81: 2004, 1990.CrossRefGoogle Scholar
Boushey, C. J., Beresford, A. A., Omenn, G. S., et al. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease: probable benefits of increasing folic acid intake. JAMA, 274: 1049, 1995.CrossRefGoogle Scholar
Duell, P. B. and Malinow, M. R.Plasma homocyst(e)ine: an important risk factor for atherosclerotic vascular disease. Curr. Opin. Lipidol., 8: 28, 1997.CrossRefGoogle Scholar
Mayer, E. L., Jacobsen, D. W. and Robinson, K.Homocysteine and coronary atherosclerosis. J. Am. Coll. Cardiol., 27: 517, 1996.CrossRefGoogle ScholarPubMed
Nygard, O., Nordrehaug, J. E., Refsum, H., et al. Plasma homocysteine levels and mortality in patients with coronary artery disease. N. Engl. J. Med., 337: 230, 1997.CrossRefGoogle ScholarPubMed
Cattaneo, M., Martinelli, I. and Manucci, P. M.Hyperhomocysteinemia as a risk factor for deep-vein thrombosis. N. Engl. J. Med., 336: 1399, 1997.Google Scholar
Falcon, C. R., Cattaneo, M., Panzeri, D., et al. High prevalence of hyperhomocyst(e)inemia in patients with juvenile venous thrombosis. Arterioscl. Thromb., 14: 1080, 1994.CrossRefGoogle Scholar
Heijer, M., Koster, T., Blom, H. U., et al. Hyperhomocysteinemia as a risk factor for deep-vein thrombosis. N. Engl. J. Med., 334: 759, 1996.CrossRefGoogle Scholar
Fermo, I., Vigano, D., Angelo, S., Paroni, R., et al. Prevalence of moderate hyperhomocysteinemia in patients with early-onset venous and arterial occlusive disease. Ann. Intern. Med., 123: 747, 1995.CrossRefGoogle ScholarPubMed
Moghadasian, M. H., McManus, B. M. and Frohlich, J. J.Homocyst(e)ine and coronary artery disease: clinical evidence and genetic and metabolic background. Arch. Int. Med., 157: 2299, 1997.CrossRefGoogle Scholar
Robinson, K., Mayer, E. L., Miller, D. P., et al. Hyperhomocysteinemia and low pyridoxal phosphate: common and independent reversible risk factors for coronary artery disease. Circulation, 92: 2825, 1995.CrossRefGoogle ScholarPubMed
Israelsson, B., Brattstorm, L. E. and Hultberg, B. L.Homocysteine and myocardial infarction. Atherosclerosis, 71: 227, 1988.CrossRefGoogle ScholarPubMed
Wu, L. L., Wu, J., Hunt, S. C., et al. Plasma homocyst(e)ine as a risk factor for early familial coronary artery disease. Clin. Chem., 40: 1361, 1994.Google Scholar
Wald, N. J., Watt, H. C., Law, M. R., et al. Homocysteine and ischemic heart disease: results of a prospective study with implications regarding prevention. Arch. Int. Med., 158: 862, 1998.CrossRefGoogle ScholarPubMed
Araki, A., Sako, Y., Fukushima, Y., et al. Plasma sulfhydryl-containing amino acids in patients with cerebral infarction and in hypertensive subjects. Atherosclerosis, 79: 139, 1989.CrossRefGoogle ScholarPubMed
Brattstrom, L., Lindgren, A., Israelsson, B., et al. Hyperhomocysteinemia in stroke: prevalence, cause and relationship to type of stroke and stroke risk factors. Eur. J. Clin. Invest., 22: 214, 1992.CrossRefGoogle Scholar
Coull, B. M., Malinow, M. R., Beamer, N., et al. Elevated plasma homocyst(e)ine concentration as a possible independent risk factor for stroke. Stroke, 21: 572, 1990.CrossRefGoogle Scholar
Molgaard, J., Malinow, M. R., Lassvik, C., et al. Hyperhomocyst(e)inaemia: an independent risk factor for intermittent claudication. J. Int. Med., 231: 273, 1992.CrossRefGoogle Scholar
Berg, M., Stehouwer, D. A., Biedrager, E., et al. Plasma homocysteine and severity of atherosclerosis in young patients with lower-limb atherosclerotic disease. Arterioscl. Thromb. Vasc. Biol., 16: 165, 1996.CrossRefGoogle ScholarPubMed
Kottke-Marchant, K., Green, R., Jacobsen, D. W., et al. High plasma homocysteine: a risk factor for arterial and venous thrombosis in patients with normal coagulation profiles. Clin. Appl. Thromb. Hemostas., 3: 239, 1997.CrossRefGoogle Scholar
Franken, D. G., Boers, G. H., Blom, H. J., et al. Treatment of mild hyperhomocysteinemia in vascular disease patients. Arterioscl. Thromb., 14: 465, 1994.CrossRefGoogle ScholarPubMed
Brattstrom, L., Israelsson, B., Norving, B., et al. Impaired homocysteine metabolism in early onset cerebral and peripheral occlusive arterial disease: effect of pyridoxine and folic acid treatment. Atherosclerosis, 81: 51, 1990.CrossRefGoogle Scholar
Brattsrom, L. E., Israelsson, B., Jeppsson, J. O., et al. Folic acid: an innocuous means to reduce plasma homocysteine. Scandin. J. Clin. Lab. Invest., 48: 215, 1988.CrossRefGoogle Scholar
Ubbink, J. B., Hayward Vermaak, W. J., Merwe, A., et al. Vitamin requirements for the treatment of hypercysteinemia in humans. J. Nutr., 124: 1927, 1994.CrossRefGoogle Scholar
Naurath, H. J., Joosten, E., Riezler, R., et al. Effects of vitamin B12, folate, and vitamin B6 supplements in elderly people with normal serum vitamin concentrations. Lancet, 346: 85, 1995.CrossRefGoogle ScholarPubMed
Landgren, P., Israelsson, B., Lindgren, A., et al. Plasma homocysteine in acute myocardial infarction: homocysteine lowering effect of folic acid. J. Int. Med., 237: 381, 1995.CrossRefGoogle ScholarPubMed
Ward, M., McNulty, H., McPartlin, J., et al. Plasma homocysteine, a risk factor for cardiovascular disease, is lowered by physiological doses of folic acid. Quart. J. Med., 909: 519, 1997.CrossRefGoogle Scholar
Cuskelly, G. J., McNulty, H., McPartlin, J. M., et al. Plasma homocysteine response to folate intervention in young women. Irish J. Med. Science, 164: 3, 1995.Google Scholar
Malinow, M. R., Duell, P. B., Hess, D. L., et al. Reduction of plasma homocyst(e)ine levels by breakfast cereal fortified with folic acid in patients with coronary heart disease. N. Engl. J. Med., 338: 1009, 1998.CrossRefGoogle Scholar
Abidgaard, U.Purification of two progressive antithrombins of human plasma. Scan. J. Clin. Lab. Invest., 19: 190, 1967.CrossRefGoogle Scholar
Kurachi, K., Schmer, G. and Hermodson, M.Inhibition of bovine factor IXa and factor Xa by anti-thrombin-III. Biochemistry, 15: 368, 1976.CrossRefGoogle Scholar
Lahiri, K., Rosenberg, R. D. and Talamo, R. C.Antithrombin-III: an inhibitor of human plasma kallikrein. Fed. Proc., 33: 642, 1974.Google Scholar
Seegers, W. H., Cole, E. R. and, Harmison, C. R.Neutralization of autoprothrombin-C activity with antithrombin. Can. J. Biochem., 42: 359, 1964.CrossRefGoogle ScholarPubMed
Walker, F. and Esmon, C.The molecular mechanism of heparin action: II. Separation of functionally different heparins by affinity chromatography. Thromb. Res., 14: 219, 1979.CrossRefGoogle Scholar
Abildgaard, U.Binding of thrombin to antithrombin III. Scan. J. Clin. Lab. Invest., 24: 23, 1969.CrossRefGoogle ScholarPubMed
Seegers, W. H., Schroer, H. and, Kagami, M.Interactivation of purified autoprothrombin I with antithrombin. Can. J. Biochem., 42: 1425, 1964.CrossRefGoogle Scholar
Stead, N., Kaplan, A. P. and, Rosenberg, R. D.Inhibition of activated factor XII by antithrombin-heparin cofactor. J. Biol. Chem., 251: 6481, 1976.Google ScholarPubMed
Vennerod, A. M., Laake, K. and Soleberg, A. K.Inactivation and binding of human plasma kallikrein by antithrombin III and heparin. Thromb. Res., 9: 457, 1976.CrossRefGoogle ScholarPubMed
Fischer, A. M., Cornu, P., Sternberg, C., et al. Antithrombin III Alger: a new homozygous ATIII variant. Thromb. Haemostas., 55: 218, 1986.Google Scholar
Fagerhol, M. and Abildgaard, U.Immunologic studies in human antithrombin III. Influence of age, sex, and use of oral contraceptives on serum concentration. Scan. J. Haematol., 7: 10, 1970.CrossRefGoogle Scholar
Howie, P., Mallinson, A. and Prentice, C.Effect of combined oestrogen–progesterone contraceptives, oestrogen, and progesterone on antiplasmin and antithrombin activity. Lancet, 2: 1329, 1990.Google Scholar
McKay, E.Immunochemical analysis of active and inactive antithrombin III. Br. J. Haematol., 46: 277, 1980.CrossRefGoogle ScholarPubMed
Peterson, C., Kelley, R. and Minard, B.Antithrombin III. Comparison of functional and immunologic assays. Am. J. Clin. Pathol., 69: 500, 1978.CrossRefGoogle Scholar
Sveger, T.Antithrombin III in adolescents. Thromb. Res., 15: 885, 1979.CrossRefGoogle ScholarPubMed
Bick, R. L.Clinical relevance of antithrombin III. Semin. Hemostas. Thromb., 8: 276, 1982.CrossRefGoogle ScholarPubMed
Candrina, R. and Goppini, A.Antithrombin III deficiency. Blood Rev., 2: 239, 1988.Google Scholar
Menache, D., O'Malley, J. P., Schorr, J. B., et al. Evaluation of the safety, recovery, half-life, and clinical efficacy of Antithrombin III (Human) in patients with hereditary antithrombin III deficiency. Blood, 75: 33, 1990.Google ScholarPubMed
Menache, D.Replacement therapy in patients with hereditary antithrombin III deficiency. Semin. Hematol., 28: 31, 1991.Google ScholarPubMed
Owen, J.Antithrombin III replacement therapy in pregnancy. Semin. Hematol., 28: 46, 1991.Google ScholarPubMed
Vinnazer, H.Antithrombin III in shock and disseminated intravascular coagulation. Clin. Appl. Thromb. Hemostas., 1: 62, 1995.CrossRefGoogle Scholar
Schwartz, R. S., Bauer, K. A., Rosenberg, R. D., et al. Clinical experience with Antithrombin III concentrate in treatment of congenital and acquired deficiency of antithrombin. Am. J. Med., 87: 53S, 1989.CrossRefGoogle ScholarPubMed
Tollefson, D. M., Majerus, D. W. and Blank, M. K.Heparin cofactor II: purification and properties of a heparin-dependent inhibitor of thrombin in human plasma. J. Biol. Chem., 257: 2162, 1982.Google Scholar
Sie, P., Fernandez, F. and Caranobe, C.Inhibition of thrombin-induced platelet aggregation and serotonin release by antithrombin III and heparin cofactor II in the presence of standard heparin, dermatan sulfate and pentosan polysulfate. Thromb. Res., 35: 231, 1984.CrossRefGoogle ScholarPubMed
Sie, P., Dupouy, D. and Pichon, J.Constitutional heparin cofactor II deficiency associated with recurrent thrombosis. Lancet, 2: 414, 1985.CrossRefGoogle ScholarPubMed
Anderson, T., Larsen, M. and Abildgaard, U.Low heparin cofactor II associated with abnormal crossed immunoelectrophoresis pattern in two Norwegian families. Thromb. Res., 47: 243, 1987.CrossRefGoogle Scholar
Bertina, R. M., , L. I. K., Engesser, L., et al. Hereditary cofactor-II deficiency and the risk of development of thrombosis. Thromb. Haemostas., 57: 196, 1987.Google ScholarPubMed
Chaunsumrit, A., Manco-Johnson, M. J. and Hathaway, W. E.Heparin cofactor II in adults and infants with thrombosis and DIC. Am. J. Hematol., 31: 109, 1989.CrossRefGoogle Scholar
Toulin, P., Vitoux, J. F. and Capron, L.Heparin cofactor II in patients with deep venous thrombosis under heparin and oral anticoagulant therapy. Thromb. Res., 49: 479, 1988.Google Scholar
Grau, E., Oliver, A. and Felez, J.Plasma and urinary heparin cofactor II levels in patients with nephrotic syndrome. Thromb. Haemostas., 60: 137, 1988.Google ScholarPubMed
Stenflo, J.Structure and function of protein C. Semin. Thromb. Hemostas., 10: 109, 1984.CrossRefGoogle ScholarPubMed
Esmon, C. T. and Esmon, N. L.Protein C activation. Semin. Thromb. Hemostas., 10: 122, 1984.CrossRefGoogle ScholarPubMed
Walker, F. J.Protein S and the regulation of activated protein C: Semin. Thromb. Hemostas., 10: 131, 1984.CrossRefGoogle ScholarPubMed
Dahlback, B.The protein C anticoagulant system: inherited defects as a basis for venous thrombosis. Thromb. Res., 77: 1, 1995.CrossRefGoogle ScholarPubMed
Griffin, J. H.Clinical studies on protein C. Semin. Thromb. Hemostas., 10: 162, 1984.CrossRefGoogle ScholarPubMed
Marlar, R. A. and Endres-Brooks, J.Recurrent thromboembolic disease due to heterozygous protein C deficiency. Thromb. Haemostas., 50: 351, 1983.Google Scholar
Broekmans, A. W.Hereditary protein C deficiency. Haemostasis, 15: 233, 1985.Google ScholarPubMed
Seligsohn, U., Berger, A. and Abend, M.Homozygous protein C deficiency manifested by massive venous thrombosis in the newborn. N. Engl. J. Med., 310: 559, 1984.CrossRefGoogle ScholarPubMed
Marciniak, E., Wilson, H. O. and Marlar, R. A.Neonatal purpura fulminans: a genetic disorder related to the absence of protein C in blood. Blood, 65: 15, 198.
Mammen, E. F.Inhibitor abnormalities. Semin. Thromb. Hemostas., 9: 42, 198.CrossRef
Reitsma, P. H., Poort, S. R., Allaart, C. F., et al. The spectrum of genetic defects in a panel of 40 Dutch families with symptomatic protein C deficiency type I: heterogeneity and founder effects. Blood, 78: 890, 199.
Comp, P. C., Nixon, R. and Esmon, C. T.Determination of functional levels of protein C, an antithrombotic protein, using thrombin/thrombomodulin complex. Blood, 63: 15, 198.
Griffin, J. H., Bezeaud, A. and Evatt, B.Functional and immunologic studies of protein C in thromboembolic disease. Blood, 62: 301a, 1987.Google Scholar
Miletich, J. P.Laboratory diagnosis of protein C. Semin. Thromb. Hemostas., 16: 169, 1998.CrossRefGoogle Scholar
Bick, R. L. Hypercoagulability and thrombosis. In Bick, R. L., Bennett, J. M., Byrnes, R. K. (eds.): Hematology: Clinical and Laboratory Practice, St. Louis, MO; CV Mosby Publishers, 1993, p. 155.Google Scholar
Marlar, R. A., Sills, R. H. and Montgomery, R. R.Protein C in commercial factor IX (F IX) concentrations (CONC) and its use in the treatment of “homozygous” protein C deficiency. Blood, 62: 303, 1998.Google Scholar
Pescatore, P., Horellou, H., Conard, J., et al. Problems of oral anticoagulation in an adult with homozygous protein C deficiency and late onset of thrombosis. Thromb. Haemostas., 69: 311, 1993.Google Scholar
Monagle, P., Andrew, M., Halton, J., et al. Homozygous protein C deficiency: description of a new mutation and successful treatment with low molecular weight heparin. Thromb. Haemostas., 79: 756, 1998.CrossRefGoogle ScholarPubMed
Broekmans, A. W., Bertina, R. M., Loeliger, E. A., et al. Protein C and the development of skin necrosis during anticoagulant therapy. Thromb. Haemostas., 49: 251, 1983.Google ScholarPubMed
Zauber, N. P. and Stark, M. W.Successful warfarin anticoagulation despite protein C deficiency and a history of warfarin necrosis. Ann. Int. Med., 104: 659, 1986.CrossRefGoogle Scholar
Samama, M., Horellou, M. H., Soria, J., et al. Successful progressive anticoagulation in a severe protein C deficiency and previous skin necrosis at the initiation of oral anticoagulation treatment. Thromb. Haemostas., 51: 132 (letter), 1984.Google Scholar
Bick, R. L. and Kaplan, H.Syndromes of thrombosis and hypercoagulability: congenital and acquired thrombophilias. Clin. Appl. Thromb. Hemostas., 4: 25, 1998.CrossRefGoogle Scholar
Nilsson, I. M. and Pandofi, M.Fibrinolytic response of the vascular wall. Thrombosis Diathesis Hemorrhagica, 40: 231, 1970.Google Scholar
Gardiner, J. E., McGann, M. A. and Berridge, C. W.Protein S as a cofactor for activated protein C in plasma and the inactivation of purified factor VIII: C. Circulation, 70: 205, 1984.Google Scholar
Fouw, N. J., Haverkate, F. and Bertina, R. M.The cofactor role of protein S in the acceleration of whole blood clot lysis by activated protein C in vitro. Blood, 67: 1189, 1986.Google ScholarPubMed
Hackeng, T. M., van't Veer, C., Meijers, J. C., et al. Human protein S inhibits prothrombinase complex activity on endothelial cells and platelets via direct interactions with factors Va and Xa. J. Biol. Chem., 269: 21051, 1994.Google ScholarPubMed
Koppelman, S. J., Hackeng, T. M., Sixma, J. J., et al. Inhibition of the intrinsic factor X activating complex by protein S: evidence for specific binding of protein S to factor VIII. Blood, 86: 1062, 1995.Google ScholarPubMed
Gladson, K. H., Griffin, J. H. and Hach, V.The incidence of protein C and protein S deficiency in 139 young thrombotic patients. Thromb. Hemostas., 59: 18, 1988.Google Scholar
Heijboer, H., Brandjes, D. P., Buller, H. R., et al. Deficiencies of coagulation-inhibiting and fibrinolytic proteins in outpatients with deep-vein thrombosis. N. Engl. J. Med., 323: 1512, 1990.CrossRefGoogle ScholarPubMed
Tabernero, M. D., Tomas, J. F., Alberca, I., et al. Incidence and clinical characteristics of hereditary disorders associated with venous thrombosis. Am. J. Hematol., 36: 249, 1991.CrossRefGoogle ScholarPubMed
Simmonds, R. E., Ireland, H., Lane, D., et al. Clarification of the risk for venous thrombosis associated with hereditary protein S deficiency by investigation of a large kindred with a characterized gene defect. Ann. Int. Med., 128: 8, 1998.CrossRefGoogle ScholarPubMed
Mahasandana, C., Suvatte, V., Marlar, R. A., et al. Neonatal purpura fulminans associated with homozygous protein S deficiency. Lancet, 335: 61, 1990.CrossRefGoogle ScholarPubMed
Broekmans, M. A., Engesser, L. and Briet, E.Clinical manifestations of hereditary protein S deficiency. Thromb. Haemostas., 54: 57, 1985.Google Scholar
Engesser, L., Broekmans, A. W., Briet, E., et al. Hereditary protein S deficiency: clinical manifestations. Ann. Int. Med., 106: 677, 1987.CrossRefGoogle ScholarPubMed
Juhan-Vague, I., Roul, C., Alessi, M. C., et al. Increased plasminogen activator inhibitor activity in non-insulin dependent diabetic patients – relationship with plasma insulin. Thromb. Haemostas., 61: 370, 1989.Google ScholarPubMed
Nalbandian, R. M., Henry, R. L. and Bick, R. L.Thrombotic thrombocytopenic purpura: an extended editorial. Semin. Thromb. Hemostas., 5: 216, 1979.CrossRefGoogle ScholarPubMed
Bick, R. L., Bishop, R. C. and Shanbrom, E.Fibrinolytic activity in acute myocardial infarction. Am. J. Clin. Pathol., 57: 359, 1972.CrossRefGoogle ScholarPubMed
Collen, D. and Juhan-Vague, I.Fibrinolysis and atherosclerosis. Semin. Thromb. Hemostas., 14: 180, 1988.CrossRefGoogle ScholarPubMed
Mansfield, M. O.Alterations in fibrinolysis associated with surgery and venous thrombosis. Br. J. Surg., 59: 754, 1972.CrossRefGoogle Scholar
Bick, R. L. and Thompson, W. B.Fibrinolytic activity: changes induced with oral contraceptives. Obstet. Gynecol., 39: 213, 1972.Google ScholarPubMed
Marsh, N. Fibrinolysis in disease. In Bick, R. L. (ed.): Fibrinolysis. New York, NY: John Wiley and Sons, 1981, p. 125.Google Scholar
Hedner, U. and Nilsson, I. M.Urokinase in serum in a clinical series. Acta Medica Scandin., 4: 185, 1971.Google Scholar
Stemerman, M. B.Vascular intimal components: precursors of thrombosis. Prog. Hemostas. Thromb., 2: 1, 1974.Google ScholarPubMed
Wight, T.Vessel proteoglycans and thrombogenesis. Prog. Hemostas. Thromb., 5: 1, 1980.Google ScholarPubMed
Mammen, E. F.Plasminogen abnormalities. Semin. Hemostas. Thromb., 9: 50, 1983.CrossRefGoogle Scholar
Aoki, N., Moroi, M. and Sakata, Y.Abnormal plasminogen. A hereditary molecular abnormality found in a patient with recurrent thrombosis. J. Clin. Invest., 61: 1186, 1978.CrossRefGoogle Scholar
Blaisdell, W.Acquired and congenital clotting syndromes. World J. Surg., 14: 664, 1990.CrossRefGoogle ScholarPubMed
Hasegawa, D. K., Tyler, B. J. and Edson, J. R.Thrombotic disease in three families with inherited plasminogen deficiency. Blood, 60: 213, 1982.Google Scholar
Sartori, M. T., Patrassi, G. M., Girolami, B., et al. Type I plasminogen deficiency should be included among familial thrombophilias. Letter. Clin. Appl. Thromb. Hemostas., 3: 218, 1997.CrossRefGoogle Scholar
Biasutti, F. D., Sulzer, I., Stucki, B., et al. Is plasminogen deficiency a thrombotic risk factor? A study on 23 thrombophilic patients and their family members. Thromb. Haemostas., 80: 167, 1998.Google Scholar
Kazama, M., Tahara, C. and Suzki, Z.Abnormal plasminogen: a case of recurrent thrombosis. Thromb. Res., 21: 517, 1981.CrossRefGoogle ScholarPubMed
Bick, R. L.Clinical hemostasis practice: The major impact of laboratory automation. Semin. Thromb. Hemostas., 9: 139, 1983.CrossRefGoogle ScholarPubMed
Nilsson, I. M. and Tehgborn, L. A.A family with thrombosis associated with high level of tissue plasminogen activator inhibitor. Haemostasis, 14: 24, 1984.Google Scholar
Petaja, M., Rasi, V. and Myllyla, G.Familial hypofibrinolysis and venous thrombosis. Br. J. Haematol., 71: 393, 1989.CrossRefGoogle ScholarPubMed
Tabernero, M. D., Estelles, A. and Vincente, V.Incidence of increased plasminogen activator inhibitor in patients with deep venous thrombosis and/or pulmonary embolism. Thromb. Res., 56: 565, 1989.CrossRefGoogle ScholarPubMed
Dawson, S., Hamsten, A. and Wiman, B.Genetic variation at the plasminogen activator inhibitor-1 locus is associated with altered levels of plasma plasminogen activator inhibitor activity. Athersclerosis Thrombosis, 11: 183, 1991.CrossRefGoogle Scholar
Li, X. N., Grtenett, H. E. and Benza, R. L.Genotype-specific transcriptional regulation of PAI-1 expression by hypertriglyceridemic VLDL and LP(a) in cultured human endothelial cells. Atherosclerosis Thrombosis Vascular Biol., 17: 3215, 1997.CrossRefGoogle Scholar
Eriksson, P., Kallin, B. and Hooft, F. M.Allele-specific increase in basal transcription of the plasminogen-activator inhibitor 1 gene is associated with myocardial infarction. National Acad. Science, USA, 92: 1851, 1995.CrossRefGoogle ScholarPubMed
Ye, S., Green, F. R. and Scarabin, P. Y.The 4G/5G genetic polymorphism in the promoter of the plasminogen activator inhibitor 1 (PAI-1) gene is associated with differences in plasma PAI-1 activity but not with the risk of myocardial infarction in the ECTIM study. Thromb. Haemosta., 74: 837, 1995.Google Scholar
Ridker, P. M., Hennekens, C. H. and Lindpaintner, K.Arterial and venous thrombosis is not associated with the 4G/5G polymorphism in the promoter of the plasminogen activator inhibitor gene in a large cohort of US men. Circulation, 95: 59, 1997.CrossRefGoogle ScholarPubMed
Hong, J. J. and Kwaan, H. C.Hereditary defects in fibrinolysis associated with thrombosis. Seminars Thrombosis Hemostasis, 25: 321, 1999.CrossRefGoogle ScholarPubMed
Mammen, E. F., Barnhart, M. I., Selik, N. R., et al.: “Sticky Platelet Syndrome”: a congenital platelet abnormality predisposing to thrombosis. Folia Haematologica, 115: 361, 1988.Google ScholarPubMed
Rubenfire, M., Blevens, R. D., Barnhart, M. I., et al. Platelet hyperaggregability in patients with chest pain and angiographically normal coronary arteries. Am. J. Cardiol., 57: 657, 1986.CrossRefGoogle ScholarPubMed
Chittoor, S., Elsehety, A. E., Roberts, G. F., et al. Sticky platelet syndrome: a case report and review of the literature. J. Clinical Applied Thrombosis Hemostasis, 4: 280, 1998.CrossRefGoogle Scholar
Mammen, E. F.Ten year's experience with the “Sticky Platelet Syndrome”. J. Clin. Appl. Thromb. Hemostas., 1: 66, 1995.CrossRefGoogle Scholar
Mammen, E. F.Sticky platelet syndrome. Seminars Thrombosis Hemostasis, 25: 361, 1999.CrossRefGoogle ScholarPubMed
Bick, R. L.Sticky Platelet Syndrome: a common cause of unexplained venous and arterial thrombosis – results of prevalence and treatment outcome. J. Clin. Appl. Thromb. Hemostas., 4: 77, 1998.CrossRefGoogle Scholar
Anderson, J. A., Bleeding and thrombosis in women. Biomedical Prog., 12: 40, 1999.Google Scholar
Berg-Damer, E., Henkes, E., Trobisch, H., et al. Sticky platelet syndrome: a cause of neurovascular thrombosis and thromboembolism. Interventional Neuroradiology, 3: 145, 1997.CrossRefGoogle Scholar
Bick, R. L.Hypercoagulability and thrombosis. Medical Clinics North America, 78: 635, 1994.CrossRefGoogle ScholarPubMed
Bick, R. L.Antiphospholipid thrombosis syndromes: etiology, pathophysiology, diagnosis and management. International J. Hematology, 65: 193, 1997.CrossRefGoogle ScholarPubMed
Oosting, J. D., Derksen, R. H. and Bobbink, I. W. G.Antiphospholipid antibodies directed against a combination of phospholipids with prothrombin, protein C or protein S: an explanation for their pathogenic mechanism? Blood, 81: 2618, 1993.Google ScholarPubMed
Bick, R. L.The antiphospholipid thrombosis syndromes: a common multidisciplinary medical problem. J. Clinical Applied Thrombosis Hemostasis, 3: 270, 1997.CrossRefGoogle Scholar
Bick, R. L. and Baker, W. F.Anticardiolipin antibodies and thrombosis. Hematology Oncology Clinics North America, 6: 1287, 1992.CrossRefGoogle ScholarPubMed
Bick, R. L. and Baker, W. F.Antiphospholipid syndrome and thrombosis. Seminars Thrombosis Hemostasis, 25: 333, 1999.CrossRefGoogle ScholarPubMed
Bick, R. L.Antiphospholipid thrombosis syndromes. Hematology Oncology Clinics North America, 17: 115, 2003.CrossRefGoogle ScholarPubMed
Bick, R. L. and Baker, W. F.The antiphospholipid and thrombosis syndromes. Medical Clinics North America, 78: 667, 1994.CrossRefGoogle ScholarPubMed
Conley, C. L. and Hartmann, R. C.A hemorrhagic disorder caused by circulating anticoagulant in patients with disseminated lupus erythematosus. J. Clin. Invest., 31: 621, 1952.Google Scholar
Criel, A., Collen, D. and Masson, P. L.A case of IgM antibodies which inhibit the contact activation of blood coagulation. Thromb. Research., 12: 833, 1978.CrossRefGoogle ScholarPubMed
Kunkel, L.Acquired circulating anticoagulants. Hematology Oncology Clinics North America, 6: 1341, 1992.CrossRefGoogle ScholarPubMed
Coller, B. S., Hultin, M. B. and Hoyer, L. W.Normal pregnancy in a patient with a prior postpartum factor VIII inhibitor: with observations on pathogenesis and prognosis. Blood, 58: 619, 1981.Google Scholar
LeFrere, J. J., Gozin, D. and Lerable, J.Circulating anticoagulant in asymptomatic persons seropositive for human immunodeficiency virus. Ann. Internal Med., 108: 771 (letter), 1988.CrossRefGoogle ScholarPubMed
Taillan, B., Roul, C. and Fuzibet, J. G.Circulating anticoagulant in patients seropositive for human immunodeficiency virus. Ann. Internal Med. (France), 87: 405, 1989.Google ScholarPubMed
Davis, S., Furie, B. and Griffin, J. H.Circulating inhibitors of blood coagulation associated with procainamide-induced lupus anticoagulants. Am. J. Hematology, 4: 401, 1978.CrossRefGoogle Scholar
Jeffrey, R. F.Transient lupus anticoagulant with fansidar therapy. Postgrad. Med. J., 62: 893, 1986.CrossRefGoogle ScholarPubMed
Morgan, M., Downs, K., Chesterman, C. N., et al. Clinical analysis of 125 patients with the lupus anticoagulant. Aust. N. Z. J. Med., 23: 151, 1993.CrossRefGoogle ScholarPubMed
Bick, R. L. and Ucar, K.Hypercoagulability and thrombosis. Hematology Oncology Clinics North America, 6: 1421, 1992.CrossRefGoogle ScholarPubMed
Schleider, M. A., Nachman, R. L. and Jaffe, E. A.A clinical study of the lupus anticoagulant. Blood, 48: 499, 1976.Google ScholarPubMed
Regan, M. G., Lackner, H. and Karpatkin, S.Platelet function and coagulation profile in lupus erythematosus. Ann. Internal Med., 81: 462, 1974.CrossRefGoogle ScholarPubMed
Mueh, J. R., Herbst, K. D. and Rapaport, S. I.Thrombosis in patients with the “lupus”-type circulating anticoagulant. Ann. Internal Med., 92: 156, 1980.CrossRefGoogle Scholar
Shapiro, S. S. and Rajagopalon, V. Hemorrhagic disorders associated with circulating inhibitors. (chapter 7) In Ratnoff, O. D. and Forbes, C. D. (eds.), Disorders of Hemostasis. Philadelphia, PA; W. B. Saunders, 1996, p. 208.Google Scholar
Kampe, C. E.Clinical syndromes associated with lupus anticoagulants. Seminars Thrombosis Hemostasis, 20: 16, 1994.CrossRefGoogle ScholarPubMed
Hinton, R. C.Neurological syndromes associated with antiphospholipid antibodies. Seminars Thrombosis Hemostasis, 20: 46, 1994.CrossRefGoogle ScholarPubMed
Kleinknecht, D., Bobrie, G., Meyer, O., et al. Recurrent thrombosis and renal vascular disease in a patient with lupus anticoagulant. Nephrology, Dialysis, Transplantation, 4: 854, 1989.CrossRefGoogle Scholar
Pope, J. M., Canny, C. L. and Bell, D. A.Cerebral ischemic events associated with endocarditis, retinal vascular disease and lupus anticoagulant. Am. J. Medicine, 90: 299–309, 1991.CrossRefGoogle ScholarPubMed
Baker, W. F. and Bick, R. L.Antiphospholipid antibodies in coronary artery disease. Seminars Thrombosis Hemostasis, 20: 27, 1994.CrossRefGoogle ScholarPubMed
Reyes, H., Dearing, L. and Shoenfeld, Y.Antiphospholipid antibodies: a critique of their heterogeneity and hegemony. Seminars Thrombosis Hemostasis, 20: 89, 1994.CrossRefGoogle ScholarPubMed
Kaczor, N. A., Bickford, N. N. and Triplett, D. A.Evaluation of different mixing study reagents and dilution effect in lupus anticoagulant testing. J. Clin. Pathol., 95: 408, 1991.CrossRefGoogle ScholarPubMed
Shapiro, S. S. and Thiagarajan, P.Lupus anticoagulants. Prog. Hemostas. Thrombosis, 6: 263, 1982.Google ScholarPubMed
Ko, J., Guaglianone, P., Wolin, M., et al. Variation in the sensitivity of an activated thromboplasin time reagent to the lupus anticoagulant. Am. J. Clin. Pathology, 99: 333 (abstract), 1993.Google Scholar
Bick, R. L.The antiphospholipid thrombosis syndromes: fact, fiction, confusion & controversy. Am. J. Clin. Path., 100: 477, 1993.CrossRefGoogle ScholarPubMed
Thiagarajan, P., Pengo, V. and Shapiro, S. S.The use of the dilute Russel viper venom time for the diagnosis of lupus anticoagulants. Blood, 68: 869, 1986.Google Scholar
McGehee, W. G., Patch, M. J. and Lingao, J. U.Detection of the lupus anticoagulant: a comparison of the kaolin clotting time with the tissue thromboplastin inhibition test. Blood, (Suppl) 62: 276a (abstract), 1983.Google Scholar
Rosove, M. H., Ismail, M. and Koziol, B. J.Lupus anticoagulants: improved diagnosis with a kaolin clotting time using rabbit brain phospholipid in standard and high concentrations. Blood, 68: 472, 1986.Google ScholarPubMed
Bick, R. L. Hypercoagulability and thrombosis (Chapter 13). In Disorders of Thrombosis and Hemostasis: Clinical and Laboratory Practice, Chicago, IL; ASCP Press, 1992, p. 261.Google Scholar
Harris, E. N. Immunology of antiphospholipid antibodies. In Lahita, R. (ed.), Systemic Lupus Erythematosus, 2nd edn., London, Churchill Livingstone, 1992, p. 305.Google ScholarPubMed
Rauch, J. and Janoff, A. S.The nature of antiphospholipid antibodies. J. Rheumatology, 19: 1782, 1992.Google ScholarPubMed
Castellarnau, C., Vila, C. L. and Sancho, M. J.Lupus anticoagulant, recurrent abortion, and prostacyclin production by cultured smooth muscle cells. Lancet, 2: 1137, 1983.CrossRefGoogle ScholarPubMed
Sanfelippo, M. J. and Drayna, C. J.Prekallikrein inhibition associated with the lupus anticoagulant: a mechanism for thrombosis. Am. J. Clin. Pathol., 77: 275, 1982.CrossRefGoogle ScholarPubMed
Bick, R. L. and Baker, W. F.Antiphospholipid and thrombosis syndromes. Seminars Thrombosis Hemostasis, 20: 3, 1994.CrossRefGoogle ScholarPubMed
Roubey, R. A. S.Autoantibodies to phospholipid-bonding plasma proteins: a new view of lupus anticoagulants and other “antiphospholipid” antibodies. Blood, 84: 2854, 1994.Google Scholar
Bick, R. L., Laughlin, H. R., Cohen, B., et al. Fetal wastage syndrome due to blood protein/platelet defects: results of prevalence studies and treatment outcome with low-dose heparin and low-dose aspirin. Clin. Applied Thrombosis Hemostasis, 1: 286, 1995.CrossRefGoogle Scholar
Bick, R. L.The antiphospholipid thrombosis (APL-T) syndromes: Characteristics and recommendations for classification and treatment. Am. J. Clin. Pathol., 96: 424, 1991.Google Scholar
Rosove, M. H. and Brewer, P. M. C.Antiphospholipid thrombosis: clinical course after the first thrombotic event in 70 patients. Ann. Internal Med., 117: 303, 1992.CrossRefGoogle ScholarPubMed
Bick, R. L. and Baker, W. F.Deep vein thrombosis: Prevalence of etiologic factors and results of management in 100 consecutive patients. Seminars Thrombosis Hemostasis, 18: 267, 1992.CrossRefGoogle ScholarPubMed
Bick, R. L., Madden, J., Heller, K. B., et al. Recurrent miscarriage: causes, evaluation, and treatment. Medscape Women's Health, 3: 1, 1998.Google ScholarPubMed
Bick, R. L. and Toofanian, A.Recurrent miscarriage syndrome: outcome in 133 patients with thrombotic disorders treatd with heparin and aspirin. J. Clinical Applied Thrombosis Hemostasis, 5 (2005), in press.Google Scholar
Bowie, E. J. W., Thompson, J. H., Pascuzzi, C. A.Thrombosis in systemic lupus erythematosus despite circulating anticoagulant. J. Lab. Clin. Med., 162: 417, 1963.Google Scholar
Bell, W. R., Boss, G. R. and Wolfson, J. S.. Circulating anticoagulant in the procainamide-induced lupus syndrome. Arch. Int. Med., 137: 1471, 1977.CrossRefGoogle ScholarPubMed
Bick, R. L. The antiphospholipid thrombosis syndromes: Lupus anticoagulants & anticardiolipin antibodies (Chapter 14). In Advances in Pathology and Laboratory Medicine, Vol. 8, Mosby, Saint Louis, MO; 8: 391,1995.
Espinoza, L. R., Hartmann, R. C.Significance of the lupus anticoagulant. Am. J. Hematology, 22: 331, 1986.CrossRefGoogle ScholarPubMed
Manoussakis, M. N., Tzioufas, A. G., Silis, M. P.High prevalence of anticardiolipin and other autoantibodies in a healthy elderly population. Clin. Exp. Immunology, 69: 557, 1987.Google Scholar
Zarrabi, M. H., Zucker, S., Miller, F.Immunologic and coagulation disorders in chlorpromazine-treated patients. Ann. Internal Med., 91: 914, 1979.CrossRefGoogle ScholarPubMed
Harris, E. N., Gharavi, A. E., Boey, M. L.Anticardiolipin antibodies: detection by radioimmunoassay and association with thrombosis in systemic lupus erythematosus. Lancet, II: 1211, 1983.CrossRefGoogle Scholar
Weidmann, C. E., Wallace, D., Peter, J.Studies of IgG, IgM and IgA antiphospholipid antibody isotypes in systemic lupus erythematosus. J. Rheumatol., 15: 74, 1988.Google ScholarPubMed
Asherson, R. A., Harris, E. N.Anticardiolipin antibodies: clinical associations. Postgrad. Med. J., 62: 1081, 1986.CrossRefGoogle ScholarPubMed
Hughes, G. V. R., Harris, E. N. and Gharavi, A. E.The anticardiolipin syndrome. J. Rheumatol., 13: 486, 1986.Google ScholarPubMed
Triplett, D. A.Clinical Significance of Antiphospholipid Antibodies. Am. Soc. Clin. Pathol. Press: Hemostasis Thrombosis Check Sample, 10: 1, 1988.Google Scholar
Derue, G., Englert, H., Harris, E.Fetal loss in systemic lupus: association with anticardiolipin antibodies. Brit. J. Obstet. Gynecol., 5: 207, 1985.CrossRefGoogle Scholar
Lubbe, W. F., Palmer, S. J., Butler, W. S.Fetal survival after prednisolone suppression of maternal lupus anticoagulant. Lancet, I: 1361, 1983.CrossRefGoogle Scholar
Harris, E. N., Gharavi, A. E., Hedge, U.Anticardiolipin antibodies in autoimmune thrombocytopenia purpura. Brit. J. Haematol., 59: 231, 1985.CrossRefGoogle Scholar
Harris, E. N., Asherson, R. A.Gharavi, A. E.Thrombocytopenia in SLE and related autoimmune disorders: association with anticardiolipin antibodies. Brit. J. Haematol., 59: 227, 1985.CrossRefGoogle Scholar
Bick, R. L. and Kaplan, H.Syndromes of thrombosis and hypercoagulability: congenital and acquired thrombophilias. Medical Clinics North America, 82: 409, 1998.CrossRefGoogle Scholar
Rosove, M. H., Brewer, P. and Runge, A.Simultaneous lupus anticoagulant and anticardiolipin assays and clinical detection of antiphospholipids. Am. J. Hematol., 32: 148, 1989.CrossRefGoogle ScholarPubMed
Tanne, D. T., Triplett, D. A. and Levine, S. R.Antiphospholipid-protein antibodies and ischemic stroke: not just cardiolipin any more. Stroke, 29: 1755, 1998.CrossRefGoogle ScholarPubMed
Bick, R. L.Discordance in antiphospholipid types in patients with arterial and venous thrombosis. J. Clinical Applied Thrombosis Hemostasis, 2005, in press.Google Scholar
McNeil, H. P., Chesterman, C. N., and Krilis, S. A.Anticardiolipin antibodies and lupus anticoagulants comprise separate antibody subgroups with different phospholipid binding characteriastics. Brit. J. Haematol., 73: 506, 1989.CrossRefGoogle Scholar
Shi, B. S., Chong, B. H. and Chesterman, C. N.Beta-2-Glycoprotein I is a requirement for anticardiolipin antibodies binding to activated platelets: differences with lupus anticoagulants. Blood, 81: 1255, 1993.Google ScholarPubMed
Harris, E. N., Hughes, G. R. V., Gharavi, A. E.Antiphospholipid antibodies: an elderly statesman dons new garments. J. Rheumatol., 14: 208, 1987.Google ScholarPubMed
Gharavi, A. E., Harris, E. N., Asherson, R. A.Anticardiolipin antibodies: isotype distribution and phospholipid specificity. Ann. Rheumatic Dis., 46: 1, 1987.CrossRefGoogle ScholarPubMed
Carreras, L., Defreyn, G. and Manchin, S.Arterial thrombosis, intrauterine death and lupus anticoagulant: detection of immunoglobulin interfering with prostacyclin formation. Lancet, 1: 244, 1981.CrossRefGoogle ScholarPubMed
Cariou, R., Tobelem, G. and Bellucci, S.Effect of lupus anticoagulant on antithrombogenic properties of endothelial cells: inhibition of thrombomodulin-dependent protein C activation. Thromb. Haemostas., 60: 54, 1988.Google ScholarPubMed
Cosgriff, T. M., Martin, B. A.Low functional and high antigenic antithrombin III level in a patient with the lupus anticoagulant. Arthritis Rheum., 24: 94, 1981.CrossRefGoogle Scholar
Khamashta, M. A., Harris, E. N. and Gharavi, A. E.Immune mediated mechanism for thrombosis: antiphospholipid antibody binding to platelet membranes. Ann. Rheum. Dis., 47: 849, 1988.CrossRefGoogle ScholarPubMed
Sanfellipo, M. J., Drayna, C. J.Prekallikrein inhibition associated with the lupus anticoagulant. Am. J. Clin. Pathol., 77: 275, 1982.CrossRefGoogle Scholar
Angeles-Cano, E., Sultan, Y. and Clauvel, J. P.Predisposing factors to thrombosis in systemic lupus erythematosus. Possible relationship to endothelial cell damage. J. Lab. Clin. Med., 94: 312, 1979.Google Scholar
Ruiz-Arguelles, G.The activated protein C resistance phenotype of the antiphospholipid syndrome may follow a relapsing course. Clinical Applied Thrombosis Hemostasis, 4: 277, 1998.CrossRefGoogle Scholar
Ginsburg, K. S., Liang, M. H., Newcomer, L.et al. Anticardiolipin antibodies and the risk for ischemic stroke and venous thrombosis. Ann. Int. Med., 117: 997, 1992.Google ScholarPubMed
Boey, M. L., Colaco, C. B. and Gharavi, A. E.Thrombosis in SLE: striking association with the presence of circulating “lupus anticoagulant”. Br. Med. J., 287: 1021, 1983.CrossRefGoogle Scholar
Elias, M. and Eldor, A.Thromboembolism in patients with the “lupus-like” circulating anticoagulant. Arch. Int. Med., 144: 510, 1984.CrossRefGoogle Scholar
Hall, S., Buettner, H. and Luthra, H. S.Occlusive retinal vascular disease in systemic lupus erythematosus. J. Rheumatol., 11: 96, 1984.Google ScholarPubMed
Asherson, R. A., Harris, E. N. and Gharavi, A. E.Arterial occlusions associated with antibodies to anticardiolipin. Arthritis Rheumatism, 28: s89 (abstr.), 1985.Google Scholar
Hamilton, M. E.Superior mesenteric artery thrombosis associated with antiphospholipid syndrome. Western J. Medicine, 155: 174, 1991.Google ScholarPubMed
Asherson, R. A., Harris, E. N. and Gharavi, A. E.Aortic arch syndrome associated with anticardiolipin antibodies and the lupus anticoagulant. Arthritis Rheumatism, 28: 594, 1985.CrossRefGoogle ScholarPubMed
Asherson, R. A., Morgan, S. H. and Harris, E. N.Arterial occlusion causing large bowel infarction: a reflection of clotting diathesis in SLE. Clin. Rheumatol., 5: 102, 1986.CrossRefGoogle ScholarPubMed
Asherson, R. A., MacKay, I. R. and Harris, E. N.Myocardial infarction in a young male with systemic lupus erythematosus, deep vein thrombosis and antiphospholipid antibodies. Br. Heart J., 56: 190, 1986.CrossRefGoogle Scholar
Gavaghan, T. P., Krilis, S. A. and Daggard, G. E.Anticardiolipin antibodies and occlusion of coronary artery bypass grafts. Lancet, II: 977, 1987.CrossRefGoogle Scholar
Morton, K. T., Gavaghan, S., Krilis, G.Coronary artery bypass graft failure: an autoimmune phenomenon? Lancet, I: 1353, 1986.CrossRefGoogle Scholar
Hamsten, A., Norberg, R. and Bjorkholm, M.Antibodies to cardiolipin in young survivors of myocardial infarction: an association with recurrent cardiovascular events. Lancet, I: 113, 1986.CrossRefGoogle Scholar
Harpaz, D. and Sidi, Y.Successful thrombolytic therapy for acute myocardial infarction in a patient with the antiphospholipid antibody syndrome. American Heart J., 122: 1492, 1991.CrossRefGoogle Scholar
Asherson, R. A., Khamashta, M. A. and Ordi-Ros, J.The “primary” antiphospholipid syndrome: major clinical and serological features. Medicine, 68: 366, 1989.CrossRefGoogle ScholarPubMed
Bick, R. L., Ismail, Y. and Baker, W. F.Coagulation abnormalities in patients with precocious coronary artery thrombosis and patients failing coronary artery bypass grafting and percutaneous transcoronary angioplasty. Seminars Thrombosis Hemostasis, 19: 411, 1993.CrossRefGoogle ScholarPubMed
Galve, E., Ordi, J. and Barquinero, J.Valvular heart disease in the primary antiphospholipid syndrome. Ann. Internal Medicine, 116: 293, 1992.CrossRefGoogle ScholarPubMed
Chartash, E. K., Lans, D. M. and Paget, S. A.Aortic insufficiency and mitral regurgitation in patients wirh systemic lupus erythematosus and the antiphospholipid syndrome. American J. Medicine, 86: 406, 1989.CrossRefGoogle Scholar
Chartash, E. K., Paget, S. A. and Lockshin, M. D.Lupus anticoagulant associated with aortic and mitral valve insufficiency. Arthritis Rheumatism, 29: 95, 1986.Google Scholar
Leung, W. H., Wong, K. L. and Wong, C. K.Association between antiphospholipid antibodies and cardiac abnormalities in patients with systemic lupus erythematosus. American J. Medicine, 89: 411, 1990.CrossRefGoogle ScholarPubMed
Coppock, M. A., Safford, R. E. and Danielson, G. K.Intracardiac thrombosis, phospholipid antibodies, and two-chambered right ventricle. British Heart J., 60: 455, 1988.CrossRefGoogle ScholarPubMed
Reisner, S. A., Blumenfeld, Z. and Brenner, B.Cardiac involvement in patients with primary antiphospholipid syndrome. Circulation(Suppl III), 82: 398, 1990.Google Scholar
Weinstein, C., Miller, M. and Axtens, R.Livido reticularis associated with increased titers of anticardiolipin antibodies in systemic lupus erythematosus. Arch. Dermatol., 123: 596, 1987.CrossRefGoogle Scholar
Eng, A. M.Cutaneous expressions of antiphospholipid syndromes. Seminars Thrombosis Hemostasis, 20: 71, 1994.CrossRefGoogle ScholarPubMed
Englert, H., Hawkes, C. and Boey, M.Dagos' Disease: association with anticardiolipin antibodies and the lupus anticoagulant. Brit. Med. J., 289, 576, 1984.CrossRefGoogle ScholarPubMed
Bird, A. G., Lendrum, R. and Asherson, R. A.Disseminated intravascular coagulation, antiphospholipid antibodies, and ischemic necrosis of extremities. Ann. Rheumatic Diseases, 46: 251, 1987.CrossRefGoogle Scholar
Wolf, P., Peter-Soyer, H. and Auer-Grumbach, P.Widespread cutaneous necrosis in a patient with rheumatoid arthritis associated with anticardiolipin antibodies. Arch. Dermatology, 127: 1739, 1991.CrossRefGoogle Scholar
Ingram, S. B., Goodnight, S. H. and Bennett, R. M.An unusual syndrome of a devastating non-inflammatory vasculopathy associated with anticardiolipin antibodies: report of two cases. Arthritis and Rheumatism, 30: 1167, 1987.CrossRefGoogle Scholar
Levine, S. R., Langer, S. L. and Albers, J. W.Sneddon's syndrome: an antiphospholipid antibody syndrome? Neurology, 38: 798, 1988.CrossRefGoogle ScholarPubMed
Frampton, G., Winer, J. B. and Cameron, J. S.Severe Guillain-Barré syndrome: an association with IgA anti-cardiolipin antibody in a series of 92 patients. J. Neuroimmunology, 19: 133, 1988.CrossRefGoogle Scholar
Levine, S. and Welch, K.The spectrum of neurologic disease associated with anticardiolipin antibodies. Arch. Neurol., 44: 876, 1987.CrossRefGoogle ScholarPubMed
Oppenheimer, S. and Hoffbrand, B.Optic neuritis and myelopathy in systemic lupus erythematosus. Can. J. Neurol. Sci., 13: 129, 1986.CrossRefGoogle ScholarPubMed
Harris, E. N., Gharavi, A. E. and Asherson, R. A.Cerebral infarction in systemic lupus: association with anticardiolipin antibodies. Clin. Exp. Rheumatology, 2: 471, 1984.Google ScholarPubMed
Williams, R. C.Cerebral infarction in systemic lupus: association with anticardiolipin antibodies. Clin. Exp. Rheumatology, 2: 3, 1984.Google ScholarPubMed
Coull, B. M., Bourdette, D. N. and Goodnight, S. H.Multiple cerebral infarctions and dementia associated with anticardiolipin antibodies. Stroke, 18: 1107, 1987.CrossRefGoogle ScholarPubMed
Asherson, R. A., Khamashta, M. A. and Hughes, G. R. V.Sneddon's syndrome. Neurology 39: 1138 (letter), 1989.CrossRefGoogle ScholarPubMed
Moral, A.Sneddon's syndrome with antiphospholipid antibodies and arteriopathy. Stroke, 22: 1327, 1991.CrossRefGoogle ScholarPubMed
Sohngen, D., Wehmeier, A. and Specker, C.Antiphospholipid antibodies in systemic lupus erythematosus and Sneddon's syndrome. Seminars Thrombosis Hemostasis, 20: 55, 1994.CrossRefGoogle ScholarPubMed
Levine, S. R., Brey, R. L. and Joseph, C. L. M.Risk of recurrent thromboembolic events in patients with focal cerebral ischemia and antiphospholipid antibodies. Stroke, 23 (Suppl. I), 29, 1992.Google ScholarPubMed
Levine, S. R., Diaczok, I. M. and Deegan, M. J.Recurrent stroke associated with thymoma and anticardiolipin antibodies. Arch. Neurology, 44: 678, 1987.CrossRefGoogle ScholarPubMed
Brey, R. L., Hart, R. G., Sherman, D. G., et al. Antiphospholipid antibodies and cerebral ischemia in young people. Neurology, 40: 1190, 1990.CrossRefGoogle ScholarPubMed
Toschi, V., Motta, A., Castelli, C., et al. High prevalence of antiphosphatidylinositol antibodies in young patients with cerebral ischemia of undetermined cause. Stroke, 29: 1759, 1998.CrossRefGoogle ScholarPubMed
Nencini, P., Baruffi, M. C., Abbate, R., et al. Lupus anticoagulant and anticardiolipin antibodies in young adults with cerebral ischemia. Stroke, 23: 189, 1992.CrossRefGoogle ScholarPubMed
Carhaupoma, J. R., Mitsias, P. and Levine, S. R.Cerebral venous thrombosis and anticardiolipin antibodies. Stroke, 28: 2363, 1997.CrossRefGoogle Scholar
Bick, R. L. and Hinton, R. C.Prevalence of hereditary and acquired coagulation protein/platelet defects in patients with cerebral ischemia. Blood, 92: (Suppl 1, part 2) 114b (abstr. 3466), 1998.Google Scholar
Levine, S. R., Brey, R. L., Sawaya, K. L., et al. Recurrent stroke and thrombo-occlusive events in the antiphospholipid syndrome. Ann. Neurology, 38: 119, 1995.CrossRefGoogle ScholarPubMed
Brey, R.for the APASS Group. Anticardiolipin antibodies are an independent risk factor for first ischemic stroke. Neurology, 43: 2069, 1993.Google Scholar
Hull, R. G., Harris, N. and Gharavi, A. E.Anticardiolipin antibodies: occurrence in Behcet's syndrome. Ann. Rheumatic Diseases, 43: 746, 1984.CrossRefGoogle ScholarPubMed
Harris, N. E. and Spinnato, J. A.Should anticardiolipin tests be performed in otherwise healthy pregnant women? Am. J. Obstetrics Gynecology, 165: 1272, 1991.CrossRefGoogle ScholarPubMed
Buchanan, N. M., Khamashta, M. A., Morton, K. E., et al. A study of 100 high-risk lupus pregnancies. American J. Reproductive Immunology, 28: 192, 1992.CrossRefGoogle ScholarPubMed
Editorial: Anticardiolipin antibodies – a risk factor for venous and arterial thrombosis. Lancet, I: 912, 1985.
Kwak, J. Y., Gilman-Sachs, A., Beaman, K. D., et al. Reproductive outcome in women with recurrent spontaneous abortions of alloimmune and autoimmune causes: preconception versus postconception treatment. American J. Obstetrics Gynecology, 166: 1787, 1992.CrossRefGoogle ScholarPubMed
Bick, R. L.Recurrent miscarriage syndrome and infertility caused by blood coagulation protein or platelet defects. Hematology Oncology Clinics North America, 14: 1117, 2000; Chin. J. Obstet. Gynecol., 28: 674, 1993.CrossRefGoogle ScholarPubMed
Parazzini, F., Acaia, B. and Faden, D.Antiphospholipid antibodies and recurrent abortion. Obstet. Gynecol., 77: 854, 1991.Google ScholarPubMed
Grandone, E., Margaglione, M. and Vecchione, G.Antiphospholipid antibodies and risk of fetal loss: a pilot report of a cross-sectional study. Thrombosis Haemostasis, 69: 597 (abstract), 1993.Google Scholar
Birdsall, M., Pattison, N. and Chamley, L.Antiphospholipid antibodies in pregnancy. Aust. N. Z. J. Obstet. Gynaecol., 32: 328, 1992.CrossRefGoogle ScholarPubMed
Maclean, M. A., Cumming, G. P. and McCall, F.The prevalence of lupus anticoagulant and anticardiolipin antibodies in women with a history of first trimester miscarriages. Brit. J. Obstet. Gynaecol., 101: 103, 1994.CrossRefGoogle ScholarPubMed
Howard, M. A., Firkin, B. G. and Healy, D. L.Lupus anticoagulant in a woman with multiple spontaneous miscarriage. Am. J. Hematology, 26: 175, 1987.CrossRefGoogle Scholar
Taylor, M., Cauchi, M. N. and Buchanan, R. R. C.The lupus anticoagulant, anticardiolipin antibodies, and recurrent miscarriage. Am. J. Reproductive Immunol., 23: 33, 1990.CrossRefGoogle ScholarPubMed
Parke, A. L., Wilson, D. and Maier, D.The prevalence of antiphospholipid antibodies in women with recurrent spontaneous abortion, women with successful pregnancies, and women who have never been pregnant. Arthritis Rheumatism, 34: 1231, 1991.CrossRefGoogle ScholarPubMed
Kochenour, N. K., Branch, D. W. and Rote, N. S.A new postpartum syndrome associated with antiphospholipid antibodies. Obstet. Gynecol., 69: 460, 1987.Google ScholarPubMed
Intrator, L., Oksenhendler, E. and Desforges, L.Anticardiolipin antibodies in HIV infected patients with or without immune thrombocytopenic purpura. Brit. J. Haematol., 67: 269, 1988.CrossRefGoogle Scholar
Canoso, R. T., Zon, L. I. and Groopman, J. E.Anticardiolipin antibodies associated with HTLV-III infection. Brit. J. Haematology, 65: 495, 1987.CrossRefGoogle ScholarPubMed
Panzer, S., Stain, C. and Hartl, H.Anticardiolipin antibodies are elevated in HIV-1 infected haemophiliacs but do not predict for disease progression. Thrombosis Haemostasis, 61: 81, 1989.Google Scholar
Stimmler, M. M., Quismorio, F. P. and McGehee, W. G.Anticardiolipin antibodies in acquired immunodeficiency syndrome. Arch. Int. Medicine, 149: 1833, 1989.CrossRefGoogle ScholarPubMed
Vaarala, O., Palosuo, T. and Kleemola, M.Anticardiolipin response in acute infections. Clin. Immunology and Immunopathology, 41: 8, 1986.CrossRefGoogle ScholarPubMed
Violi, F., Ferro, D. and Quintarelli, C.Dilute aPTT prolongation by antiphospholipid antibodies in patients with liver cirrhosis. Thrombosis Haemostasis, 63: 183, 1990.Google ScholarPubMed
Harrison, R. L., Alperin, J. B. and Kumar, D.Concurrent lupus anticoagulants and prothrombin deficiency due to phenytoin use. Arch. Pathology Laboratory Medicine, 111: 719, 1987.Google ScholarPubMed
Lillicrap, D. P., Pinto, M. and Benford, K.Heterogeneity of laboratory test results for antiphospholipid antibodies in patients treated with chlorpromazine and other phenothiazines. Am. J. Clin. Pathology, 93: 771, 1990.CrossRefGoogle ScholarPubMed
Walenga, J. M. and Bick, R. L.Heparin-induced thrombocytopenia, paradoxical thromboembolism and other side effects of heparin therapy. Cardiology Clinics: Annual of Drug Therapy, 2: 123, 1998.Google Scholar
Girolami, B., Prandoni, P., Rossi, L., et al. Transaminase elevation in patients treated with unfractionated heparin or low molecular weight heparin for venous thromboembolism. Clinical Applied Thrombosis Hemostasis, 4: 126, 1998.CrossRefGoogle Scholar
Schved, J. F., Dupuy-Fons, C. and Biron, C.A prospective epidemiological study on the occurrence of antiphospholipid antibody: the Montpellier Antiphospholipid (MAP) Study. Haemostasis, 24: 175, 1994.Google ScholarPubMed
Vila, P., Hernandez, M. C. and Lopez-Fernandez, M. F.Prevalence, follow-up and clinical significance of the anticardiolipin antibodies in normal subjects. Thrombosis Haemostasis, 72: 209, 1994.Google ScholarPubMed
Bick, R. L. and Ancypa, D.The antiphospholipid and thrombosis syndromes: clinical and laboratory correlates. Clinics Laboratory Medicine, 15: 63, 1995.Google ScholarPubMed
Falcon, C. R., Hoffer, A. M., Forastiero, R. R., et al. Clinical significance of various ELISA assays for detecting antiphospholipid antibodies. Thrombosis Haemostasis, 64: 21, 1990.Google ScholarPubMed
Loizou, S., McCrea, J. D., Rudge, A. C., et al. Measurement of anti-cardiolipin antibodies by an enzyme-linked immunosorbent assay (ELISA): standardization and quantitation of results. Clin. Exp. Immunology, 62: 738, 1985.Google Scholar
Reyes, H., Dearing, L., Bick, R. L., et al. Laboratory diagnosis of antiphospholipid syndromes. Clinics Laboratory Medicine, 15: 85, 1995.Google ScholarPubMed
Triplett, D. A. Laboratory evaluation of circulating anticoagulants. (Chapter 98) In Hematology: Clinical and Laboratory Practice, ed. Bick, R. L., Bennett, R. M., Brynes, R. K., et al. St. Louis, MO, C. V. Mosby Publisher, 1993, pp. 1539–48.Google Scholar
Mannucci, P. M., Canciani, M. T., Mari, D., et al. The varied sensitivity of partial thromboplastin and prothrombin time reagents in the demonstration of the lupus-like inhibitor. Scand. J. Haematology, 22: 423, 1979.CrossRefGoogle Scholar
Bick, R. L., Pascoe, H. R. and Laughlin, W. R.Efficacy of four common activated partial thromboplastin times in screening for the lupus anticoagulant. Blood, 84: 82 (abstract), 1994.Google Scholar
Saxena, R., Saraya, A. K., Kotte, V. K., et al. Evaluation of four coagulation tests to detect plasma lupus anticoagulants. Am. J. Clinical Pathology, 96: 755, 1991.CrossRefGoogle ScholarPubMed
Exner, T., Triplett, D. A., Taberner, D., et al. Guidelines for testing and revised criteria for lupus anticoagulants. Thrombosis Haemostasis, 65: 320, 1991.Google ScholarPubMed
Bell, H. G. and Alton, H. G.A brain extract as a substitute for platelet suspensions in the thromboplastin generation test. Nature, 174: 880, 1954.CrossRefGoogle ScholarPubMed
Rauch, J., Tannenbaum, M. and Janoff, A. S.Distinguishing plasma lupus anticoagulants from anti-factor antibodies using hexagonal (II) phase phospholipids. Thrombosis Haemostasis, 62: 892, 1989.Google ScholarPubMed
Cabral, A. R., Amigo, M. C., Cabiedes, J., et al. The antiphospholipid/cofactor syndromes: a primary variant with antibodies to beta-2-glycoprotein-1 but no antibodies detectable in standard antiphospholipid assays. American J. Medicine, 101: 472, 1996.CrossRefGoogle ScholarPubMed
Falcon, C. R., Hoffer, A. M. and Carreras, L. O.Antiphosphatidylinositol antibodies as markers of the antiphospholipid syndrome. Thrombosis Haemostasis, 63: 321, 1990.Google ScholarPubMed
Falcon, C. R., Hoffer, A. M. and Carreras, L. O.Evaluation of the clinical and laboratory associations of antiphosphatidylethanolamine antibodies. Thrombosis Research, 59: 383, 1990.CrossRefGoogle ScholarPubMed
Sorice, M., Circella, A., Garofalo, G. T., et al. Anticardiolipin and anti-beta-2-GPI are two distinct populations of antibodies. Thrombosis Haemostasis, 75: 303, 1996.Google Scholar
Martinuzzo, M. E., Forastiero, R. R. and Carreras, L. O.Anti-beta-2-glycoprotein I antibodies: detection and association with thrombosis. Br. J. Haematology, 89: 397, 1995.CrossRefGoogle ScholarPubMed
Staub, H. L., Harris, E. N., Khamashta, M. A., et al. Antibody to phosphatidylethanolamine in a patient with lupus anticoagulant and thrombosis. Ann. Rheumatic Diseases, 48: 166, 1989.CrossRefGoogle Scholar

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  • Hereditary and acquired thrombophilia in pregnancy
    • By Rodger L. Bick, M.D., Ph.D., F.A.C.P., Professor of Medicine and Pathology, University of Texas Southwestern Medical Center; Director: Dallas Thrombosis Clinical Center, Dallas, Texas; Director: Pacific Thrombosis Clinical Center, Southern California, USA, William F. Baker, Jr., M.D., F.A.C.P., Associate Clinical Professor of Medicine, Center for Health Sciences, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, CA, USA, Thrombosis, Hemostasis, and Special Hematology Clinic, Kern Medical Center, Bakersfield; California Clinical Thrombosis Center, Bakersfield, California, USA
  • Edited by Rodger L. Bick, University of Texas Southwestern Medical Center, Dallas, Eugene P. Frenkel, University of Texas Southwestern Medical Center, Dallas, William F. Baker, University of California, Los Angeles, Ravi Sarode, University of Texas Southwestern Medical Center, Dallas
  • Book: Hematological Complications in Obstetrics, Pregnancy, and Gynecology
  • Online publication: 01 February 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511526978.006
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  • Hereditary and acquired thrombophilia in pregnancy
    • By Rodger L. Bick, M.D., Ph.D., F.A.C.P., Professor of Medicine and Pathology, University of Texas Southwestern Medical Center; Director: Dallas Thrombosis Clinical Center, Dallas, Texas; Director: Pacific Thrombosis Clinical Center, Southern California, USA, William F. Baker, Jr., M.D., F.A.C.P., Associate Clinical Professor of Medicine, Center for Health Sciences, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, CA, USA, Thrombosis, Hemostasis, and Special Hematology Clinic, Kern Medical Center, Bakersfield; California Clinical Thrombosis Center, Bakersfield, California, USA
  • Edited by Rodger L. Bick, University of Texas Southwestern Medical Center, Dallas, Eugene P. Frenkel, University of Texas Southwestern Medical Center, Dallas, William F. Baker, University of California, Los Angeles, Ravi Sarode, University of Texas Southwestern Medical Center, Dallas
  • Book: Hematological Complications in Obstetrics, Pregnancy, and Gynecology
  • Online publication: 01 February 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511526978.006
Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

  • Hereditary and acquired thrombophilia in pregnancy
    • By Rodger L. Bick, M.D., Ph.D., F.A.C.P., Professor of Medicine and Pathology, University of Texas Southwestern Medical Center; Director: Dallas Thrombosis Clinical Center, Dallas, Texas; Director: Pacific Thrombosis Clinical Center, Southern California, USA, William F. Baker, Jr., M.D., F.A.C.P., Associate Clinical Professor of Medicine, Center for Health Sciences, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, CA, USA, Thrombosis, Hemostasis, and Special Hematology Clinic, Kern Medical Center, Bakersfield; California Clinical Thrombosis Center, Bakersfield, California, USA
  • Edited by Rodger L. Bick, University of Texas Southwestern Medical Center, Dallas, Eugene P. Frenkel, University of Texas Southwestern Medical Center, Dallas, William F. Baker, University of California, Los Angeles, Ravi Sarode, University of Texas Southwestern Medical Center, Dallas
  • Book: Hematological Complications in Obstetrics, Pregnancy, and Gynecology
  • Online publication: 01 February 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511526978.006
Available formats
×