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  5.     <title>UTas ePrints - Polymorphisms of the tissue factor pathway inhibitor gene are associated with venous thromboembolism in the antiphospholipid syndrome and carriers of factor V Leiden</title>
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  13.     <meta content="Lincz, L.F." name="eprints.creators_name" />
  14. <meta content="Adams, M.J." name="eprints.creators_name" />
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  23. <meta content="Polymorphisms of the tissue factor pathway inhibitor gene
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  29. <meta content="antiphospholipid syndrome, factor V Leiden, tissue factor
  30. pathway inhibitor, venous thrombosis" name="eprints.keywords" />
  31. <meta content="The definitive version is available online at www.bloodcoagulation.com/" name="eprints.note" />
  32. <meta content="Polymorphisms within the tissue factor pathway inhibitor (TFPI) gene may determine TFPI expression and increase the risk of venous thromboembolism (VTE) in predisposed individuals. We tested this hypothesis by comparing TFPI activity and the frequency of common TFPI polymorphisms, -33T->C, -399C->T and -287T->C, in patients with antiphospholipid syndrome (APS) (n = 24) or factor V Leiden (n = 44) who had a history of VTE (n = 26), compared with those without VTE (n = 42) and also with normal control individuals (n = 56). TFPI activity was measured using a modified amidolytic assay and genotypes were determined by polymerase chain reaction and restriction fragment length polymorphism. We found that only APS patients with a history of venous thrombosis had TFPI activity levels significantly different from control individuals (1.77 +/- 0.60 vs 0.77 +/- 0.19 U/ml; P = 0.0001), and this was associated with inheritance of the TFPI -33C allele (1.70 +/- 0.72 U/ml for TC/CC genotypes vs 0.97 +/- 0.56 U/ml for TT; P = 0.01). Multivariate analysis of APS and factor V Leiden patients revealed that the greatest independent contributor to VTE was TFPI activity (adjusted odds ratio = 16.84; 95% confidence interval = 2.47-114.36, P = 0.004), while inheritance of either the TFPI -33C or -399T alleles each increased the odds of VTE by nearly 13 times (95% confidence interval = 2.39-69.91, P = 0.003; and 95% confidence interval = 2.25-71.23, P = 0.004, respectively). These results indicate that the TFPI -33T->C and -399C->T polymorphisms are significantly associated with venous thrombosis in the presence of other risk factors, especially APS, and may be clinically relevant in patients who are prone to hypercoagulability." name="eprints.abstract" />
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  44. <meta content="1 Wun TC, Kretzmer KK, Girard TJ, Miletich JP, Broze GJ Jr. Cloning and
  45. characterization of a cDNA coding for the lipoprotein-associated
  46. coagulation inhibitor shows that it consists of three tandem Kunitz-type
  47. inhibitory domains. J Biol Chem 1988; 263:6001-6004.
  48. 2 Broze GJ Jr. Tissue factor pathway inhibitor and the current concept
  49. of blood coagulation. Blood Coagul Fibrinolysis 1995; 6 (Suppl 1):
  50. S7-S13.
  51. 3 Iversen N, Lindahl AK, Abildgaard U. Elevated TFPI in malignant disease:
  52. relation to cancer type and hypercoagulation. Br J Haematol 1998;
  53. 102:889-895.
  54. 4 He M, Wen Z, He X, Xiong S, Liu F, Xu J, et al. Observation on tissue factor
  55. pathway and some other coagulation parameters during the onset of acute
  56. cerebrocardiac thrombotic diseases. Thromb Res 2002; 107:223-228.
  57. 5 Amini-Nekoo A, Futers TS, Moia M, Mannucci PM, Grant PJ, Ariens RA.
  58. Analysis of the tissue factor pathway inhibitor gene and antigen levels in
  59. relation to venous thrombosis. Br J Haematol 2001; 113:537-543.
  60. 6 Adams MJ, Donohoe S, Mackie IJ, Machin SJ. Antitissue factor pathway
  61. inhibitor activity in patients with primary antiphospholipid syndrome. Br J
  62. Haematol 2001; 114:375-379.
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  64. and involvement in disease. J Pathol 2006; 208:327-339.
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  66. on chromosome 2 influences levels of tissue factor pathway inhibitor:
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  68. 25:1489-1492.
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  70. TFPI V264M mutation and venous thromboembolic disease. Thromb
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  89. and the risk for venous thromboembolism in the adult Danish population.
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  92. Tissue factor pathway inhibitor and the risk of recurrent venous
  93. thromboembolism. Thromb Haemost 2005; 94:787-790.
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  97. 18 Moatti D, Haidar B, Fumeron F, Gauci L, Boudvillain O, Seknadji P, et al.
  98. A new T-287C polymorphism in the 50 regulatory region of the tissue factor
  99. pathway inhibitor gene. Association study of the T-287C and C-399T
  100. polymorphisms with coronary artery disease and plasma TFPI levels.
  101. Thromb Haemost 2000; 84:244-249.
  102. 19 Moatti D, Seknadji P, Galand C, Poirier O, Fumeron F, Desprez S, et al.
  103. Polymorphisms of the tissue factor pathway inhibitor (TFPI) gene in patients
  104. with acute coronary syndromes and in healthy subjects: impact of the
  105. V264M substitution on plasma levels of TFPI. Arterioscler Thromb Vasc
  106. Biol 1999; 19:862-869.
  107. 20 Sandset PM, Larsen ML, Abildgaard U, Lindahl AK, Odegaard OR.
  108. Chromogenic substrate assay of extrinsic pathway inhibitor (EPI): levels in
  109. the normal population and relation to cholesterol. Blood Coagul
  110. Fibrinolysis 1991; 2:425-433.
  111. 21 Ameziane N, Seguin C, Borgel D, Fumeron F, Moatti D, Alhenc-Gelas M,
  112. et al. The -33T->C polymorphism in intron 7 of the TFPI gene influences
  113. the risk of venous thromboembolism, independently of the factor V Leiden
  114. and prothrombin mutations. Thromb Haemost 2002; 88:195-199.
  115. 22 Miyata T, Sakata T, Kumeda K, Uchida K, Tsushima M, Fujimura H, et al.
  116. C-399T polymorphism in the promoter region of human tissue factor
  117. pathway inhibitor (TFPI) gene does not change the plasma TFPI antigen
  118. level and does not cause venous thrombosis. Thromb Haemost 1998;
  119. 80:345-346.
  120. 23 Moatti D, Meirhaeghe A, Ollivier V, Bauters C, Amouyel P, de Prost D.
  121. Polymorphisms of the tissue factor pathway inhibitor gene and the risk of
  122. restenosis after coronary angioplasty. Blood Coagul Fibrinolysis 2001;
  123. 12:317-323.
  124. 24 Akarsu M, Demirkan F, Ozsan GH, Onen F, Yuksel F, Ozkan S, et al.
  125. Increased levels of tissue factor pathway inhibitor may reflect disease
  126. activity and play a role in thrombotic tendency in Behcet's disease. Am J
  127. Hematol 2001; 68:225-230.
  128. 25 Amengual O, Atsumi T, Khamashta MA, Hughes GR. The role of the tissue
  129. factor pathway in the hypercoagulable state in patients with the
  130. antiphospholipid syndrome. Thromb Haemost 1998; 79:276-281.
  131. 26 Wakita Y, Wada H, Nakase T, Nakasaki T, Shimura M, Hiyoyama K, et al.
  132. Aberrations of the tissue factor pathway in patients positive for lupus
  133. anticoagulant. Clin Appl Thromb Hemost 1999; 5:10-15.
  134. 27 Kiraz S, Ertenli I, Benekli M, Haznedaroglu IC, Calguneri M, Celik I, et al.
  135. Clinical significance of hemostatic markers and thrombomodulin in
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  138. 28 Adams M, Breckler L, Stevens P, Thom J, Baker R, Oostryck R. Antitissue
  139. factor pathway inhibitor activity in subjects with antiphospholipid syndrome
  140. is associated with increased thrombin generation. Haematologica 2004;
  141. 89:985-990.
  142. 29 Eitzman DT, Westrick RJ, Bi X, Manning SL, Wilkinson JE, Broze GJ, et al.
  143. Lethal perinatal thrombosis in mice resulting from the interaction of tissue
  144. factor pathway inhibitor deficiency and factor V Leiden. Circulation 2002;
  145. 105:2139-2142.
  146. 30 van 't Veer C, Kalafatis M, Bertina RM, Simioni P, Mann KG. Increased
  147. tissue factor-initiated prothrombin activation as a result of the Arg506 ->
  148. Gln mutation in factor VLEIDEN. J Biol Chem 1997; 272:20721-20729.
  149. 31 Hubbard AR, Weller LJ, Gray E. Measurement of tissue factor pathway
  150. inhibitor in normal and postheparin plasma. Blood Coagul Fibrinolysis
  151. 1994; 5:819-823.
  152. 32 Jeske W, Hoppensteadt D, Fareed J, Bermes E. Measurement of functional
  153. and immunologic levels of tissue factor pathway inhibitor. Some
  154. methodologic considerations. Blood Coagul Fibrinolysis 1995; 6 (Suppl 1):
  155. S73-S80.
  156. 33 Adams MJ, Oostryck R. A comparative study of functional assays for tissue
  157. factor pathway inhibitor using normal plasma and clinical samples. Blood
  158. Coagul Fibrinolysis 2000; 11:327-333.
  159. 34 Bognacki J, Hammelburger J. Functional and immunologic methods for the
  160. measurement of human tissue factor pathway inhibitor. Blood Coagul
  161. Fibrinolysis 1995; 6 (Suppl 1):S65-S72.
  162. 35 Bajaj MS, Birktoft JJ, Steer SA, Bajaj SP. Structure and biology of tissue
  163. factor pathway inhibitor. Thromb Haemost 2001; 86:959-972." name="eprints.referencetext" />
  164. <meta content="Lincz, L.F. and Adams, M.J. and Scorgie, F.E. and Thom, J. and Baker, Ross I. and Seldon, M. (2007) Polymorphisms of the tissue factor pathway inhibitor gene are associated with venous thromboembolism in the antiphospholipid syndrome and carriers of factor V Leiden. Blood Coagulation and Fibrinolysis, 18 (6). pp. 559-564. ISSN 0957-5235" name="eprints.citation" />
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  177. <meta content="Polymorphisms within the tissue factor pathway inhibitor (TFPI) gene may determine TFPI expression and increase the risk of venous thromboembolism (VTE) in predisposed individuals. We tested this hypothesis by comparing TFPI activity and the frequency of common TFPI polymorphisms, -33T->C, -399C->T and -287T->C, in patients with antiphospholipid syndrome (APS) (n = 24) or factor V Leiden (n = 44) who had a history of VTE (n = 26), compared with those without VTE (n = 42) and also with normal control individuals (n = 56). TFPI activity was measured using a modified amidolytic assay and genotypes were determined by polymerase chain reaction and restriction fragment length polymorphism. We found that only APS patients with a history of venous thrombosis had TFPI activity levels significantly different from control individuals (1.77 +/- 0.60 vs 0.77 +/- 0.19 U/ml; P = 0.0001), and this was associated with inheritance of the TFPI -33C allele (1.70 +/- 0.72 U/ml for TC/CC genotypes vs 0.97 +/- 0.56 U/ml for TT; P = 0.01). Multivariate analysis of APS and factor V Leiden patients revealed that the greatest independent contributor to VTE was TFPI activity (adjusted odds ratio = 16.84; 95% confidence interval = 2.47-114.36, P = 0.004), while inheritance of either the TFPI -33C or -399T alleles each increased the odds of VTE by nearly 13 times (95% confidence interval = 2.39-69.91, P = 0.003; and 95% confidence interval = 2.25-71.23, P = 0.004, respectively). These results indicate that the TFPI -33T->C and -399C->T polymorphisms are significantly associated with venous thrombosis in the presence of other risk factors, especially APS, and may be clinically relevant in patients who are prone to hypercoagulability." name="DC.description" />
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  291.     <h1 class="ep_tm_pagetitle">Polymorphisms of the tissue factor pathway inhibitor gene are associated with venous thromboembolism in the antiphospholipid syndrome and carriers of factor V Leiden</h1>
  292.     <p style="margin-bottom: 1em" class="not_ep_block"><span class="person_name">Lincz, L.F.</span> and <span class="person_name">Adams, M.J.</span> and <span class="person_name">Scorgie, F.E.</span> and <span class="person_name">Thom, J.</span> and <span class="person_name">Baker, Ross I.</span> and <span class="person_name">Seldon, M.</span> (2007) <xhtml:em>Polymorphisms of the tissue factor pathway inhibitor gene are associated with venous thromboembolism in the antiphospholipid syndrome and carriers of factor V Leiden.</xhtml:em> Blood Coagulation and Fibrinolysis, 18 (6). pp. 559-564. ISSN 0957-5235</p><p style="margin-bottom: 1em" class="not_ep_block"></p><table style="margin-bottom: 1em" class="not_ep_block"><tr><td valign="top" style="text-align:center"><a href="http://eprints.utas.edu.au/1768/1/Lincz_et_al_2007.pdf"><img alt="[img]" src="http://eprints.utas.edu.au/style/images/fileicons/application_pdf.png" class="ep_doc_icon" border="0" /></a></td><td valign="top"><a href="http://eprints.utas.edu.au/1768/1/Lincz_et_al_2007.pdf"><span class="ep_document_citation">PDF</span></a> - Full text restricted - Requires a PDF viewer<br />111Kb</td></tr></table><p style="margin-bottom: 1em" class="not_ep_block">Official URL: <a href="http://dx.doi.org/10.1097/MBC.0b013e3281eec977">http://dx.doi.org/10.1097/MBC.0b013e3281eec977</a></p><div class="not_ep_block"><h2>Abstract</h2><p style="padding-bottom: 16px; text-align: left; margin: 1em auto 0em auto">Polymorphisms within the tissue factor pathway inhibitor (TFPI) gene may determine TFPI expression and increase the risk of venous thromboembolism (VTE) in predisposed individuals. We tested this hypothesis by comparing TFPI activity and the frequency of common TFPI polymorphisms, -33T-&gt;C, -399C-&gt;T and -287T-&gt;C, in patients with antiphospholipid syndrome (APS) (n = 24) or factor V Leiden (n = 44) who had a history of VTE (n = 26), compared with those without VTE (n = 42) and also with normal control individuals (n = 56). TFPI activity was measured using a modified amidolytic assay and genotypes were determined by polymerase chain reaction and restriction fragment length polymorphism. We found that only APS patients with a history of venous thrombosis had TFPI activity levels significantly different from control individuals (1.77 +/- 0.60 vs 0.77 +/- 0.19 U/ml; P = 0.0001), and this was associated with inheritance of the TFPI -33C allele (1.70 +/- 0.72 U/ml for TC/CC genotypes vs 0.97 +/- 0.56 U/ml for TT; P = 0.01). Multivariate analysis of APS and factor V Leiden patients revealed that the greatest independent contributor to VTE was TFPI activity (adjusted odds ratio = 16.84; 95% confidence interval = 2.47-114.36, P = 0.004), while inheritance of either the TFPI -33C or -399T alleles each increased the odds of VTE by nearly 13 times (95% confidence interval = 2.39-69.91, P = 0.003; and 95% confidence interval = 2.25-71.23, P = 0.004, respectively). These results indicate that the TFPI -33T-&gt;C and -399C-&gt;T polymorphisms are significantly associated with venous thrombosis in the presence of other risk factors, especially APS, and may be clinically relevant in patients who are prone to hypercoagulability.</p></div><table style="margin-bottom: 1em" cellpadding="3" class="not_ep_block" border="0"><tr><th valign="top" class="ep_row">Item Type:</th><td valign="top" class="ep_row">Article</td></tr><tr><th valign="top" class="ep_row">Additional Information:</th><td valign="top" class="ep_row">The definitive version is available online at www.bloodcoagulation.com/</td></tr><tr><th valign="top" class="ep_row">Keywords:</th><td valign="top" class="ep_row">antiphospholipid syndrome, factor V Leiden, tissue factor&#13;
  293. pathway inhibitor, venous thrombosis</td></tr><tr><th valign="top" class="ep_row">Subjects:</th><td valign="top" class="ep_row"><a href="http://eprints.utas.edu.au/view/subjects/321008.html">320000 Medical and Health Sciences &gt; 321000 Clinical Sciences &gt; 321008 Haematology</a></td></tr><tr><th valign="top" class="ep_row">ID Code:</th><td valign="top" class="ep_row">1768</td></tr><tr><th valign="top" class="ep_row">Deposited By:</th><td valign="top" class="ep_row"><span class="ep_name_citation"><span class="person_name">Dr Murray J Adams</span></span></td></tr><tr><th valign="top" class="ep_row">Deposited On:</th><td valign="top" class="ep_row">27 Sep 2007</td></tr><tr><th valign="top" class="ep_row">Last Modified:</th><td valign="top" class="ep_row">09 Jan 2008 02:30</td></tr><tr><th valign="top" class="ep_row">ePrint Statistics:</th><td valign="top" class="ep_row"><a target="ePrintStats" href="/es/index.php?action=show_detail_eprint;id=1768;">View statistics for this ePrint</a></td></tr></table><p align="right">Repository Staff Only: <a href="http://eprints.utas.edu.au/cgi/users/home?screen=EPrint::View&amp;eprintid=1768">item control page</a></p>
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