The plasminogen activator inhibitor-1 gene, hypofibrinolysis, and osteonecrosis

Clinical Orthopaedics and Related Research

Volumn 366, Issue , 1999, Pages 133-146

  Glueck, Charles J ^a,b   Fontaine, Robert N ^a   Gruppo, Ralph ^a   Stroop, Davis ^a   Sieve Smith, Luann ^a   Tracy, Trent ^a   Wang, Ping ^a  

^a UNIVERSITY OF CINCINNATI COLLEGE OF MEDICINE   (United States)

^b JEWISH HOSPITAL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

5,10 METHYLENETETRAHYDROFOLATE REDUCTASE (FADH2); ACTIVATED PROTEIN C; BLOOD CLOTTING FACTOR 5; CARDIOLIPIN ANTIBODY; DNA; GENE PRODUCT; HOMOCYSTEINE; LIPOPROTEIN A; LUPUS ANTICOAGULANT; PLASMINOGEN ACTIVATOR INHIBITOR 1; PROTEIN C; PROTEIN S; PROTHROMBIN; TISSUE PLASMINOGEN ACTIVATOR;

ADULT; AGED; ARTICLE; BLOOD CLOTTING TEST; BONE NECROSIS; CONTROLLED STUDY; FEMALE; FIBRINOLYSIS; GENE; GENETIC POLYMORPHISM; HUMAN; MAJOR CLINICAL STUDY; MALE; MUTATION; POLYMERASE CHAIN REACTION; PRIORITY JOURNAL; THROMBOPHILIA;

EID: 0032820732     PISSN: 0009921X     EISSN: 15281132     Source Type: Journal    
DOI: 10.1097/00003086-199909000-00017     Document Type: Article

References (42)

1. Balasa VV, Gruppo RA, Glueck CJ, et al: The relationships of mutations in the methylenetetrahydrofolate reductase, prothrombin, and plasminogen activator inhibitor-1 gene to plasma levels of homocysteine, prothrombin, and plasminogen activator inhibitor-1 in children and adults. Thromb Haemost In Press. 1999. 81:739-744, 1999.
2. Brandt G, Gruppo R, Glueck CJ, et al: Sensitivity, specificity, and predictive value of modified assays for activated protein C resistance in children. Thromb Haemost 79:567-570, 1998.
3. Eriksson P, Kallin B, van't Hooft FM, Bavenholm P, Hamsten A: Allele-specific increase in basal transcription of the plasminogen-activator inhibitor 1 gene is associated with myocardial infarction. Proc Natl Acad Sci USA 92:1851-1855, 1995.
4. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group: ECAT angina pectoris study: Baseline associations of haemostatic factors with extent of coronary arteriosclerosis and other coronary risk factors in 3000 patients with angina pectoris undergoing coronary angiography. Eur Heart J 14:8-17, 1993.
5. Frosst P, Blom HJ, Milos R, et al: A candidate genetic risk factor for vascular disease: A common mutation in methylenetetrahydrofolate reductase. Nature Genetics 10:111-113, 1995.
6. Glueck CJ, Bell H, Vadlamani L, Gupta A, et al: Heritable thrombophilia and hypofibrinolysis. Arch Ophthalmol 117:43-49, 1999.
7. Glueck CJ, Brandt G, Gruppo R, et al: Resistance to activated protein C and Legg-Perthes disease. Clin Orthop 338:139-152, 1997.
8. Glueck CJ, Crawford A, Roy D, et al: Association of antithrombotic factor deficiencies and hypofibrinolysis with Legg-Perthes disease. J Bone Joint Surg 78A:3-13, 1996.
9. Glueck CJ, Fontaine RN, Gupta A, Alasmi M: Myocardial infarction in a 35 year old man with homocysteinemia, high plasminogen activator inhibitor activity, and resistance to activated protein C. Metabolism 46:1470-1472, 1997.
10. Glueck CJ, Freiberg R, Crawford A, et al: Second-hand smoke, hypofibrinolysis, and childhood osteonecrosis of the hip, Legg-Perthes disease. Clin Orthop 352:159-167, 1998.
11. Glueck CJ, Freiberg R, Glueck HI, et al: Hypofibrinolysis: A common, major cause of osteonecrosis. Am J Hematol 45:156-166, 1994.
12. Glueck CJ, Freiberg R, Glueck HI, et al: Idiopathic osteonecrosis, hypofibrinolysis, high plasminogen activator inhibitor, high lipoprotein(a), and therapy with Stanozolol. Am J Hematol 48:213-220, 1995.
13. Glueck CJ, Freiberg, R, Gruppo R, et al: Thrombophilia and Hypofibrinolysis: Reversible Pathogenetic Etiologies of Osteonecrosis in Adults and in Children (Legg-Perthes Disease). AOA International Symposium on Osteonecrosis. In Urbaniak JR, Jones Jr JP (eds). Osteonecrosis: Etiology, Diagnosis, and Treatment. Rosemont, IL, American Academy of Orthopaedic Surgeons 105-110, 1997.
14. Glueck CJ, Freiberg RA, Gruppo R, et al: Amelioration of osteonecrosis by treatment of thrombophilia and hypofibrinolysis. J Invest Med 46:227A, 1998. Abstract.
15. Glueck CJ, Freiberg R, Tracy T, Stroop D, Wang P: Thrombophilia and hypofibrinolysis: Pathoetiologies of osteonecrosis. Clin Orthop 334:43-56, 1997.
16. Glueck CJ, Glueck HI, Mieczkowski L, et al: Familial high plasminogen activator inhibitor with hypofibrinolysis, a new pathophysiologic cause of osteonecrosis? Thromb Haemost 69:460-465, 1993.
17. Glueck CJ, Glueck HI, Tracy T, et al: Relationships between lipoprotein (a), lipids, apolipoproteins, basal and stimulated fibrinolytic regulators, and D-dimer. Metabolism 42:236-246, 1993.
18. Glueck CJ, Glueck HI, Welch M, et al: Familial idiopathic osteonecrosis mediated by familial hypofibrinolysis with high levels of plasminogen activator inhibitor. Thromb Haemost 71:195-198, 1994.
19. Glueck CJ, McMahon RE, Bouquot J, et al: Thrombophilia, hypofibrinolysis, and alveolar osteonecrosis of the jaw. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 81:557-560, 1996.
20. Glueck CJ, McMahon RE, Bouquot J, et al: Heterozygosity for the Leiden mutation of the factor V gene, a common pathoetiology for osteonecrosis of the jaw, with thrombophilia augmented by exogenous estrogens. J Lab Clin Med 130:540-543, 1997.
21. Glueck CJ, McMahon RE, Bouquot JE, et al: A preliminary pilot study of treatment of thrombophilia and hypofibrinolysis and amelioration of the pain of osteonecrosis of the jaws. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 85:64-73, 1998.
22. Glueck CJ, Rorick MH, Schmerler M, et al: Hypofibrinolytic and atherogenic risk factors for stroke. J Lab Clin Med 125:319-325, 1995.
23. Glueck CJ, Shaw P, Lang JE, et al: Evidence that homocysteine is an independent risk factor for atherosclerosis in hyperlipidemic patients. Am J Cardiol 75:132-136, 1995.
24. Gruppo R, Glueck CJ, McMahon RE, et al: The pathophysiology of alveolar osteonecrosis of the jaw: Anticardiolipin antibodies, thrombophilia, and hypofibrinolysis. Pathophysiology of osteonecrosis of the jaw. J Lab Clin Med 127:481-489, 1996.
25. Hamsten A, de Faire U, Walldius G, et al: Plasminogen activator inhibitor in plasma: Risk factor for recurrent myocardial infarction. Lancet 2:3-9, 1987.
26. Henry M, Tregouet DA, Alessi MC, et al: Metabolic determinants are much more important than genetic polymorphisms in determining the PAI-1 activity and antigen plasma concentrations: A family study with part of the Stanislas Cohort. Arterioscler Thromb Vasc Biol 18:84-91, 1998.
27. Jones Jr JP: Risk Factors Potentially Activating Intravascular Coagulation and Causing Nontraumatic Osteonecrosis. In Urbaniak JR, Jones Jr JP (eds). Osteonecrosis: Etiology, Diagnosis, and Treatment, Rosemont IL, American Academy of Orthopaedic Surgeons 89-97, 1997.
28. Korompilias AV, Gilkeson GS, Ortel TL, Seaber AV, Urbaniak JR: Anticardiolipin antibodies and osteonecrosis of the femoral head. Clin Orthop 345:174-180, 1997.
29. Korompilas AV, Ortel TL, Gilkeson GS, et al: Hypercoagulability and Osteonecrosis. In Urbaniak JR, Jones Jr JP (eds). Osteonecrosis: Etiology, Diagnosis, and Treatment. Rosemont IL, American Academy of Orthopaedic Surgeons 111-117, 1997.
30. Lang IM, Moster KM, Schleef RR: Elevated expression of urokinase-like plasminogen activator and plasminogen activator inhibitor type 1 during the vascular remodeling associated with pulmonary thromboembolism. Arterioscler Thromb Vasc Biol 18:808-815, 1998.
31. Loskutoff DJ, Swadey M, Keeton M, Schneidermann J: Regulation of PAI-1 gene expression in vivo. Thromb Haemost 70:135-137, 1993.
32. Miller SA, Dykes DD, Polesky HF: A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Res 16:1215-1217, 1988.
33. Nagasawa K, Ishii Y, Mayumi T, et al: Avascular necrosis of bone in systemic lupus erythematosus: Possible role of haemostatic abnormalities. Ann Rheum Dis 48:672-676, 1989.
34. Nilsson IM, Krook H, Sternby NH, Soderberg E, Soderstrom N: Severe thrombotic disease in a young man with bone marrow and skeletal changes and with a high content of an inhibitor in the fibrinolytic system. Acta Med Scand 169:323-337, 1961.
35. Ossei-Gerning N, Mansfield MW, Stickland MH, Wilson IJ, Grant PJ: Plasminogen activator inhibitor-1 promotor 4G/5G genotype and plasma levels in relation to a history of myocardial infarction in patients characterized by coronary angiography. Arterioscler Thromb Vasc Biol 17:33-37, 1997.
36. Pierre-Jacques H, Glueck CJ, Mont MA, Hungerford DS: Familial heterozygous protein S deficiency in a patient who had multifocal osteonecrosis. J Bone Joint Surg 79A:1079-1084, 1997.
37. Poort SR, Rosendaal FR, Reitsma PH, Bertina RM: 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 88:3698-3703, 1996.
38. Snedecor GW, Cochran WG: Statistical Methods. Ed 7. Ames, IA, Iowa State University Press 1980.
39. Sprengers ED, Kluft C: Plasminogen activator inhibitors. Blood 69:381-387, 1987.
40. Van Meijer M, Pannekoek H: Structure of plasminogen activator inhibitor 1 (PAI-1) and its function in fibrinolysis: An update. Fibrinolysis 9:263-276, 1995.
41. Van Veldhuizen PJ, Neff J, Murphey MD, Bodensteiner D, Skikne BS: Decreased fibrinolytic potential in patients with idiopathic avascular necrosis and transient osteoporosis of the hip. Am J Hematol 44:243-248, 1993.
42. Velazquez E, Mendoza SG, Wang P, Glueck CJ: Metformin therapy is associated with a decrease in plasma plasminogen activator inhibitor-1, lipoprotein (a), and immunoreactive insulin levels in patients with the polycystic ovary syndrome. Metabolism 46:454-457, 1997.