Advanced glycation end-product pentosidine is not a relevant marker of disease activity in patients with rheumatoid arthritis

Title:

Advanced glycation end-product pentosidine is not a relevant marker of disease activity in patients with rheumatoid arthritis

Creator:

Ladislav Šenolt, Martin Braun, Jiří Vencovský, Liliana Šedová, and Karel Pavelka

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:0d09a9ad-0628-45d4-adcc-d640a2701176
uuid:0d09a9ad-0628-45d4-adcc-d640a2701176
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, revmatologie, revmatoidní artritida, matrix, rheumatology, rheumatoid arthritis, pentosidine, advanced glycation end-product (AGE), cartilage oligomeric matrix protein (COMP), anti-CCP antibodies, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Advanced glycation end-product (AGE) pentosidine has previously been demonstrated in different tissues and body fluids. It was suggested as a novel marker for evaluating the pathologic activity in rheumatoid arthritis (RA). In this study we analyzed the relation between pentosidine and markers of inflammation, cartilage turnover, immune response, and disease status of RA. Using HPLC, we analyzed pentosidine in serum and synovial fluid from 39 patients with RA and in serum from 38 healthy controls. Cartilage oligomeric matrix protein (COMP) and antibodies to CCP (anti-CCP) were measured by ELISA. Clinical disease status was assessed by Disease Activity Score 28 (DAS 28) and functional status by Health Assessment Questionnaire (HAQ). We demonstrated significantly higher serum levels of pentosidine in RA patients in comparison with controls. Pentosidine in serum significantly correlated with pentosidine in synovial fluid. Serum pentosidine levels were associated with erythrocyte sedimentation rate (p<0.03) but not with CRP, COMP, anti-CCP antibodies, DAS 28, or HAQ. In contrast to previous studies, we could not show any correlation of pentosidine levels with inflammatory status, clinical disease activity, markers of immune response, or cartilage breakdown. However, AGEs can be suggested as important players participating in joint destruction rather than markers of disease activity., L. Šenolt, M. Braun, J. Vencovský, L. Šedová, K. Pavelka., and Obsahuje bibliografii a bibliografické odkazy

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2007 Volume:56 | Number:6

Harvested from:

CDK

Metadata only:

false