Anti-Domain I β2-Glycoprotein I Antibodies and Activated Protein C Resistance Predict Thrombosis in Antiphospholipid Syndrome: TAC(I)T Study.


Journal

The journal of applied laboratory medicine
ISSN: 2576-9456
Titre abrégé: J Appl Lab Med
Pays: England
ID NLM: 101693884

Informations de publication

Date de publication:
01 11 2020
Historique:
received: 08 02 2020
accepted: 24 04 2020
pubmed: 24 6 2020
medline: 16 10 2021
entrez: 24 6 2020
Statut: ppublish

Résumé

Antibodies binding to domain I of β2-glycoprotein I (aDI) and activated protein C (APC) resistance are associated with an increased risk of thrombosis in cross-sectional studies. The objective of this study was to assess their predictive value for future thromboembolic events in patients with antiphospholipid antibodies (aPL) or antiphospholipid syndrome. This prospective multicenter cohort study included consecutive patients with aPL or systemic lupus erythematosus. We followed 137 patients (43.5 ± 15.4 year old; 107 women) for a mean duration of 43.1 ± 20.7 months. We detected aDI IgG antibodies by ELISA in 21 patients. An APC sensitivity ratio (APCsr) was determined using a thrombin generation-based test. The APCsr was higher in patients with anti-domain I antibodies demonstrating APC resistance (0.75 ± 0.13 vs 0.48 ± 0.20, P < 0.0001). In univariate analysis, the hazard ratio (HR) for thrombosis over time was higher in patients with aDI IgG (3.31 [95% CI, 1.15-9.52]; P = 0.03) and patients with higher APC resistance (APCsr >95th percentile; HR, 6.07 [95% CI, 1.69-21.87]; P = 0.006). A sensitivity analysis showed an increased risk of higher aDI IgG levels up to HR 5.61 (95% CI, 1.93-16.31; P = 0.01). In multivariate analysis, aDI IgG (HR, 3.90 [95% CI, 1.33-11.46]; P = 0.01) and APC resistance (HR, 4.98 [95% CI, 1.36-18.28]; P = 0.02) remained significant predictors of thrombosis over time. Our study shows that novel tests for antibodies recognizing domain I of β2-glycoprotein I and functional tests identifying APC resistance are significant predictors of thrombosis over time and may be useful for risk stratification.

Sections du résumé

BACKGROUND
Antibodies binding to domain I of β2-glycoprotein I (aDI) and activated protein C (APC) resistance are associated with an increased risk of thrombosis in cross-sectional studies. The objective of this study was to assess their predictive value for future thromboembolic events in patients with antiphospholipid antibodies (aPL) or antiphospholipid syndrome.
METHODS
This prospective multicenter cohort study included consecutive patients with aPL or systemic lupus erythematosus. We followed 137 patients (43.5 ± 15.4 year old; 107 women) for a mean duration of 43.1 ± 20.7 months.
RESULTS
We detected aDI IgG antibodies by ELISA in 21 patients. An APC sensitivity ratio (APCsr) was determined using a thrombin generation-based test. The APCsr was higher in patients with anti-domain I antibodies demonstrating APC resistance (0.75 ± 0.13 vs 0.48 ± 0.20, P < 0.0001). In univariate analysis, the hazard ratio (HR) for thrombosis over time was higher in patients with aDI IgG (3.31 [95% CI, 1.15-9.52]; P = 0.03) and patients with higher APC resistance (APCsr >95th percentile; HR, 6.07 [95% CI, 1.69-21.87]; P = 0.006). A sensitivity analysis showed an increased risk of higher aDI IgG levels up to HR 5.61 (95% CI, 1.93-16.31; P = 0.01). In multivariate analysis, aDI IgG (HR, 3.90 [95% CI, 1.33-11.46]; P = 0.01) and APC resistance (HR, 4.98 [95% CI, 1.36-18.28]; P = 0.02) remained significant predictors of thrombosis over time.
CONCLUSIONS
Our study shows that novel tests for antibodies recognizing domain I of β2-glycoprotein I and functional tests identifying APC resistance are significant predictors of thrombosis over time and may be useful for risk stratification.

Identifiants

pubmed: 32572467
pii: 5861164
doi: 10.1093/jalm/jfaa072
doi:

Substances chimiques

beta 2-Glycoprotein I 0

Types de publication

Journal Article Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1242-1252

Informations de copyright

© American Association for Clinical Chemistry 2020. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Auteurs

Stephane Zuily (S)

Nancy University Hospital, Vascular Medicine Division and Regional Competence Center for Rare Vascular and Systemic Autoimmune Diseases, Nancy, France.
Inserm, U1116, Nancy, France.
Nancy University, Nancy, France.
University of Lorraine, Nancy, France.

Bas de Laat (B)

Synapse Research Institute, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, The Netherlands.
Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, The Netherlands.

Francis Guillemin (F)

University of Lorraine, Nancy, France.
Inserm, CIC-EC CIE1433, Nancy, France.

Hilde Kelchtermans (H)

Synapse Research Institute, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, The Netherlands.
Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, The Netherlands.

Nadine Magy-Bertrand (N)

CHRU de Besançon, Internal Medicine Department, Besançon, France.

Hélène Desmurs-Clavel (H)

Department of Internal Medicine, CHU de Lyon, Lyon, France.

Marc Lambert (M)

CHRU de Lille, Department of Internal Medicine, Lille, France.

Vincent Poindron (V)

CHU de Strasbourg, Internal Medicine and Clinical Immunology Department, Strasbourg, France.

Emmanuel de Maistre (E)

CHU de Dijon, Hematology Department, Dijon, France.

Virginie Dufrost (V)

Nancy University Hospital, Vascular Medicine Division and Regional Competence Center for Rare Vascular and Systemic Autoimmune Diseases, Nancy, France.
Inserm, U1116, Nancy, France.
Nancy University, Nancy, France.
University of Lorraine, Nancy, France.

Jessie Risse (J)

Nancy University Hospital, Vascular Medicine Division and Regional Competence Center for Rare Vascular and Systemic Autoimmune Diseases, Nancy, France.
Inserm, U1116, Nancy, France.
Nancy University, Nancy, France.
University of Lorraine, Nancy, France.

Zakera Shums (Z)

CHU de Dijon, Hematology Department, Dijon, France.

Gary L Norman (GL)

INOVA Diagnostics, San Diego, CA.

Philip G de Groot (PG)

Synapse Research Institute, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, The Netherlands.
Clinical Chemistry and Haematology, University Medical Centre (UMC) Utrecht, Utrecht, The Netherlands.

Patrick Lacolley (P)

Nancy University Hospital, Vascular Medicine Division and Regional Competence Center for Rare Vascular and Systemic Autoimmune Diseases, Nancy, France.
Inserm, U1116, Nancy, France.
Nancy University, Nancy, France.
University of Lorraine, Nancy, France.

Thomas Lecompte (T)

Nancy University Hospital, Hematology Laboratory, Nancy, France.

Véronique Regnault (V)

Nancy University Hospital, Vascular Medicine Division and Regional Competence Center for Rare Vascular and Systemic Autoimmune Diseases, Nancy, France.
Inserm, U1116, Nancy, France.
Nancy University, Nancy, France.
University of Lorraine, Nancy, France.

Denis Wahl (D)

Nancy University Hospital, Vascular Medicine Division and Regional Competence Center for Rare Vascular and Systemic Autoimmune Diseases, Nancy, France.
Inserm, U1116, Nancy, France.
Nancy University, Nancy, France.
University of Lorraine, Nancy, France.

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