IFABP2 as a new prognostic biomarker for secondary non-response in rheumatoid arthritis.


Journal

International immunopharmacology
ISSN: 1878-1705
Titre abrégé: Int Immunopharmacol
Pays: Netherlands
ID NLM: 100965259

Informations de publication

Date de publication:
Jun 2023
Historique:
received: 22 12 2022
revised: 09 03 2023
accepted: 22 03 2023
medline: 1 6 2023
pubmed: 13 4 2023
entrez: 12 4 2023
Statut: ppublish

Résumé

Increased intestinal permeability promotes the translocation of bacterial products from the local microbiome to the circulation, inducing inflammation and increasing clinical activity in rheumatoid arthritis (RA). This study evaluates whether intestinal fatty acid binding protein 2 (IFABP2) serum levels are prognostic biomarkers of non-response to conventional synthetic disease-modifying antirheumatic drug therapy (csDMARDs) in RA. The therapeutic schemes administered to 60 women with RA for at least 18 months were assessed retrospectively, and the treatment response was classified according to the change in DAS28-ESR over time. Serum levels of IFABP2 and TNF-α were determined by ELISA. Receiver operating characteristics (ROC) curve analysis and logistic regression models were used to assess the predictive value and the association of IFABP2 with the non-responder phenotype in RA patients. Eleven women had a responder phenotype, 23 had a primary non-responder phenotype, and 26 had a secondary non-responder phenotype. Secondary non-responders showed higher DAS28-ESR (P = 0.009) and higher IFABP2 serum levels compared to the responder group (P = 0.023) and the primary non-responder group (P = 0.018). IFABP2 serum levels were positively correlated with chloroquine dose (r = 0.581, P = 0.007) and negatively correlated with total cholesterol (r = -0.456, P = 0.019) in secondary non-responders. The area under the curve (AUC) value of IFABP2 for predicting secondary non-response was 0.736, and IFABP2 serum levels > 9.311 ng/mL were associated with secondary non-response to csDMARDs (OR = 6.00, P = 0.003). IFABP2 serum levels are potentially a new biomarker predictive of secondary non-response to csDMARDs in RA, although our findings should be validated externally and in a larger cohort.

Sections du résumé

BACKGROUND BACKGROUND
Increased intestinal permeability promotes the translocation of bacterial products from the local microbiome to the circulation, inducing inflammation and increasing clinical activity in rheumatoid arthritis (RA). This study evaluates whether intestinal fatty acid binding protein 2 (IFABP2) serum levels are prognostic biomarkers of non-response to conventional synthetic disease-modifying antirheumatic drug therapy (csDMARDs) in RA.
METHODS METHODS
The therapeutic schemes administered to 60 women with RA for at least 18 months were assessed retrospectively, and the treatment response was classified according to the change in DAS28-ESR over time. Serum levels of IFABP2 and TNF-α were determined by ELISA. Receiver operating characteristics (ROC) curve analysis and logistic regression models were used to assess the predictive value and the association of IFABP2 with the non-responder phenotype in RA patients.
RESULTS RESULTS
Eleven women had a responder phenotype, 23 had a primary non-responder phenotype, and 26 had a secondary non-responder phenotype. Secondary non-responders showed higher DAS28-ESR (P = 0.009) and higher IFABP2 serum levels compared to the responder group (P = 0.023) and the primary non-responder group (P = 0.018). IFABP2 serum levels were positively correlated with chloroquine dose (r = 0.581, P = 0.007) and negatively correlated with total cholesterol (r = -0.456, P = 0.019) in secondary non-responders. The area under the curve (AUC) value of IFABP2 for predicting secondary non-response was 0.736, and IFABP2 serum levels > 9.311 ng/mL were associated with secondary non-response to csDMARDs (OR = 6.00, P = 0.003).
CONCLUSION CONCLUSIONS
IFABP2 serum levels are potentially a new biomarker predictive of secondary non-response to csDMARDs in RA, although our findings should be validated externally and in a larger cohort.

Identifiants

pubmed: 37044032
pii: S1567-5769(23)00411-3
doi: 10.1016/j.intimp.2023.110090
pii:
doi:

Substances chimiques

Antirheumatic Agents 0
Biomarkers 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

110090

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Oscar Zaragoza-García (O)

Faculty of Chemical-Biological Sciences, Universidad Autónoma de Guerrero, Chilpancingo, Guerrero, Mexico.

Ilse Adriana Gutiérrez-Pérez (IA)

Faculty of Chemical-Biological Sciences, Universidad Autónoma de Guerrero, Chilpancingo, Guerrero, Mexico.

Olivia Briceño (O)

Infectious Diseases Research Center, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico.

José Rafael Villafan-Bernal (JR)

Laboratory of Immunogenomics and Metabolic Diseases, Instituto Nacional de Medicina Genomica, Mexico City, Mexico.

José Eduardo Navarro-Zarza (JE)

Department of Medical Internal. Hospital General Dr. RaymundAbarca Alarcón. Chilpancingo, Guerrero, Mexico.

Isela Parra-Rojas (I)

Faculty of Chemical-Biological Sciences, Universidad Autónoma de Guerrero, Chilpancingo, Guerrero, Mexico.

Ramcés Falfán-Valencia (R)

HLA Laboratory, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico.

Iris Paola Guzmán-Guzmán (IP)

Faculty of Chemical-Biological Sciences, Universidad Autónoma de Guerrero, Chilpancingo, Guerrero, Mexico. Electronic address: pao_nkiller@yahoo.com.mx.

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Classifications MeSH