Different Biomarkers of Response to Treatment with Selective Jak-1 Inhibitors in Rheumatoid Arthritis

© 2023 The Author(s). Published by IMR Press..

BACKGROUND: Rheumatoid arthritis (RA) is a systemic autoimmune disease that causes progressive joint damage. The Janus kinase (JAK) inhibitors (JAK-I) represent a new therapeutic option for RA patients, blocking the intracellular JAK-STAT pathway. Today, no studies have been conducted to determine whether new biomarkers could better reflect disease activity in patients treated with JAK-I than traditional disease activity indicators. Thus, the aim of our study was to determine additional disease activity biomarkers in RA patients receiving selective JAK-1 inhibitors.

METHODS: we enrolled 57 patients with RA: 34 patients were treated with Upadacitinib (UPA) and 23 patients with Filgotinib (FIL). All patients were evaluated for clinimetry with DAS28 and Crohn's Disease Activity Index (CDAI), number of tender and swollen joints, Visual Analogic Scale (VAS), Physician Global Assessment (PhGA), and Health Assessment Questionnaire (HAQ), at baseline and at the 12th week of treatment. Lymphocyte subpopulations, complete blood count, erythrocyte sedimentation rate (ESR), C-Reactive Protein (CRP), anti-cyclic citrullinated peptide antibodies (APCA), rheumatoid factor (RF) IgM, interleukin 6 (IL-6), circulating calprotectin (cCLP), tumor necrosis factor α (TNFα), soluble urokinase Plasminogen Activator Receptor (suPAR), complement functional activity were measured at baseline and after the 12th week of treatment.

RESULTS: in both groups of patients, we documented a significant reduction in the clinimetric parameters DAS28, CDAI, number of tender joints, number of swollen joints, VAS, PhGA, and HAQ. Moreover, significant differences were reported for laboratory parameters of ESR, CRP, IL-6, suPAR, cCLP, and PLT/L ratio in both groups. However, no difference was demonstrated between the two groups for changes in renal, hepatic, and lipid parameters.

CONCLUSIONS: the suPAR and cCLP levels may lead towards a different therapeutic choice between UPA and FIL, with the expression of two different RA pathophenotypes directing FIL towards a lymphocyte-poor form and UPA towards a myeloid form of RA.

Medienart:

E-Artikel

Erscheinungsjahr:

2023

Erschienen:

2023

Enthalten in:

Zur Gesamtaufnahme - volume:28

Enthalten in:

Frontiers in bioscience (Landmark edition) - 28(2023), 8 vom: 23. Aug., Seite 176

Sprache:

Englisch

Beteiligte Personen:

Benucci, Maurizio [VerfasserIn]
Gobbi, Francesca Li [VerfasserIn]
Fusi, Paola [VerfasserIn]
Damiani, Arianna [VerfasserIn]
Russo, Edda [VerfasserIn]
Guiducci, Serena [VerfasserIn]
Manfredi, Mariangela [VerfasserIn]
Grossi, Valentina [VerfasserIn]
Infantino, Maria [VerfasserIn]
Amedei, Amedeo [VerfasserIn]

Links:

Volltext

Themen:

9007-41-4
Biomarkers
C-Reactive Protein
EC 2.7.10.2
Filgotinib
Interleukin-6
JAK inhibitors
Janus Kinases
Journal Article
Receptors, Urokinase Plasminogen Activator
Rheumatoid arthritis
STAT Transcription Factors
Upadacitinib

Anmerkungen:

Date Completed 13.09.2023

Date Revised 13.09.2023

published: Print

Citation Status MEDLINE

doi:

10.31083/j.fbl2808176

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM361626606