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Does anti-TNF therapy cause any change in platelet activation in ankylosing spondylitis patients? A comparative study.

Authors
  • Orüm, Hüseyin
  • Pamuk, Gülsüm Emel
  • Pamuk, Omer Nuri
  • Demir, Muzaffer
  • Turgut, Burhan
Type
Published Article
Journal
Journal of Thrombosis and Thrombolysis
Publisher
Springer-Verlag
Publication Date
Feb 01, 2012
Volume
33
Issue
2
Pages
154–159
Identifiers
DOI: 10.1007/s11239-011-0663-9
PMID: 22173846
Source
Medline
License
Unknown

Abstract

Recently, it has been reported that ankylosing spondylitis (AS) was characterised by endothelial dysfunction and the development of atherosclerotic complications. In this study, we evaluated platelet and endothelial activation parameters in AS patients. Fiftynine AS patients and 22 healthy controls were included. The clinical features and acute phase parameters were evaluated. In all patients and healthy controls, platelet-monocyte complexes (PMC), platelet-neutrophil complexes, basal and ADP-stimulated P-selectin (CD62P) expression were determined by flow cytometry; soluble E-selectin (sE-selectin) and soluble CD40L (sCD40L) were determined by ELISA. AS patients were divided into two groups as active and inactive by using BASDAI. In 15 AS patients, the evaluated parameters were assessed before and after 12 weeks of anti-TNF therapy. PMC and sCD40L levels in AS patients were significantly higher than in the control group (P values 0.013 and 0.016). The evaluated variables were similar in active and inactive AS groups (P > 0.05). There were no significant changes in platelet and endothelial activation parameters in AS patients after anti-TNF therapy (P > 0.05). Platelet activation which is reflected by high levels of PMC and sCD40L might be responsible for the increased frequency of atherosclerosis in AS. The platelet activation in our AS patients was not associated with disease activity and did not improve after anti-TNF therapy.

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