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Decreased platelet size is associated with platelet activation and anti-phospholipid syndrome in systemic lupus erythematosus

Lood, Christian LU ; Tydén, Helena LU ; Gullstrand, Birgitta LU ; Nielsen, Christoffer T. ; Heegaard, Niels H. ; Linge, Petrus LU ; Jönsen, Andreas LU ; Hesselstrand, Roger LU ; Kahn, Robin LU and Bengtsson, Anders A. LU (2017) In Rheumatology (Oxford, England) 56(3). p.408-416
Abstract

Objectives: . SLE is an autoimmune disease with increased cardiovascular morbidity and platelet activation. In the general population, increased platelet size predicts platelet reactivity and cardiovascular disease. The aim of this study was to investigate whether platelet size related to platelet activation and cardiovascular disease in SLE.

Methods: . Fresh blood samples from SLE patients ( n = 148), healthy volunteers ( n = 79) and disease controls ( n = 40) were analysed for platelet size and activation by flow cytometry, ELISA and cell count. Associations to manifest cardiovascular disease, venous thrombosis and APS were adjusted for traditional cardiovascular risk factors using logistic regression analysis.

Results: .... (More)

Objectives: . SLE is an autoimmune disease with increased cardiovascular morbidity and platelet activation. In the general population, increased platelet size predicts platelet reactivity and cardiovascular disease. The aim of this study was to investigate whether platelet size related to platelet activation and cardiovascular disease in SLE.

Methods: . Fresh blood samples from SLE patients ( n = 148), healthy volunteers ( n = 79) and disease controls ( n = 40) were analysed for platelet size and activation by flow cytometry, ELISA and cell count. Associations to manifest cardiovascular disease, venous thrombosis and APS were adjusted for traditional cardiovascular risk factors using logistic regression analysis.

Results: . SLE patients had decreased platelet size as compared with healthy controls ( P = 0.003). In SLE, decreased platelet size was related to increased platelet activation, in particular microparticle formation ( P < 0.0001, r = -0.46) and release of serotonin from dense granules ( P < 0.001, r = 0.57). SLE patients with aCL had decreased platelet size ( P = 0.02) and aCL decreased platelet size in vitro ( P = 0.007). In contrast to the general population, increased platelet size was not associated with cardiovascular disease. Instead, decreased platelet size was associated with secondary APS, even after adjusting for traditional cardiovascular risk factors ( P = 0.01, odds ratio 3.58).

Conclusion: . Platelet size is decreased in SLE patients and associated with microparticle formation and APS. Future studies are needed to determine the underlying mechanism(s) as well as the potential predictive value of small platelets for disease complications in SLE.

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author
; ; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
anti-cardiolipin antibody, anti-phospholipid syndrome, cardiovascular disease, microparticle, platelet, systemic lupus erythematosus, thrombosis
in
Rheumatology (Oxford, England)
volume
56
issue
3
pages
9 pages
publisher
Oxford University Press
external identifiers
  • pmid:28031442
  • wos:000397052200012
  • scopus:85021854997
ISSN
1462-0332
DOI
10.1093/rheumatology/kew437
language
English
LU publication?
yes
id
8407a397-8726-46c8-8ff3-efc48042dd8e
date added to LUP
2017-08-21 11:38:23
date last changed
2024-03-17 17:11:20
@article{8407a397-8726-46c8-8ff3-efc48042dd8e,
  abstract     = {{<p>Objectives: . SLE is an autoimmune disease with increased cardiovascular morbidity and platelet activation. In the general population, increased platelet size predicts platelet reactivity and cardiovascular disease. The aim of this study was to investigate whether platelet size related to platelet activation and cardiovascular disease in SLE.</p><p>Methods: . Fresh blood samples from SLE patients ( n = 148), healthy volunteers ( n = 79) and disease controls ( n = 40) were analysed for platelet size and activation by flow cytometry, ELISA and cell count. Associations to manifest cardiovascular disease, venous thrombosis and APS were adjusted for traditional cardiovascular risk factors using logistic regression analysis.</p><p>Results: . SLE patients had decreased platelet size as compared with healthy controls ( P = 0.003). In SLE, decreased platelet size was related to increased platelet activation, in particular microparticle formation ( P &lt; 0.0001, r = -0.46) and release of serotonin from dense granules ( P &lt; 0.001, r = 0.57). SLE patients with aCL had decreased platelet size ( P = 0.02) and aCL decreased platelet size in vitro ( P = 0.007). In contrast to the general population, increased platelet size was not associated with cardiovascular disease. Instead, decreased platelet size was associated with secondary APS, even after adjusting for traditional cardiovascular risk factors ( P = 0.01, odds ratio 3.58).</p><p>Conclusion: . Platelet size is decreased in SLE patients and associated with microparticle formation and APS. Future studies are needed to determine the underlying mechanism(s) as well as the potential predictive value of small platelets for disease complications in SLE.</p>}},
  author       = {{Lood, Christian and Tydén, Helena and Gullstrand, Birgitta and Nielsen, Christoffer T. and Heegaard, Niels H. and Linge, Petrus and Jönsen, Andreas and Hesselstrand, Roger and Kahn, Robin and Bengtsson, Anders A.}},
  issn         = {{1462-0332}},
  keywords     = {{anti-cardiolipin antibody; anti-phospholipid syndrome; cardiovascular disease; microparticle; platelet; systemic lupus erythematosus; thrombosis}},
  language     = {{eng}},
  month        = {{03}},
  number       = {{3}},
  pages        = {{408--416}},
  publisher    = {{Oxford University Press}},
  series       = {{Rheumatology (Oxford, England)}},
  title        = {{Decreased platelet size is associated with platelet activation and anti-phospholipid syndrome in systemic lupus erythematosus}},
  url          = {{http://dx.doi.org/10.1093/rheumatology/kew437}},
  doi          = {{10.1093/rheumatology/kew437}},
  volume       = {{56}},
  year         = {{2017}},
}