Treatment of thrombosis in antiphospholipid syndrome

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

Antiphospholipid syndrome (APS) is an acquired cause of venous thromboembolism (VTE), i.e., deep vein thrombosis and/or pulmonary embolism in patients with systemic lupus erythematosus or other autoimmune diseases, as well as in the general population. Antiphospholipid antibodies (aPLs), particularly lupus anticoagulant, are important thrombotic risks factors [1]. Growing evidence demonstrates that aPLs, particularly antibodies specific for β2 glycoprotein I, are not merely a marker of thrombophilia but are pathogenic, directly contributing to hypercoagulability. Current management of VTE in patients with APS does not substantially differ from that in the general population of patients with VTE and without APS. However, a more problematic monitoring of the anticoagulant treatment, both in the acute and in the long-term management, and the high risk of recurrences makes the treatment of VTE in patients with APS more challenging and deserves some special considerations. The intensity and duration of anticoagulation with vitamin K antagonists (VKA) for longer-term secondary prophylaxis are therefore important issues.

Original languageEnglish
Title of host publicationAntiphospholipid Antibody Syndrome: From Bench to Bedside
PublisherSpringer International Publishing
Pages185-192
Number of pages8
ISBN (Print)9783319110448, 9783319110431
DOIs
Publication statusPublished - Jan 1 2015

Fingerprint

Antiphospholipid Syndrome
Venous Thromboembolism
Thrombosis
Antiphospholipid Antibodies
Thrombophilia
Lupus Coagulation Inhibitor
Vitamin K
Risk Management
Therapeutics
Pulmonary Embolism
Venous Thrombosis
Systemic Lupus Erythematosus
Anticoagulants
Population
Autoimmune Diseases
Glycoproteins
Recurrence
Antibodies

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Braham, S., Bucciarelli, P., & Moia, M. (2015). Treatment of thrombosis in antiphospholipid syndrome. In Antiphospholipid Antibody Syndrome: From Bench to Bedside (pp. 185-192). Springer International Publishing. https://doi.org/10.1007/978-3-319-11044-8_15

Treatment of thrombosis in antiphospholipid syndrome. / Braham, Simon; Bucciarelli, Paolo; Moia, Marco.

Antiphospholipid Antibody Syndrome: From Bench to Bedside. Springer International Publishing, 2015. p. 185-192.

Research output: Chapter in Book/Report/Conference proceedingChapter

Braham, S, Bucciarelli, P & Moia, M 2015, Treatment of thrombosis in antiphospholipid syndrome. in Antiphospholipid Antibody Syndrome: From Bench to Bedside. Springer International Publishing, pp. 185-192. https://doi.org/10.1007/978-3-319-11044-8_15
Braham S, Bucciarelli P, Moia M. Treatment of thrombosis in antiphospholipid syndrome. In Antiphospholipid Antibody Syndrome: From Bench to Bedside. Springer International Publishing. 2015. p. 185-192 https://doi.org/10.1007/978-3-319-11044-8_15
Braham, Simon ; Bucciarelli, Paolo ; Moia, Marco. / Treatment of thrombosis in antiphospholipid syndrome. Antiphospholipid Antibody Syndrome: From Bench to Bedside. Springer International Publishing, 2015. pp. 185-192
@inbook{64bd850883c14dd2863cd0f6fb49473f,
title = "Treatment of thrombosis in antiphospholipid syndrome",
abstract = "Antiphospholipid syndrome (APS) is an acquired cause of venous thromboembolism (VTE), i.e., deep vein thrombosis and/or pulmonary embolism in patients with systemic lupus erythematosus or other autoimmune diseases, as well as in the general population. Antiphospholipid antibodies (aPLs), particularly lupus anticoagulant, are important thrombotic risks factors [1]. Growing evidence demonstrates that aPLs, particularly antibodies specific for β2 glycoprotein I, are not merely a marker of thrombophilia but are pathogenic, directly contributing to hypercoagulability. Current management of VTE in patients with APS does not substantially differ from that in the general population of patients with VTE and without APS. However, a more problematic monitoring of the anticoagulant treatment, both in the acute and in the long-term management, and the high risk of recurrences makes the treatment of VTE in patients with APS more challenging and deserves some special considerations. The intensity and duration of anticoagulation with vitamin K antagonists (VKA) for longer-term secondary prophylaxis are therefore important issues.",
author = "Simon Braham and Paolo Bucciarelli and Marco Moia",
year = "2015",
month = "1",
day = "1",
doi = "10.1007/978-3-319-11044-8_15",
language = "English",
isbn = "9783319110448",
pages = "185--192",
booktitle = "Antiphospholipid Antibody Syndrome: From Bench to Bedside",
publisher = "Springer International Publishing",

}

TY - CHAP

T1 - Treatment of thrombosis in antiphospholipid syndrome

AU - Braham, Simon

AU - Bucciarelli, Paolo

AU - Moia, Marco

PY - 2015/1/1

Y1 - 2015/1/1

N2 - Antiphospholipid syndrome (APS) is an acquired cause of venous thromboembolism (VTE), i.e., deep vein thrombosis and/or pulmonary embolism in patients with systemic lupus erythematosus or other autoimmune diseases, as well as in the general population. Antiphospholipid antibodies (aPLs), particularly lupus anticoagulant, are important thrombotic risks factors [1]. Growing evidence demonstrates that aPLs, particularly antibodies specific for β2 glycoprotein I, are not merely a marker of thrombophilia but are pathogenic, directly contributing to hypercoagulability. Current management of VTE in patients with APS does not substantially differ from that in the general population of patients with VTE and without APS. However, a more problematic monitoring of the anticoagulant treatment, both in the acute and in the long-term management, and the high risk of recurrences makes the treatment of VTE in patients with APS more challenging and deserves some special considerations. The intensity and duration of anticoagulation with vitamin K antagonists (VKA) for longer-term secondary prophylaxis are therefore important issues.

AB - Antiphospholipid syndrome (APS) is an acquired cause of venous thromboembolism (VTE), i.e., deep vein thrombosis and/or pulmonary embolism in patients with systemic lupus erythematosus or other autoimmune diseases, as well as in the general population. Antiphospholipid antibodies (aPLs), particularly lupus anticoagulant, are important thrombotic risks factors [1]. Growing evidence demonstrates that aPLs, particularly antibodies specific for β2 glycoprotein I, are not merely a marker of thrombophilia but are pathogenic, directly contributing to hypercoagulability. Current management of VTE in patients with APS does not substantially differ from that in the general population of patients with VTE and without APS. However, a more problematic monitoring of the anticoagulant treatment, both in the acute and in the long-term management, and the high risk of recurrences makes the treatment of VTE in patients with APS more challenging and deserves some special considerations. The intensity and duration of anticoagulation with vitamin K antagonists (VKA) for longer-term secondary prophylaxis are therefore important issues.

UR - http://www.scopus.com/inward/record.url?scp=84944617201&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84944617201&partnerID=8YFLogxK

U2 - 10.1007/978-3-319-11044-8_15

DO - 10.1007/978-3-319-11044-8_15

M3 - Chapter

SN - 9783319110448

SN - 9783319110431

SP - 185

EP - 192

BT - Antiphospholipid Antibody Syndrome: From Bench to Bedside

PB - Springer International Publishing

ER -