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Concerted Actions by PIICP, CTXII, and TNF-α in Patients with Juvenile Idiopathic Arthritis

Overview
Journal Biomolecules
Publisher MDPI
Date 2021 Apr 30
PMID 33924892
Citations 2
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Abstract

Joint destruction in juvenile idiopathic arthritis (JIA), initiated in the early, preclinical stage of the disease, is diagnosed on the basis of clinical evaluation and radiographic imaging. The determination of circulating cartilage-matrix turnover markers can facilitate the diagnosis and application of better and earlier treatment strategies for JIA. We have shown that 96 JIA patients have elevated levels of procollagen II C-terminal propeptide (PIICP), reflecting the extent of joint cartilage biosynthesis, and C-telopeptide of type II collagen (CTXII), a biomarker of the resorption of this tissue. Patients who did not respond to treatment had particularly high levels of these markers. JIA treatment resulted in the normalization of these markers in remissive patients, but not in those with active JIA. We showed correlations between examined variables and inflammatory process indicators, i.e., C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and tumor necrosis factor-α (TNF-α). The TNF-α of patients responding to treatment correlated with PIICP, especially in the patients before treatment (r = 0.898, < 0.001). Significant changes in serum PIICP during JIA therapy suggest its potential diagnostic utility in the monitoring of disease activity and the possibility of its use in assessing treatment towards remission. Understanding changes in type II collagen metabolism over the course of the discussed arthritis may allow the implementation of both new diagnostic tools and new therapeutic strategies in children with JIA.

Citing Articles

GAAGs, COMP, and YKL-40 as Potential Markers of Cartilage Turnover in Blood of Children with Juvenile Idiopathic Arthritis Treated with Etanercept-Relationship with ADAMTS4, ADAMTS5, and PDGF-BB.

Dabkowska K, Wojdas M, Kuznik-Trocha K, Wisowski G, Gruenpeter A, Komosinska-Vassev K J Clin Med. 2022; 11(17).

PMID: 36079004 PMC: 9457057. DOI: 10.3390/jcm11175069.


The Effects of TNF-α Inhibition on the Metabolism of Cartilage: Relationship between KS, HA, HAPLN1 and ADAMTS4, ADAMTS5, TOS and TGF-β1 Plasma Concentrations in Patients with Juvenile Idiopathic Arthritis.

Kuznik-Trocha K, Winsz-Szczotka K, Lachor-Motyka I, Dabkowska K, Wojdas M, Olczyk K J Clin Med. 2022; 11(7).

PMID: 35407621 PMC: 8999578. DOI: 10.3390/jcm11072013.

References
1.
Araki Y, Mimura T . Matrix Metalloproteinase Gene Activation Resulting from Disordred Epigenetic Mechanisms in Rheumatoid Arthritis. Int J Mol Sci. 2017; 18(5). PMC: 5454818. DOI: 10.3390/ijms18050905. View

2.
Martini A, Ravelli A, Avcin T, Beresford M, Burgos-Vargas R, Cuttica R . Toward New Classification Criteria for Juvenile Idiopathic Arthritis: First Steps, Pediatric Rheumatology International Trials Organization International Consensus. J Rheumatol. 2018; 46(2):190-197. DOI: 10.3899/jrheum.180168. View

3.
Briot K, Roux C, Gossec L, Charni N, Kolta S, Dougados M . Effects of etanercept on serum biochemical markers of cartilage metabolism in patients with spondyloarthropathy. J Rheumatol. 2008; 35(2):310-4. View

4.
Grounds M, Radley H, Gebski B, Bogoyevitch M, Shavlakadze T . Implications of cross-talk between tumour necrosis factor and insulin-like growth factor-1 signalling in skeletal muscle. Clin Exp Pharmacol Physiol. 2008; 35(7):846-51. DOI: 10.1111/j.1440-1681.2007.04868.x. View

5.
Lundell A, Erlandsson M, Bokarewa M, Liivamagi H, Uibo K, Tarraste S . Low Serum IGF-1 in Boys with Recent Onset of Juvenile Idiopathic Arthritis. J Immunol Res. 2019; 2018:3856897. PMC: 6304197. DOI: 10.1155/2018/3856897. View