血液学指标在评估强直性脊柱炎患者的疾病活动性和对α-抗肿瘤坏死因子药物的治疗反应方面的临床实用性

Dilek Tezcan, M. K. Körez, Selda Hakbi̇len, Mustafa Emin Kaygisiz, Semral Gülcemal, Sema Yi̇lmaz
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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.\nResults: 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. 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摘要

背景:强直性脊柱炎(AS)是一种影响免疫细胞比例的慢性炎症性疾病。肿瘤坏死因子α(TNF-α)在强直性脊柱炎的发病机制中起着至关重要的作用,TNF抑制剂是治疗强直性脊柱炎患者最有效的药物。近年来,有报道称血常规指标是全身炎症的标志物,与许多恶性肿瘤和慢性炎症性疾病的诊断和预后有关。本研究旨在探讨接受 TNF 抑制剂治疗的 AS 患者的血液学参数与临床参数、疾病严重程度和治疗反应之间的关系:方法:本研究从风湿病科招募了326名参与者。参与者分为健康对照组(n = 178)和强直性脊柱炎组(n = 148)。中性粒细胞、淋巴细胞、单核细胞和血小板计数、中性粒细胞-淋巴细胞比值(NLR)、单核细胞-淋巴细胞比值(MLR)、血小板-淋巴细胞比值(PLR)、血小板计数(PCT)、平均血小板体积(MPV)、红细胞分布宽度(RDW)、血小板计数(PCT)、平均血小板体积(MPV)、分析了每位受试者的红细胞分布宽度(RDW)、全身炎症指数(SII)、全身炎症反应指数(SIRI)、集群全身炎症指数(AISI)和 RPR 水平。结果:RDW、PLR、NLR、MLR、SIRI、AISI 和 SII 均高于健康对照组,除 SIRI 外,其他指标均随治疗而下降。治疗后,HLA-B27 阳性患者的 AISI 和 SII 下降明显。MPV 低于健康对照组,并随治疗而升高。活动期强直性脊柱炎患者的SII、SIRI和AISI明显高于非活动期患者。此外,它们还与红细胞沉降率(ESR)、C反应蛋白(CRP)和巴斯强直性脊柱炎疾病活动指数(BASDAI)相关:结论:SII、AISI 和 SIRI 可能是显示疾病激活和评估抗肿瘤坏死因子-α 治疗效果的重要标志物。
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ANKİLOZAN SPONDİLİT HASTALARINDA HASTALIK AKTİVİTESİ VE ANTİ-TÜMÖR NEKROZ FAKTÖRÜ ALFA AJANLAR İLE TEDAVİ YANITINI DEĞERLENDİRMEDE HEMATOLOJİK ENDEKSLERİN KLİNİK YARARLILIĞI
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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