Abstract

Background: Ankylosing spondylitis (AS) is a chronic inflammatory disease which influences the proportion of immune cells. Tumor necrosis factor alpha (TNF-α) is essential in the pathogenesis of AS, and TNF inhibitors are the most effective treatment for AS patients. In recent years, routine blood parameters were reported as markers of systemic inflammation associated with the diagnosis and prognosis of numerous malignancies and chronic inflammatory diseases. This study aimed to investigate the relationship between haematological parameters and clinical parameters, disease severity and treatment response in AS patients treated with TNF inhibitors. Methods: A total of 326 participants were recruited from the rheumatology department in this study. Participants were divided into healthy controls (n = 178) and AS (n = 148). Neutrophil, lymphocyte, monocyte and platelet counts, neutrophil-lymphocyte ratio (NLR), monocyte-lymphocyte ratio (MLR), platelet-lymphocyte ratio (PLR), platelet crit (PCT), mean platelet volume (MPV), red cell distribution width (RDW), systemic inflammatory index (SII), systemic inflammatory response index (SIRI), cluster systemic inflammation index (AISI) and RPR levels were analyzed for each participant. They were compared between healthy control, AS patients during the pre-treatment phase and three months after the treatment. Results: RDW, PLR, NLR, MLR, SIRI, AISI and SII were higher than healthy controls and decreased with treatment except SIRI. The decrease in AISI and SII after treatment was significant in HLA-B27 positive patients. MPV was lower than healthy controls and increased with treatment. SII, SIRI and AISI were significantly higher in the active AS patients than in the inactive patient. Also, they were correlated with erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). Conclusion: SII, AISI, and SIRI may be valuable markers for demonstrating disease activation and evaluating the effectiveness of anti‐TNF‐α therapy.

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