Clinical Significance of β2 Glycoprotein I Dependent Anticardiolipin Antibody, Lupus Anticoagulant and Antinuclear Antibodies in Patients with Recurrent Miscarriages

1999 ◽  
pp. 272-276
Author(s):  
Mayumi Ogasawara ◽  
Koji Aoki ◽  
Kinue Katano ◽  
Tomomi Aoyama ◽  
Kaoru Suzumori
Keyword(s):  
Clinical Significance ◽  
Lupus Anticoagulant ◽  
Antinuclear Antibodies ◽  
Anticardiolipin Antibody ◽  
Recurrent Miscarriages ◽  
Glycoprotein I

Anti-β2-glycoprotein I Antibody: Specificity and Clinical Significance

Lupus ◽  
1996 ◽  
Vol 5 (5) ◽  
pp. 378-380 ◽  
Author(s):  
T Koike ◽  
E Matsuura
Keyword(s):  
Conformational Change ◽  
Clinical Significance ◽  
Clinical Course ◽  
Oxidized Ldl ◽  
Anticardiolipin Antibody ◽  
Antibody Specificity ◽  
Glycoprotein I ◽  
Cryptic Epitopes ◽  
Oxygen Atoms

Cardiolipin binding of IgG-class anticardiolipin antibody (aCL) depends on the existence of β2-glycoprotein I (β2-GPI). We developed an EIA system that enables detection of antibodies against β2-GPI, without the presence of cardiolipin. This system involves use of irradiated polystyrene plates, in which oxygen atoms are introduced onto the surfaces of the plates. β2-GPI bound to the surface of these plates is assumed to undergo a conformational change that exposes normally cryptic epitopes. Anti-β2-GPI antibody measured using this EIA system showed good correlation with aCL measured by conventional EIA methods and may prove useful in evaluating the risk of thrombosis and monitoring the clinical course in patients with SLE. Utilizing this EIA system and β2-GPI-deleted mutants, we found that the fourth domain of β2-GPI is involved in expression of one of the cryptic epitopes recognized by aCL. We also found that oxidized LDL are sequentially targeted by β2-GPI and aCL.

Anti β2-glycoprotein I antibodies: Clinical significance

Lupus ◽  
1998 ◽  
Vol 7 (2_suppl) ◽  
pp. 107-109 ◽  
Author(s):  
A Tincani ◽  
L Spatola ◽  
M Cinquini ◽  
R Cattaneo ◽  
P Meroni ◽  
...  
Keyword(s):  
Antibody Response ◽  
Clinical Significance ◽  
Antiphospholipid Syndrome ◽  
Clinical Evaluation ◽  
Fetal Loss ◽  
Anticardiolipin Antibody ◽  
Apoptotic Bodies ◽  
Glycoprotein I ◽  
Antigenic Complex ◽  
Direct Target

The introduction of anticardiolipin antibody (aCL) assay, described in 1983, was able to focus much attention on the study of patients suffering from thrombosis, repeated fetal loss and thrombocytopenia, and allowing the identification of the so called antiphospholipid syndrome (APS). The identification of β2 glycoprotein I (β22GPI) as an essential component of the antigenic complex recognized by aCL suggested that this molecule could be a direct target of the antibody response. Since then, different groups have described ELISAs for the detection of anti β2GPI antibodies, applied to the clinical evaluation of patients with APS, and showing an overall better specificity. Recently, anti β2GPI were also shown to bind apoptotic bodies resulting in an alteration of their physiological clearance with the triggering of TNFα release. This observation suggests that anti β2GPI may also modify the immunogenicity of apoptotic bodies and of the autoantigens that they contain.

scholarly journals Hyperhomocysteinemia Relates to the Subtype of Antiphospholipid Antibodies in Non-SLE Patients

2007 ◽  
Vol 13 (4) ◽  
pp. 398-403 ◽  
Author(s):  
Wei Hsi Chen ◽  
Hung Sheng Lin ◽  
Yi Fen Kao ◽  
Min Yu Lan ◽  
Jia Shou Liu
Keyword(s):  
Lupus Anticoagulant ◽  
Methylenetetrahydrofolate Reductase ◽  
Homocysteine Level ◽  
Anticardiolipin Antibody ◽  
Plasma Homocysteine ◽  
Serum Folate ◽  
Antiphospholipid Antibody ◽  
Glycoprotein I ◽  
Abnormal Increase

Abnormal increases of antiphospholipid antibody and plasma homocysteine levels are recently emerging as nonlipidic risk factors for cerebral atherogenesis and thrombosis. Both antiphospholipid antibody and homocysteine share many similar bioeffects in hemostasis, but their interaction is still inconsistent. In this study, we examined the relation between the plasma homocysteine level and lupus anticoagulant, anticardiolipin antibody, and anti-β2-glycoprotein I antibody in patients with noncardiac cerebral ischemia. Systemic lupus erythrematosus patients were excluded. The results showed a higher frequency of moderate hyperhomocysteinemia in patients with an abnormal increase of lupus anticoagulant only. Neither the serum folate and cobalamin levels nor methylenetetrahydrofolate reductase allele mutation contributes to this result. Accordingly, homocysteine interacts with lupus anticoagulant to promote cerebral atherosclerosis and ischemia. The role of vasculopathic or prothrombotic autoantibody generation in response to specific pathological change such as hyperhomocysteinemia warrants further investigation.

scholarly journals Laboratory methods to detect antiphospholipid antibodies

Hematology ◽  
2014 ◽  
Vol 2014 (1) ◽  
pp. 321-328 ◽  
Author(s):  
Steven A. Krilis ◽  
Bill Giannakopoulos
Keyword(s):  
Clinical Significance ◽  
Antiphospholipid Antibodies ◽  
Lupus Anticoagulant ◽  
Solid Phase ◽  
Evidence Based ◽  
Diagnostic Utility ◽  
Laboratory Methods ◽  
Detailed Review ◽  
Glycoprotein I ◽  
Beta 2

Abstract This chapter reviews several important themes pertaining to the antiphospholipid syndrome (APS), including a description of the clinical features, a discussion of the main autoantigen, beta 2-glycoprotein I (β2GPI), and insights into the characteristics of the pathogenic anti-β2GPI autoantibodies. Evidence-based considerations for when to test for APS are explored, along with the clinical significance of patients testing positive on multiple APS assays, so-called triple positivity. A detailed review of recently published laboratory guidelines for the detection of lupus anticoagulant and the solid-phase anticardiolipin and anti-β2GPI ELISAs is undertaken. Finally, a brief review of nonclassification criteria laboratory assays with potential future diagnostic utility is presented.

Increased Levels of β2-Glycoprotein I (aca-Cofactor) in Patients with Lupus Anticoagulant

1992 ◽  
Vol 67 (03) ◽  
pp. 386-386 ◽  
Author(s):  
M Galli ◽  
S Cortelazzo ◽  
M Daldossi ◽  
T Barbui
Keyword(s):  
Lupus Anticoagulant ◽  
Glycoprotein I

Synchronized Inhibition of the Phospholipid Mediated Autoactivation of Factor XII in Plasma by β2-glycoprotein I and Anti-β2-glycoprotein I

1995 ◽  
Vol 73 (05) ◽  
pp. 798-804 ◽  
Author(s):  
Inger Schousboe ◽  
Margit Søe Rasmussen
Keyword(s):  
Lupus Erythematosus ◽  
Lupus Anticoagulant ◽  
Response Curve ◽  
Inhibitory Effect ◽  
Factor Xii ◽  
High Antibody ◽  
Contact Activation ◽  
Maximal Inhibition ◽  
Lupus Anticoagulants ◽  
Glycoprotein I

SummaryLupus anticoagulants are a group of antibodies commonly found in patients with autoimmune diseases such as systemic lupus erythematosus. Lupus anticoagulants inhibit phospholipid dependent coagulation and may bind to negatively charged phospholipids. Recent studies have suggested an association between anti-β2-glycoprotein I and a lupus anticoagulant, whose activity is frequently dependent on the presence of β2-glycoprotein I. Based on these observations, the effect of anti-β2-glycoprotein I on the autoactivation of factor XII in plasma was investigated. Autoactivation initiated by the presence of negatively charged phospholipids, but not by sulfatide, was strongly inhibited by immunoaffinity purified anti-β2-glycoprotein I. The dose-response curve of anti-β2-gly coprotein I was identical with that of a precipitating antibody, showing no inhibition at low and high antibody dilutions and maximal inhibition at an intermediate dilution. At high antibody concentrations, an increased rate of factor Xlla activation was observed. This increase was of the same magnitude as the decreased rate observed in plasma supplemented with the same amount of β2-glycoprotein I as in the plasma itself. This confirms the inhibitory effect of β2-GP-I on the contact activation and shows that inhibition is effective on the autoactivation of factor XII in plasma. The inhibitory action of β2-glycoprotein I was independent of the inhibition caused by the anti- β2-glycoprotein I/β2-glycoprotein I complex suggesting a synchronized inhibition of factor XII autoactivation by β2-glycoprotein I and anti-β2-gly coprotein I. The inhibition caused by the antibody is suggested to be caused by a reduced availability of negatively charged phospholipids due to the binding of the anti-β2- GP-I/β2-GP-I complex. This complex may be a lupus anticoagulant.

scholarly journals Diagnostic Challenges on the Laboratory Detection of Lupus Anticoagulant

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 844
Author(s):  
Armando Tripodi
Keyword(s):  
Lupus Anticoagulant ◽  
Clinical Laboratory ◽  
External Quality Assessment ◽  
State Of The Art ◽  
Diagnostic Procedures ◽  
External Quality ◽  
Glycoprotein I ◽  
Current State ◽  
Clinical Laboratories

Lupus anticoagulant (LA) is one of the three laboratory parameters (the others being antibodies to either cardiolipin or β2-glycoprotein I) which defines the rare but potentially devastating condition known as antiphospholipid syndrome (APS). Testing for LA is a challenging task for the clinical laboratory because specific tests for its detection are not available. However, proper LA detection is paramount for patients’ management, as its persistent positivity in the presence of (previous or current) thrombotic events, candidate for long term anticoagulation. Guidelines for LA detection have been established and updated over the last two decades. Implementation of these guidelines across laboratories and participation to external quality assessment schemes are required to help standardize the diagnostic procedures and help clinicians for appropriate management of APS. This article aims to review the current state of the art and the challenges that clinical laboratories incur in the detection of LA.

scholarly journals No Association of Homocysteine, Anticardiolipin Antibody, and Anti-β2 Glycoprotein I Antibody With Portal Venous System Thrombosis in Liver Cirrhosis

2021 ◽  
Vol 27 ◽  
pp. 107602962110109
Author(s):  
Le Wang ◽  
Xiaozhong Guo ◽  
Xiangbo Xu ◽  
Shixue Xu ◽  
Juqiang Han ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Portal Vein ◽  
Anticardiolipin Antibody ◽  
Venous System ◽  
Common Complication ◽  
Portal Venous System ◽  
Main Portal Vein ◽  
Glycoprotein I ◽  
Cirrhotic Patients ◽  
Clinically Significant

Portal venous system thrombosis (PVST), a common complication of liver cirrhosis, is closely associated with thrombophilia. To explore the association of homocysteine (Hcy), anticardiolipin antibody (aCL), and anti-β2 glycoprotein I antibody (aβ2GPI), which are possible thrombophilic factors, with PVST in liver cirrhosis. Overall, 654 non-malignant patients (219 with and 435 without liver cirrhosis) admitted between January 2016 and June 2020 were retrospectively evaluated. Presence of PVST, degree of main portal vein (MPV) thrombosis, and clinically significant PVST were identified. Hcy level, hyperhomocysteinemia (HHcy), aCL positivity, and aβ2GPI positivity were compared according to the presence of liver cirrhosis and PVST. Positive aβ2GPI was significantly more frequent in patients with liver cirrhosis than those without, but Hcy level and proportions of HHcy and positive aCL were not significantly different between them. PVST could be evaluated in 136 cirrhotic patients. Hcy level [10.57 μmol/L (2.71-56.82) versus 9.97 μmol/L (2.05-53.44); P = 0.796] and proportions of HHcy [4/44 (9.1%) versus 13/81 (16.0%); P = 0.413] and positive aCL [1/23 (4.3%) versus 10/52 (19.2%); P = 0.185] and aβ2GPI [9/23 (39.1%) versus 21/52 (40.4%); P = 0.919] were not significantly different between cirrhotic patients with and without PVST. There was still no significant association of Hcy level, HHcy, aCL, or aβ2GPI with PVST based on Child-Pugh classification, MPV thrombosis >50%, and clinically significant PVST. Hcy, aCL, and aβ2GPI may not be associated with PVST in liver cirrhosis, suggesting that routine screening for Hcy, aCL, and aβ2GPI should be unnecessary in such patients.

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