Antiphospholipid Antibody‐Induced Trophoblast Responses are Differentially Modulated by Viral dsRNA and Viral ssRNA

Mesothelioma-associated antiphospholipid antibody syndrome presenting with cutaneous infarction and neuropathy

British Journal of Dermatology ◽

10.1046/j.1365-2133.1998.02289.x ◽

1998 ◽

Vol 138 (6) ◽

pp. 1092-1094 ◽

Cited By ~ 10

Author(s):

Tucker ◽

Coulson ◽

Salman ◽

Kendra ◽

Johnson

Keyword(s):

Antiphospholipid Antibody ◽

Antiphospholipid Antibody Syndrome

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Plasma Levels of Lipoprotein(a) Are Elevated in Patients with the Antiphospholipid Antibody Syndrome

Thrombosis and Haemostasis ◽

10.1055/s-0038-1642454 ◽

1994 ◽

Vol 71 (04) ◽

pp. 424-427 ◽

Cited By ~ 42

Author(s):

Masahide Yamazaki ◽

Hidesaku Asakura ◽

Hiroshi Jokaji ◽

Masanori Saito ◽

Chika Uotani ◽

...

Keyword(s):

Plasma Levels ◽

Active Form ◽

Plasminogen Activator Inhibitor ◽

Arterial System ◽

Control Group ◽

Antiphospholipid Antibody ◽

Antiphospholipid Antibody Syndrome ◽

Lipoprotein A ◽

Soluble Thrombomodulin ◽

Relationship Of

SummaryThe mechanisms underlying clinical abnormalities associated with the antiphospholipid antibody syndrome (APAS) have not been elucidated. We measured plasma levels of lipoprotein(a) [Lp(a)], the active form of plasminogen activator inhibitor (active PAI), thrombin-antithrombin III complex (TAT) and soluble thrombomodulin (TM), to investigate the relationship of these factors to thrombotic events in APAS. Mean plasma levels of Lp(a), TAT, active PAI and TM were all significantly higher in patients with aPL than in a control group of subjects. Plasma levels of Lp(a) and active PAI were significantly higher in patients with aPL and arterial thromboses than in patients with aPL but only venous thromboses. There was a significant correlation between plasma levels of Lp(a) and active PAI in patients with aPL. These findings suggest that patients with aPL are in hypercoagulable state. High levels of Lp(a) in plasma may impair the fibrinolytic system resulting in thromboses, especially in the arterial system.

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The Interaction of β2 Glycoprotein-I and Heparin and Its Effect on β2 Glycoprotein-I Antiphospholipid Antibody Cofactor Function in Plasma

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648918 ◽

1994 ◽

Vol 72 (04) ◽

pp. 578-581 ◽

Cited By ~ 3

Author(s):

T McNally ◽

S E Cotterell ◽

I J Mackie ◽

D A Isenberg ◽

S J Machin

Keyword(s):

Solid Phase ◽

Pharmaceutical Preparations ◽

Enzyme Linked Immunosorbent Assay ◽

Antiphospholipid Antibody ◽

Biological Functions ◽

Dermatan Sulphate ◽

Glycoprotein I ◽

Crossed Immunoelectrophoresis ◽

Calcium Heparin ◽

Cofactor Activity

Summaryβ2 glycoprotein-I (β2GPI), a cofactor for antiphospholipid antibody (aPA) binding, binds to many anionic macromolecules including heparin. The nature of this interaction with heparin is not well understood and its effect on the purported biological functions of β2GPI is unknown.We have examined the interactions of dermatan sulphate (DS) and different pharmaceutical preparations of heparin with β2GPI by crossed immunoelectrophoresis (CIE) and investigated the effect of these agents on plasma levels of p2GPI antigen (β2GPI: Ag) by a standardised enzyme linked immunosorbent assay (ELISA). P2GPI aPA cofactor activity (β2GPI:Cof) was also measured using a modified solid phase an-ti-phosphatidylserine (aPS) ELISA. CIE results confirmed a heparin-β2GPI interaction with unfractionated (UF) heparin. β2GPI:Ag levels were unaffected by any of the preparations investigated. There were no significant differences in β2GPI:Cof activities of the samples containing LMW heparins or DS but levels of β2GPI:Cof were increased in samples containing UF sodium and calcium heparin preparations (0.5 IU/ml Monoparin, p <0.05, and 10 IU/ml Liquemin and Calcipa-rine, p <0.05).

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The Risk of Recurrent Venous Thromboembolism in Patients with and without Factor V Leiden

Thrombosis and Haemostasis ◽

10.1055/s-0038-1656023 ◽

1997 ◽

Vol 77 (04) ◽

pp. 624-628 ◽

Cited By ~ 139

Author(s):

Sabine Eichinger ◽

Ingrid Pabinger ◽

Andreas Stümpfien ◽

Mirko Hirschl ◽

Christine Bialonczyk ◽

...

Keyword(s):

Oral Anticoagulant Therapy ◽

Oral Anticoagulants ◽

Factor V Leiden ◽

Multicenter Trial ◽

Observation Time ◽

Antiphospholipid Antibody ◽

Antiphospholipid Antibody Syndrome ◽

Factor V ◽

Increased Risk ◽

Recurrent Vte

SummaryThromboprophylaxis with oral anticoagulants up to six months is established in patients after a first venous thromboembolic event (VTE). The risk of recurrent VTE is still considerable thereafter, and it is uncertain whether some patients might benefit from extended anticoagulation. We performed a prospective, multicenter trial (4 thrombosis centers) and evaluated in 380 patients with a first or recurrent VTE (patients with a deficiency of antithrombin, protein C, protein S or plasminogen; cancer; or an antiphospholipid antibody syndrome were excluded) the risk of recurrence after discontinuation of secondary thromboprophylaxis with oral anticoagulants. It was the aim of the study to evaluate whether patients with factor V Leiden are at an increased risk of recurrent VTE. 112 (29.5%) patients were carriers of factor V Leiden (26.9% heterozygous, 2.6% homozygous). After a median observation time of 19.3 months the overall recurrence rate of VTE was 9.9%. Recurrent deep vein thrombosis and/or pulmonary embolism occurred in 26 of 268 patients without factor V Leiden (9.7%) and in 10 of 112 patients with factor V Leiden (8.9%). The probability of recurrent VTE two years after discontinuation of oral anticoagulants was 12.4% (95% Cl 7.8-17) in patients without factor V Leiden and was 10.6% (95% Cl 3.8-17.4) in carriers of the mutation. This difference was statistically not significant. Patients with factor V Leiden are not at a higher risk of recurrent VTE within two years after discontinuation of oral anticoagulants than patients without factor V Leiden. Balancing the risk of recurrent VTE and bleeding from oral. anticoagulants, patients with factor V Leiden are not likely to benefit from oral anticoagulant therapy extended beyond six months.

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