scholarly journals THU0253 Triple positivity to antiphospholipid antibodies in primary antiphospholipid syndrome: increased risk of arterial thromboses and abortions

2017 ◽  
Author(s):  
F Signorelli ◽  
G Balbi ◽  
RA Levy
Keyword(s):  
Antiphospholipid Syndrome ◽  
Antiphospholipid Antibodies ◽  
Primary Antiphospholipid Syndrome ◽  
Increased Risk

scholarly journals Flare of Antiphospholipid Syndrome in the Course of COVID-19

TH Open ◽  
2020 ◽  
Vol 04 (03) ◽  
pp. e207-e210 ◽  
Author(s):  
Alexandre Thibault Jacques Maria ◽  
Isabelle Diaz-Cau ◽  
Jean-Marc Benejean ◽  
Anaïs Nutz ◽  
Aurélie Schiffmann ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Severe Acute Respiratory Syndrome ◽  
Antiphospholipid Syndrome ◽  
Antiphospholipid Antibodies ◽  
Adrenal Glands ◽  
Primary Antiphospholipid Syndrome ◽  
Increased Risk ◽  
Risk For Thrombosis

AbstractWe report the case of a 48-year-old man followed since 2013 for primary antiphospholipid syndrome (APLS) revealed by venous thromboembolism in the presence of antiphospholipid antibodies (APL-Abs, anticardiolipin and anti-β-2-glycoprotein-1), who decompensated in the course of coronavirus disease (COVID-19). Despite efficient anticoagulation, he suffered bilateral adrenal glands hemorrhage and limb arterial ischemia. The tropism of severe acute respiratory syndrome coronavirus-2 for endothelium can lead to microangiopathy and increased risk for thrombosis. If APL-Abs positivity can be an epiphenomenon under inflammatory and prothrombotic conditions, COVID-19 was herein responsible for disseminated thrombosis and a threat of catastrophic APLS, despite efficient anticoagulation.

scholarly journals Immunogenicity, Safety and Antiphospholipid Antibodies After SARS-CoV-2 Vaccine in Patients With Primary Antiphospholipid Syndrome

2021 ◽  
Author(s):  
Flavio Signorelli ◽  
Gustavo Guimarães Moreira Balbi ◽  
Nadia Emi Aikawa ◽  
Clovis Artur Almeida Silva ◽  
Léonard de Vinci Kanda Kupa ◽  
...  
Keyword(s):  
Antiphospholipid Syndrome ◽  
Antiphospholipid Antibodies ◽  
Neutralizing Antibodies ◽  
Thrombotic Event ◽  
Control Group ◽  
Blood Collection ◽  
Primary Antiphospholipid Syndrome ◽  
Increased Risk ◽  
Excellent Safety Profile ◽  
Induced Changes

Abstract Background: Coronavirus disease 19 (COVID-19) has an increased risk of coagulopathy with high frequency of antiphospholipid antibodies (aPL). The recent reports of thrombosis associated with the adenovirus-based vaccines raises concern that SARS-CoV-2 immunization in primary antiphospholipid syndrome (PAPS) patients may trigger a dysregulated immune response with possible clotting complications. Therefore, the objectives of this study were to assess immunogenicity, aPL production and safety of Sinovac-Coronavac in PAPS patients.Methods: This prospective controlled phase 4 study of SARS-CoV-2-naïve PAPS patients and a control group (CG) consisted of a two-dose Sinovac-CoronaVac (D0/D28) and blood collection before vaccination (D0), at D28 and 6 weeks after second dose (D69) for immunogenicity/aPL levels. Outcomes were seroconversion (SC) rates of anti-SARS-CoV-2 S1/S2 IgG and/or neutralizing antibodies (NAb) at D28/D69. Safety and aPL production were also assessed. Results: Forty-four PAPS patients and 132 CG had comparable age (p=0.982) and sex (p>0.999). At D69, both groups had high and comparable SC (83.9% vs. 93.5%, p=0.092) and GMT [50.2(95%CI 34.5-73.2) vs. 61.7 (95%CI 52.8-72.3), p=0.249] as well as NAb positivity (77.4% vs. 78.7%, p=0.440), and NAb-activity [64.3% (49.0-77.0) vs. 60.9% (45.6-81.3), p=0.689]. Of note, for D28, the antibody response was very low and also similar in both groups SC (25.8% vs. 30.6% p=0.609). Antiphospholipid levels remained stable throughout the study at D0 vs D28 vs D69 (IgG aCL, p=0.058; IgM aCL, p=0.091; IgG aβ2GPI, p=0.513 and IgM aβ2GPI, p=0.468). Thrombotic event up to 6 months or other moderate/severe side effects were not observed.Conclusions: We provide novel evidence that Sinovac-CoronaVac vaccine has a high immunogenicity and excellent safety profile in PAPS. We further demonstrated that this vaccine did not trigger thrombosis or induced changes in aPL-related antibodies production. Our findings strongly support the recommendation of SARS-CoV-2 vaccination for PAPS patients.Trial registration: ClinicalTrials.gov - Identifier: NCT04754698 first registered on February 8th, 2021.

Long-term use of hydroxychloroquine reduces antiphospholipid antibodies levels in patients with primary antiphospholipid syndrome

2016 ◽  
Vol 65 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Entela Nuri ◽  
Mara Taraborelli ◽  
Laura Andreoli ◽  
Marta Tonello ◽  
Maria Gerosa ◽  
...  
Keyword(s):  
Antiphospholipid Syndrome ◽  
Antiphospholipid Antibodies ◽  
Primary Antiphospholipid Syndrome

The clonal analysis of anticardiolipin antibodies in a single patient with primary antiphospholipid syndrome reveals an extreme antibody heterogeneity

Blood ◽  
2001 ◽  
Vol 97 (12) ◽  
pp. 3820-3828 ◽  
Author(s):  
Patricia Lieby ◽  
Anne Soley ◽  
Honey Levallois ◽  
Benedicte Hugel ◽  
Jean-Marie Freyssinet ◽  
...  
Keyword(s):  
Antiphospholipid Syndrome ◽  
Antiphospholipid Antibodies ◽  
Polyclonal Antibodies ◽  
Single Cells ◽  
Expression System ◽  
Baculovirus Expression System ◽  
Clonal Analysis ◽  
Primary Antiphospholipid Syndrome ◽  
Single Patient ◽  
Prothrombotic State

The mechanism underlying the prothrombotic state that characterizes the primary antiphospholipid syndrome proves to be difficult to define mainly because of the variety of the phospholipid and protein targets of antiphospholipid antibodies that have been described. Much of the debate is related to the use of polyclonal antibodies during the different antiphospholipid assays. To better describe the antiphospholipid antibodies, a strategy was designed to analyze the reactivity of each one antibody making up the polyclonal anticardiolipin activity, breaking down this reactivity at the clonal level. This was performed in a single patient with primary antiphospholipid syndrome by combining (1) the antigen-specific selection of single cells sorted by flow cytometry using structurally bilayered labeled anionic phospholipids and (2) the cloning of immunoglobulin (Ig) variable (V) region genes originating from individual IgG anticardiolipin-specific B cells by a single-cell polymerase chain reaction technique. The corresponding V regions were cloned in order to express human recombinant antibodies in insect cells by a baculovirus expression system. The molecular analysis, the fine specificity, and the protein cofactor dependency of the first 5 monoclonal IgG anticardiolipins are reported here. This clonal analysis reveals the extreme heterogeneity of these antibodies, which could account for the difficulties in the previous attempts to define the pathogenic antiphospholipid response. This approach should help to unravel the complex antiphospholipid immune response and the mechanism of the prothrombotic state associated with these antibodies, but it could also shed some light on their possible origins.

Coagulation Activation and Fibrinolytic imbalance in Subjects with Idiopathic Antiphospholipid Antibodies -A Crucial Role for Acquired Free Protein S Deficiency

1996 ◽  
Vol 76 (02) ◽  
pp. 190-194 ◽  
Author(s):  
Paul R J Ames ◽  
Catello Tommasino ◽  
Luigi Iannaccone ◽  
Massimo Brillante ◽  
Renato Cimino ◽  
...  
Keyword(s):  
Antiphospholipid Syndrome ◽  
Antiphospholipid Antibodies ◽  
Thrombin Generation ◽  
Protein S ◽  
Venous Occlusion ◽  
Cross Sectional Study ◽  
Primary Antiphospholipid Syndrome ◽  
Cross Sectional ◽  
Free Protein ◽  
Asymptomatic Subjects

SummaryTo explore the coagulation/fibrinolytic balance and its relation with free protein S (f-PS) in subjects with antiphospholipid antibodies (aPLs) outside the setting of autoimmune inflammatory disorders, we carried out a cross-sectional study on 18 thrombotic patients with primary antiphospholipid syndrome and 18 apparently healthy subjects with persistence of idiopathic aPLs. Prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT) and D-Dimer (D-D) were taken as markers of thrombin generation and fibrin turnover. Mean F1+2 levels were higher in thrombotic (p = 0.006) and non-thrombotic subjects (p = 0.0001) than in controls as were those of D-D (p <0.0001 and p = 0.003 respectively). TAT levels did not differ. Lower mean levels of f-PS were found in thrombotic (p = 0.0006) and non-thrombotic subjects (p = 0.002) than in controls. Within both groups, mean Fl+2 levels were higher in subjects who had low f-PS levels compared to those with normal f-PS levels (p = 0.01). Gender analysed data revealed blunted tPA release (venous occlusion test) in thrombotic females (from 16.80 ± 0.79 to 21.3 ± 3.9 ng/nl, NS) but not in thrombotic males (from 18.2 ± 2.0 to 33.7 ± 4.9 ng/ml, p = 0.01) nor in asymptomatic subjects of either sex. Also, in both patient groups females had higher mean PAI than males (p <0.0002) and than control females (p <0.02). Low free protein S was found in 100% of non-thrombotic and in 90% of thrombotic patients with defective fibrinolysis. These data are consistent with increased thrombin generation, accelerated fibrin turnover and fibrinolysis abnormalities also in asymptomatic carriers of aPLs and highlight a central role for acquired f-PS deficiency in the thrombotic tendency of the antiphospholipid syndrome.

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