ArticleInflammopharmacology2019
IL-1β, IL-17A, CRP and biologics history might serve as potential markers for clinical response to etanercept in rheumatoid arthritis patients.
Article in Inflammopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Serum TNFα levels at 24 h after certolizumab pegol predict effectiveness at week 12 in patients with rheumatoid arthritis from TSUBAME study.Arthritis research & therapy · 2021Trial
- Defining immune cell phenotypes that distinguish treatment responders and non-responders in RA.Seminars in arthritis and rheumatism · 2025Review
- Measurement of pre-treatment inflammatory cytokine levels is valuable for prediction of treatment efficacy to tumor necrosis factor inhibitor in axial spondyloarthritis patients.International journal of rheumatic diseases · 2022Article
- MiR-223-3p inhibits inflammation and pyroptosis in monosodium urate-induced rats and fibroblast-like synoviocytes by targeting NLRP3.Clinical and experimental immunology · 2021Article
- Toward Overcoming Treatment Failure in Rheumatoid Arthritis.Frontiers in immunology · 2021Review
- Effect of Moxibustion on the Serum Levels of MMP-1, MMP-3, and VEGF in Patients with Rheumatoid Arthritis.Evidence-based complementary and alternative medicine : eCAM · 2020Article
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2 authors.
Funding
Abstract
This study aimed to explore the predictive value of 10 serum cytokines for clinical response to etanercept (ETN) in rheumatoid arthritis (RA) patients. Totally 128 active RA patients were enrolled, and their serum cytokines levels were detected by enzyme-linked immune sorbent assay at baseline. All patients received ETN treatment for 24 weeks, and clinical response to ETN was assessed at week 4 (W4), week 12 (W12) and week 24 (W24). There were 40 (31.3%), 74 (57.8%) and 94 (73.4%) patients who achieved clinical response at W4, W12 and W24, respectively. Based on the clinical response status at W24, patients were divided into responders and non-responders. Baseline levels of interleukin (IL)-1β and IL-17A were higher in responders, while baseline levels of tumor necrosis factor (TNF)-α, IL-6, 1L-8, IL-21, IL-23, intercellular cell adhesion molecule-1 (ICAM-1) and vascular endothelial growth factor (VEGF) were similar in responders compared with non-responders. Responders had less of a history of biologics, and higher baseline level of C-reactive protein (CRP) compared with non-responders. Further analysis revealed that CRP and IL-1β were independent factors predicting increased clinical response. Subsequent receiver operating characteristics (ROC) curve analysis illustrated that the combination of CRP and IL-1β (AUC: 0.730, 95% CI 0.636-0.824) well distinguished responders from non-responders. In conclusion, IL-1β, IL-17A, CRP and biologics history would serve as potential markers for clinical response to ETN in RA patients.
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