The concomitant presence of lupus anticoagulant, anticardiolipin and anti-β2-glycoprotein i antibodies could be associated with acquired activated protein c resistance in non-systemic lupus erythematosus patients

2003 ◽  
Vol 121 (3) ◽  
pp. 527-529 ◽  
Author(s):  
Laura Gennari ◽  
Alicia Blanco ◽  
María Fabiana Alberto ◽  
Silvia Grosso ◽  
María Angela Lazzari
Blood ◽  
2001 ◽  
Vol 97 (4) ◽  
pp. 844-849 ◽  
Author(s):  
Christoph Male ◽  
Lesley Mitchell ◽  
James Julian ◽  
Patricia Vegh ◽  
Penny Joshua ◽  
...  

Abstract Acquired activated protein C resistance (APCR) has been hypothesized as a possible mechanism by which antiphospholipid antibodies (APLAs) cause thrombotic events (TEs). However, available evidence for an association of acquired APCR with APLAs is limited. More importantly, an association of acquired APCR with TEs has not been demonstrated. The objective of the study was to determine, in pediatric patients with systemic lupus erythematosus (SLE), whether (1) acquired APCR is associated with the presence of APLAs, (2) APCR is associated with TEs, and (3) there is an interaction between APCR and APLAs in association with TEs. A cross-sectional cohort study of 59 consecutive, nonselected children with SLE was conducted. Primary clinical outcomes were symptomatic TEs, confirmed by objective radiographic tests. Laboratory testing included lupus anticoagulants (LAs), anticardiolipin antibodies (ACLAs), APC ratio, protein S, protein C, and factor V Leiden. The results revealed that TEs occurred in 10 (17%) of 59 patients. Acquired APCR was present in 18 (31%) of 58 patients. Acquired APCR was significantly associated with the presence of LAs but not ACLAs. Acquired APCR was also significantly associated with TEs. There was significant interaction between APCR and LAs in the association with TEs. Presence of both APCR and LAs was associated with the highest risk of a TE. Protein S and protein C concentrations were not associated with the presence of APLAs, APCR, or TEs. Presence of acquired APCR is a marker identifying LA-positive patients at high risk of TEs. Acquired APCR may reflect interference of LAs with the protein C pathway that may represent a mechanism of LA-associated TEs.


2009 ◽  
Vol 124 (1) ◽  
pp. 127-131 ◽  
Author(s):  
Junzo Nojima ◽  
Yoshinori Iwatani ◽  
Kiyoshi Ichihara ◽  
Hidehiro Tsuneoka ◽  
Toshizo Ishikawa ◽  
...  

Lupus ◽  
2002 ◽  
Vol 11 (11) ◽  
pp. 730-735 ◽  
Author(s):  
F-J Muñoz-Rodríguez ◽  
J-C Reverter ◽  
J Font ◽  
D Tàssies ◽  
G Espinosa ◽  
...  

2009 ◽  
Vol 53 (3) ◽  
pp. 188-189 ◽  
Author(s):  
Juzo Matsuda ◽  
Kengo Gohchi ◽  
Miyo Tsukamoto ◽  
Moritaka Gotoh ◽  
Noriko Saitoh ◽  
...  

1998 ◽  
Vol 80 (12) ◽  
pp. 936-941 ◽  
Author(s):  
Marion Tannenbaum ◽  
Carolyn Neville ◽  
Paul Fortin ◽  
Joyce Rauch

SummaryWe have previously demonstrated that lupus anticoagulant antibodies from patients with systemic lupus erythematosus (SLE) specifically recognize hexagonal (II) phase phosphatidylethanolamine (PE), but not bilayer PE (Thromb Haemost 1989; 62: 892). In those studies, the involvement of proteins in this recognition was not evaluated. To address this issue, we have isolated IgG lupus anticoagulant antibodies from the plasma of SLE patients and evaluated the inhibition of lupus anticoagulant activity by hexagonal (II) phase PE in the presence and absence of purified plasma proteins. All six of the IgG lupus anticoagulant antibodies tested were inhibited by hexagonal (II) phase PE in the presence, but not the absence, of human prothrombin. In contrast, little or no inhibition was observed with prothrombin alone or with PE in combination with either β2-glycoprotein I or annexin V. These data indicate that, for certain lupus anticoagulant antibodies, inhibition by hexagonal (II) phase PE is dependent on prothrombin, suggesting that these antibodies recognize a complex of PE and prothrombin.


2021 ◽  
Vol 11 (1) ◽  
pp. 69
Author(s):  
Maria Efthymiou ◽  
Philip J. Lane ◽  
David Isenberg ◽  
Hannah Cohen ◽  
Ian J. Mackie

Background: Acquired activated protein C resistance (APCr) has been identified in antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE). Objective: To assess agreement between the ST-Genesia® and CAT analysers in identifying APCr prevalence in APS/SLE patients, using three thrombin generation (TG) methods. Methods: APCr was assessed with the ST-Genesia using STG-ThromboScreen and with the CAT using recombinant human activated protein C and Protac® in 105 APS, 53 SLE patients and 36 thrombotic controls. Agreement was expressed in % and by Cohen's kappa coefficient. Results: APCr values were consistently lower with the ST-Genesia® compared to the CAT, using either method, in both APS and SLE patients. Agreement between the two analysers in identifying APS and SLE patients with APCr was poor (≤65.9%, ≤0.20) or fair (≤68.5%, ≥0.29), regardless of TG method, respectively; no agreement was observed in thrombotic controls. APCr with both the ST Genesia and the CAT using Protac®, but not the CAT using rhAPC, was significantly greater in triple antiphospholipid antibody (aPL) APS patients compared to double/single aPL patients (p < 0.04) and in thrombotic SLE patients compared to non-thrombotic SLE patients (p < 0.05). Notably, the ST-Genesia®, unlike the CAT, with either method, identified significantly greater APCr in pregnancy morbidity (median, confidence intervals; 36.9%, 21.9–49.0%) compared to thrombotic (45.7%, 39.6–55.5%) APS patients (p = 0.03). Conclusion: Despite the broadly similar methodology used by CAT and ST-Genesia®, agreement in APCr was poor/fair, with results not being interchangeable. This may reflect differences in the TG method, use of different reagents, and analyser data handling.


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