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<title>UTas ePrints - Anti-tissue factor pathway inhibitor activity in patients with primary antiphospholipid syndrome</title>
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<meta content="Adams, M.J." name="eprints.creators_name" />
<meta content="Donohoe, S." name="eprints.creators_name" />
<meta content="Mackie, I.J." name="eprints.creators_name" />
<meta content="Machin, S.J." name="eprints.creators_name" />
<meta content="article" name="eprints.type" />
<meta content="2007-09-10" name="eprints.datestamp" />
<meta content="2008-01-08 15:30:00" name="eprints.lastmod" />
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<meta content="Anti-tissue factor pathway inhibitor activity in patients with
primary antiphospholipid syndrome" name="eprints.title" />
<meta content="pub" name="eprints.ispublished" />
<meta content="321008" name="eprints.subjects" />
<meta content="restricted" name="eprints.full_text_status" />
<meta content="TFPI, antiphospholipid syndrome, anti-TFPI
activity, factor Xa, thrombosis." name="eprints.keywords" />
<meta content="The definitive version is available at www.blackwell-synergy.com" name="eprints.note" />
<meta content="The association between antiphospholipid antibodies
and an increased risk of thrombosis in antiphospholipid
syndrome (aPS) patients is probably caused by
numerous mechanisms, including the effects of antibodies
to phospholipid-binding proteins such as b2-glycoprotein I
and prothrombin. In this study, we investigated the
inhibition of tissue factor pathway inhibitor (TFPI) in 33
patients with primary antiphospholipid syndrome (PAPS).
TFPI was measured in PAPS patients using an amidolytic
assay, dependent on the generation of activated factor X
(Fxa), and this was compared with 55 healthy subjects.
Functional levels of TFPI (mean plus or minus SD) were significantly
lower in PAPS patients (0.89 plus or minus 0.37 U/ml) than the
control group (1.05 plus or minus 0.15 U/ml) (P = 0.02). The difference
was caused by a subset of five patients who had TFPI
levels below the lower 99% confidence interval of the
normal reference range, representing increased FXa generation
in the assay system. IgG fractions were isolated from
these five patients and five control subjects, then incorporated
into normal plasma to measure FXa generation in the
TFPI assay system. FXa generation was increased when
polyclonal rabbit anti-human TFPI IgG (P less than 0.0001) or
PAPS IgG (P = 0.0001) were added to normal plasma,
demonstrating inhibition of TFPI. The apparent anti-TFPI
activity demonstrated in the five subjects with PAPS in this
study may represent a significant new mechanism for
thrombosis in patients with aPS, as it implies that increased
tissue factor FVIIa-mediated thrombin generation might
occur." name="eprints.abstract" />
<meta content="2001" name="eprints.date" />
<meta content="published" name="eprints.date_type" />
<meta content="British Journal of Haematology" name="eprints.publication" />
<meta content="114" name="eprints.volume" />
<meta content="375-379" name="eprints.pagerange" />
<meta content="10.1046/j.1365-2141.2001.02923.x" name="eprints.id_number" />
<meta content="UNSPECIFIED" name="eprints.thesis_type" />
<meta content="TRUE" name="eprints.refereed" />
<meta content="http://dx.doi.org/10.1046/j.1365-2141.2001.02923.x" name="eprints.official_url" />
<meta content="Adams, M.J. & Oostryck, R. (1997) Further investigations of lupus
anticoagulant interference in a functional assay for tissue factor
pathway inhibitor. Thrombosis Research, 87, 245±249.
Adams, M.J., Dunstan, R.A. & Oostryck, R. (1995) Interference by
lupus anticoagulant in a functional assay for tissue factor
pathway inhibitor. Thrombosis Research, 80, 435±550.
Amengual, O., Atsumi, T., Khamashta, M.A. & Hughes, G.R. (1998)
The role of the tissue factor pathway in the hypercoagulable state
in patients with the antiphospholipid syndrome. Thrombosis and
Haemostasis, 79, 276±281.
Broze, G.J., Warren, L.A., Novotny, W.F., Higuchi, D.A., Girard, J.J. &
Miletich, J.P. (1988) The lipoprotein-associated coagulation
inhibitor that inhibits the factor VII-tissue factor complex also
inhibits factor Xa: insight into its possible mechanism of action.
Blood, 71, 335±343.
Cakir, B., Arnett, F.C. & Roubey, R.A.S. (2000) Autoantibodies to
tissue factor pathway inhibitor (TFPI) are associated with arterial
thrombosis/stroke. Journal of Autoimmunity, 15, A11(Abstract).
Exner, T., Triplett, D.A., Taberner, D. & Machin, S.J. (1991)
Guidelines for testing and revised criteria for lupus anticoagulants.
Thrombosis and Haemostasis, 65, 320±322.
Greaves, M., Cohen, H., Machin, S.J. & Mackie, I.J. (2000) Guidelines
on the investigation and management of the antiphospholipid
syndrome. British Journal of Haematology, 109, 704±715.
Harris, E.N. & Hughes, G.R. (1987) Standardising the anticardiolipin
antibody test. Lancet., 1, 277.
Harris, E.N., Baguley, E., Asherson, R.A. & Hughes, G.R. (1987)
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British Journal of Rheumatology, 26, 19.
Hughes, G.R., Harris, N.N. & Gharavi, A.E. (1986) The anticardiolipin
syndrome. Journal of Rheumatology, 13, 486±489.
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antibodies interfere with tissue factor pathway inhibitor?
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Kiraz, S., Ertenli, I., Benekli, M., Haznedaroglu, I.C., Calguneri, M.,
Celik, I., Apras, S. & Kirazli, S. (1999) Clinical significance of
hemostatic markers and thrombomodulin in systemic lupus
erythematosus: evidence for a prothrombotic state. Lupus, 8,
737±741.
Love, P.E. & Santoro, S.A. (1990) Antiphospholipid antibodies:
anticardiolipin and the lupus anticoagulant in systemic lupus
erythematosus (SLE) and in non-SLE disorders. Prevalence and
clinical significance. Annals of Internal Medicine, 112, 682±698.
McNally, T., Mackie, I.J., Machin, S.J. & Isenberg, D.A. (1995)
Increased levels of beta 2-glycoprotein-I antigen and beta 2-
glycoprotein-I binding antibodies are associated with a history of
thromboembolic complications in patients with SLE and primary
antiphospholipid syndrome. British Journal of Rheumatology, 34,
1031±1036.
McNeil, H.P., Simpson, R.J., Chesterman, C.N. & Krilis, S.A. (1990)
Anti-phospholipid antibodies are directed against a complex
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4114.
Salemink, I., Blezer, R., Willems, G.M., Galli, M., Bevers, E. &
Lindhout, T. (2000) Antibodies to û2-glycoprotein-I associated
with antiphospholipid syndrome suppress the inhibitory activity
of tissue factor pathway inhibitor. Thrombosis and Haemostasis, 84,
653±656.
Sandset, P.M., Abildgaard, U. & Pettersen, M. (1987) A sensitive
assay of extrinsic coagulation pathway inhibitor (EPI) in plasma
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Wakita, Y., Wada, H., Nakase, T., Nakasaki, T., Shimura, M.,
Hiyoyama, K., Mori, Y., Gabazza, E.C., Nishikawa, M., Deguchi, K.
& Shiku, H. (1999) Aberrations of the tissue factor pathway in
patients positive for lupus anticoagulant. Clinical and Applied
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Wilson, W.A., Gharavi, A.E., Koike, T., Lockshin, M.D., Branch,
D.W., Piette, J.C., Brey, R., Derksen, R., Harris, E.N., Hughes, G.R.,
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Arthritis and Rheumatism, 42, 1309±1311." name="eprints.referencetext" />
<meta content="Adams, M.J. and Donohoe, S. and Mackie, I.J. and Machin, S.J. (2001) Anti-tissue factor pathway inhibitor activity in patients with primary antiphospholipid syndrome. British Journal of Haematology, 114 . pp. 375-379." name="eprints.citation" />
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primary antiphospholipid syndrome" name="DC.title" />
<meta content="Adams, M.J." name="DC.creator" />
<meta content="Donohoe, S." name="DC.creator" />
<meta content="Mackie, I.J." name="DC.creator" />
<meta content="Machin, S.J." name="DC.creator" />
<meta content="321008 Haematology" name="DC.subject" />
<meta content="The association between antiphospholipid antibodies
and an increased risk of thrombosis in antiphospholipid
syndrome (aPS) patients is probably caused by
numerous mechanisms, including the effects of antibodies
to phospholipid-binding proteins such as b2-glycoprotein I
and prothrombin. In this study, we investigated the
inhibition of tissue factor pathway inhibitor (TFPI) in 33
patients with primary antiphospholipid syndrome (PAPS).
TFPI was measured in PAPS patients using an amidolytic
assay, dependent on the generation of activated factor X
(Fxa), and this was compared with 55 healthy subjects.
Functional levels of TFPI (mean plus or minus SD) were significantly
lower in PAPS patients (0.89 plus or minus 0.37 U/ml) than the
control group (1.05 plus or minus 0.15 U/ml) (P = 0.02). The difference
was caused by a subset of five patients who had TFPI
levels below the lower 99% confidence interval of the
normal reference range, representing increased FXa generation
in the assay system. IgG fractions were isolated from
these five patients and five control subjects, then incorporated
into normal plasma to measure FXa generation in the
TFPI assay system. FXa generation was increased when
polyclonal rabbit anti-human TFPI IgG (P less than 0.0001) or
PAPS IgG (P = 0.0001) were added to normal plasma,
demonstrating inhibition of TFPI. The apparent anti-TFPI
activity demonstrated in the five subjects with PAPS in this
study may represent a significant new mechanism for
thrombosis in patients with aPS, as it implies that increased
tissue factor FVIIa-mediated thrombin generation might
occur." name="DC.description" />
<meta content="2001" name="DC.date" />
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<h1 class="ep_tm_pagetitle">Anti-tissue factor pathway inhibitor activity in patients with primary antiphospholipid syndrome</h1>
<p style="margin-bottom: 1em" class="not_ep_block"><span class="person_name">Adams, M.J.</span> and <span class="person_name">Donohoe, S.</span> and <span class="person_name">Mackie, I.J.</span> and <span class="person_name">Machin, S.J.</span> (2001) <xhtml:em>Anti-tissue factor pathway inhibitor activity in patients with primary antiphospholipid syndrome.</xhtml:em> British Journal of Haematology, 114 . pp. 375-379.</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/1780/1/Adams_et_al_2001.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/1780/1/Adams_et_al_2001.pdf"><span class="ep_document_citation">PDF</span></a> - Full text restricted - Requires a PDF viewer<br />151Kb</td></tr></table><p style="margin-bottom: 1em" class="not_ep_block">Official URL: <a href="http://dx.doi.org/10.1046/j.1365-2141.2001.02923.x">http://dx.doi.org/10.1046/j.1365-2141.2001.02923.x</a></p><div class="not_ep_block"><h2>Abstract</h2><p style="padding-bottom: 16px; text-align: left; margin: 1em auto 0em auto">The association between antiphospholipid antibodies
and an increased risk of thrombosis in antiphospholipid
syndrome (aPS) patients is probably caused by
numerous mechanisms, including the effects of antibodies
to phospholipid-binding proteins such as b2-glycoprotein I
and prothrombin. In this study, we investigated the
inhibition of tissue factor pathway inhibitor (TFPI) in 33
patients with primary antiphospholipid syndrome (PAPS).
TFPI was measured in PAPS patients using an amidolytic
assay, dependent on the generation of activated factor X
(Fxa), and this was compared with 55 healthy subjects.
Functional levels of TFPI (mean plus or minus SD) were significantly
lower in PAPS patients (0.89 plus or minus 0.37 U/ml) than the
control group (1.05 plus or minus 0.15 U/ml) (P = 0.02). The difference
was caused by a subset of five patients who had TFPI
levels below the lower 99% confidence interval of the
normal reference range, representing increased FXa generation
in the assay system. IgG fractions were isolated from
these five patients and five control subjects, then incorporated
into normal plasma to measure FXa generation in the
TFPI assay system. FXa generation was increased when
polyclonal rabbit anti-human TFPI IgG (P less than 0.0001) or
PAPS IgG (P = 0.0001) were added to normal plasma,
demonstrating inhibition of TFPI. The apparent anti-TFPI
activity demonstrated in the five subjects with PAPS in this
study may represent a significant new mechanism for
thrombosis in patients with aPS, as it implies that increased
tissue factor FVIIa-mediated thrombin generation might
occur.</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 at www.blackwell-synergy.com</td></tr><tr><th valign="top" class="ep_row">Keywords:</th><td valign="top" class="ep_row">TFPI, antiphospholipid syndrome, anti-TFPI
activity, factor Xa, 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 > 321000 Clinical Sciences > 321008 Haematology</a></td></tr><tr><th valign="top" class="ep_row">ID Code:</th><td valign="top" class="ep_row">1780</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">10 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=1780;">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&eprintid=1780">item control page</a></p>
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