The impact of anti-TNF treatment on Wnt signaling, noggin, and cytokine levels in axial spondyloarthritis.


Journal

Clinical rheumatology
ISSN: 1434-9949
Titre abrégé: Clin Rheumatol
Pays: Germany
ID NLM: 8211469

Informations de publication

Date de publication:
May 2022
Historique:
received: 04 06 2021
accepted: 16 01 2022
revised: 20 12 2021
pubmed: 22 1 2022
medline: 4 5 2022
entrez: 21 1 2022
Statut: ppublish

Résumé

Anti-tumor necrosis factor (anti-TNF) agents are commonly used in treatment of axial spondyloarthritis (axSpA), but clinical and radiological improvement is not achieved in all patients. We aimed to investigate the impact of anti-TNFs on inflammatory and noninflammatory parameters in patients with axSpA. In this longitudinal study, 30 biologic naïve axSpA patients with high disease activity and 30 healthy controls were enrolled. All patients were treated with anti-TNF agents for 6 months. ASDAS-CRP, BASDAI, BASFI, BASMI, patient and physician global assessments were evaluated. C-reactive protein, COX2, TNF-α IL-6, IL-17, IL-22, IL-23, IL-33, sclerostin, dickkopf-1, and noggin levels were evaluated at baseline and at 6 months of anti-TNF treatment. At baseline, axSpA patients had significantly higher median (IQR) TNF-α levels, 34.4 (31.4-37.03) vs. 18.1 (12.1-28.4) pg/ml (p < 0.001), and lower DKK1, 446.7 (356.9-529.3) vs. 1088.7 (951.7-1244.4) pg/ml, and sclerostin, 312.4 (140.8-412.7) vs. 412.3 (295.4-512.8) pg/ml, compared to healthy controls (all p < 0.001). The median (IQR) serum levels of IL-17, IL-22, and IL-33 increased significantly after 6 months of anti-TNF treatment, from 93.3 (85.1-104.8) to 102.1 (86.6-114.6) pg/ml (p = 0.026), 159.2 (151.9-178.4) to 183.5 (156.3-304.6) pg/ml (p = 0.033), and 127.8 (106.6-186.1) to 147.06 (128.5-213.4) pg/ml (p = 0.016), respectively. Sclerostin and DKK-1 levels increased significantly after anti-TNF treatment from 312.4 (140.8-412.7) to 405.1 (276.3-452.5) pg/ml (p = 0.018) and 446.7 (356.9-529.3) to 881.3 (663.1-972.2) pg/ml (p < 0.001), while there was no significant change in noggin level. Many inflammatory cytokines increase after anti-TNF treatment and noggin is not affected by anti-TNF treatment in AxSpA. Noggin might be a therapeutic target in patients with axSpA. • Anti-TNF therapy is not sufficient for complete blockage of the inflammatory process in axial spondyloarthritis. • The increase in IL-17, IL-22, and IL-33 may decrease the efficiency of anti-TNF therapy. • Noggin might be a therapeutic target as a complementary or alternative approach to anti-TNF therapy in axial spondyloarthritis.

Identifiants

pubmed: 35059881
doi: 10.1007/s10067-022-06070-w
pii: 10.1007/s10067-022-06070-w
doi:

Substances chimiques

Cytokines 0
Interleukin-17 0
Interleukin-33 0
Tumor Necrosis Factor Inhibitors 0
Tumor Necrosis Factor-alpha 0
C-Reactive Protein 9007-41-4

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1381-1389

Subventions

Organisme : Gazi Üniversitesi
ID : 01/2019-34.

Informations de copyright

© 2022. International League of Associations for Rheumatology (ILAR).

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Auteurs

Nuh Atas (N)

Division of Rheumatology, Department of Internal Medicine, Gazi University Faculty of Medicine, 06100, Ankara, Turkey. nuhatas2008@gmail.com.

Bağdagül Çakır (B)

Department of Clinical Biochemistry, Alab Laboratory, Ankara, Turkey.

Fatih Bakır (F)

Department of Clinical Biochemistry, Lokman Hekim University, Ankara, Turkey.

Murat Uçar (M)

Department of Radiology, Gazi University Faculty of Medicine, Ankara, Turkey.

Hasan Satış (H)

Division of Rheumatology, Department of Internal Medicine, Gazi University Faculty of Medicine, 06100, Ankara, Turkey.

Gizem Tuğçe Güz (GT)

Department of Internal Medicine, Gazi University Faculty of Medicine, Ankara, Turkey.

Kübra Durmuş Demirel (KD)

Department of Internal Medicine, Gazi University Faculty of Medicine, Ankara, Turkey.

Hakan Babaoğlu (H)

Division of Rheumatology, Department of Internal Medicine, Gazi University Faculty of Medicine, 06100, Ankara, Turkey.

Reyhan Bilici Salman (RB)

Division of Rheumatology, Department of Internal Medicine, Gazi University Faculty of Medicine, 06100, Ankara, Turkey.

Aslıhan Avanoğlu Güler (AA)

Division of Rheumatology, Department of Internal Medicine, Gazi University Faculty of Medicine, 06100, Ankara, Turkey.

Hazan Karadeniz (H)

Division of Rheumatology, Department of Internal Medicine, Gazi University Faculty of Medicine, 06100, Ankara, Turkey.

Şeminur Haznedaroğlu (Ş)

Division of Rheumatology, Department of Internal Medicine, Gazi University Faculty of Medicine, 06100, Ankara, Turkey.

Berna Göker (B)

Division of Rheumatology, Department of Internal Medicine, Gazi University Faculty of Medicine, 06100, Ankara, Turkey.

Mehmet Akif Öztürk (MA)

Division of Rheumatology, Department of Internal Medicine, Gazi University Faculty of Medicine, 06100, Ankara, Turkey.

Abdurrahman Tufan (A)

Division of Rheumatology, Department of Internal Medicine, Gazi University Faculty of Medicine, 06100, Ankara, Turkey.

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