|Year : 2019 | Volume
| Issue : 3 | Page : 180-181
Platelet activation markers in juvenile idiopathic arthritis
Pandiarajan Vignesh, Surjit Singh
Department of Pediatrics, Advanced Pediatrics Centre, Allergy Immunology Unit, Post Graduate Institute of Medical Education and Research, Chandigarh, India
|Date of Web Publication||30-Oct-2019|
Prof. Surjit Singh
Department of Pediatrics, Advanced Pediatrics Centre, Allergy Immunology Unit, Post Graduate Institute of Medical Education and Research, Chandigarh - 160 012
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Vignesh P, Singh S. Platelet activation markers in juvenile idiopathic arthritis. Indian J Rheumatol 2019;14:180-1
Platelets are recognized to play an important role in hemostasis and tissue repair. The pro-inflammatory function of platelets was first elucidated in tissue models of atherosclerosis. Platelets get activated at sites of inflammation or endothelial damage, and the activated platelets can, in turn, augment inflammation by secreting pro-inflammatory cytokines, recruitment of neutrophils and monocytes, and activation of alternate complement pathway. The role of activated platelets in propagation of inflammation and in thrombus formation is increasingly being recognized in several rheumatological disorders.,,
Activation of platelets has been implicated in pathogenesis of vasculitides such as Kawasaki disease, polyarteritis nodosa, and antineutrophil cytoplasmic antibody-associated vasculitis. Reports of increased activity of secretory phospholipase A2 and platelet-activating factor in the synovium of patients with rheumatoid arthritis (RA) suggest that platelet activation may have a role in pathogenesis of inflammatory arthritides., To the best of our knowledge, platelet activation markers have not previously been studied in juvenile idiopathic arthritis (JIA).
Platelet microparticles (PMPs) are very small-sized fragments (0.1–1 μm diameter) that are derived from activated or apoptotic platelets. Apart from their role in coagulation, PMPs have also been shown to play a role in cell-to-cell communication and alter adaptive immune responses. Boilard et al. demonstrated elevated levels of PMPs in the synovial fluid of patients with RA and also showed that PMPs have a pro-inflammatory action. In the same study, collagen receptor glycoprotein VI was found to activate the formation of PMPs in the rheumatoid synovium.
In this issue of the journal, Kumar et al. report on flow cytometry-based assay of PMPs in 26 children with JIA. They found that levels of PMPs are significantly elevated during disease activity when compared with disease-inactive states. However, the levels did not bear a direct correlation with conventional inflammatory markers such as erythrocyte sedimentation rate and C-reactive protein. The results of this study provide preliminary evidence that platelet activation does occur during active phase of JIA. However, whether this platelet activation is the cause or effect of disease activity in JIA remains conjectural.
This is an exciting area of research, and the authors need to be complimented for their novel initiative. However, more work needs to be done to decipher the precise role of platelet activation in rheumatological disorders. The immunological cross-talk between platelets, synovium, and inflammatory cells needs to be studied at length to enhance our understanding of disease pathogenesis of such complex conditions. Analysis of other sensitive markers such as leukocyte–platelet aggregates along with PMPs in both synovial fluid and blood would need to be explored in future studies. Serial assessment of platelet activation markers may have prognostic significance and could help the clinician in assessing disease activity.
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