Associations of Platelet Count with Inflammation and Response to Anti-TNF-α Therapy in Patients with Ankylosing Spondylitis

Abstract

Background: Increased platelet count has been reported in ankylosing spondylitis (AS) patients, but its clinical significance is still largely elusive. The objective of this study was to evaluate the clinical role of platelet count in AS patients, especially its impact on treatment outcomes. Methods: A case-control study containing 35 AS patients receiving anti-tumor necrosis factor-α (anti-TNF-α) therapy and 45 healthy controls was performed, and AS patients were followed at least 6 months after anti-TNF-α therapy. A systematic review and metaanalysis of studies containing relevant data on outcomes of interest was also performed. Results: AS patients had significantly higher platelet count than controls (p 0.0001), and the significantly increased platelet count in AS patients was confirmed in a metaanalysis of 14 studies involving 1,223 AS patients and 913 controls (mean difference 39.61, 95% CI 27.89-51.34, p < 0.001). Besides, platelet count was significantly correlated with ESR (p < 0.001) and was moderately correlated with ASDAS-CRP score (p 0.002). Moreover, anti-TNF-α therapy could reduce platelet count in AS patients at the first month and the effect was maintained through the treatment duration. In the prospective follow-up study of those 35 AS patients, those responders to anti-TNF-α therapy had significantly lower platelet count than nonresponders (p 0.015). Logistic regression analysis suggested that lower platelet count was associated with higher possibility of achieving good response to anti-TNF-α therapy in AS patients (odds ratio 2.26; 95% CI 1.06-4.82; p 0.035). Conclusion: This study suggested that platelet count was associated with inflammation severity and treatment outcomes in AS patients, and elevated platelet count was a promising biomarker of poorer response to anti-TNF-α therapy. The findings above need to be validated in more future studies.

Systemic immune-inflammation index and other inflammatory parameters in patients receiving biological or targeted synthetic DMARDs for inflammatory rheumatic disease

“…In another study in ankylosing spondylitis, platelet count was correlated with disease activity, and anti-TNF treatment decreased the platelet count. In regression analysis, a high platelet count may predict a poorer response to anti-TNF-α therapy [24]. Similar to our results, in the last study conducted in 2020, NLR, PLR, MPV and CRP decreased after the biological treatment, including infliximab, etanercept, adalimumab and ustekinumab, and this result was independent of drug [8]…”

​Circulating Cytokines in Myocardial Infarction Are Associated With Coronary Blood Flow

“…In particular, TNFa is a pleiotropic cytokine that is involved in atherothrombosis in several pathways: TNF-a increases the expression of adhesion molecules by endothelium and as well enhances leukocyte adhesion and rolling (46), and it is involved in the implementation of endothelial dysfunction via increase of reactive oxygen species production and impairment of NO-mediated vasodilation (47)(48)(49)(50). Finally, there is evidence of increased platelet aggregation upon TNF-a stimulation (51)(52)(53)(54). MIP-1b was shown to be released by macrophages and smooth muscle cells in atherosclerotic plaques.…”

Systemic immune‐inflammation index is associated with disease activity in patients with ankylosing spondylitis

“…In addition, they are also important mediators of inflammatory response. Studies have shown that the peripheral blood PLT count in patients with AS is higher than that in healthy individuals 29,30 . Although the specific mechanisms involving PLTs in the pathogenesis of AS are not clear, it has been reported that activation of PLTs by thrombin, histamine, tumor necrosis factor‐α, and interleukin (IL)‐12 leads to adhesion between activated PLTs and neutrophils, monocytes, eosinophils, and T lymphocyte subsets, which may be a key factor in the activation of inflammatory pathways 31 .…”

“…Studies have shown that the peripheral blood PLT count in patients with AS is higher than that in healthy individuals. 29,30 Although the specific mechanisms involving PLTs in the pathogenesis of AS are not clear, it has been reported that activation of PLTs by thrombin, histamine, tumor necrosis factorα, and interleukin (IL)-12 leads to adhesion between activated PLTs and neutrophils, monocytes, eosinophils, and T lymphocyte subsets, which may be a key factor in the activation of inflammatory pathways. 31 Furthermore, platelet factor 4 (chemokine [C-X-C motif] ligand 4) is the most abundant protein in the alpha granules of PLTs, and the first member of the chemokine family to be recognized in PLTs.…”