Abstract
This study aimed at evaluating the clinical relevance of glycoprotein profiles during the earliest phases of rheumatoid arthritis (RA) as biomarkers of cardiovascular (CV) risk and treatment response. Then, GlycA and GlycB serum levels were measured using 1H-nuclear magnetic resonance in 82 early RA patients, 14 clinically-suspect arthralgia (CSA), and 28 controls. Serum glycosyltransferase activity was assessed by a colorimetric assay. Subclinical CV disease was assessed by Doppler-ultrasound. We found that GlycA and GlycB serum levels were increased in RA (both p < 0.001), but not in CSA, independently of cardiometabolic risk factors. Increased serum glycosyltransferase activity paralleled GlycA (r = 0.405, p < 0.001) and GlycB levels (r = 0.327, p = 0.005) in RA. GlycA, but not GlycB, was associated with atherosclerosis occurrence (p = 0.012) and severity (p = 0.001). Adding GlycA to the mSCORE improved the identification of patients with atherosclerosis over mSCORE alone, increasing sensitivity (29.7 vs. 68.0%) and accuracy (55.8 vs. 76.6%) and allowing reclassification into more appropriate risk categories. GlycA-reclassification identified patients with impaired lipoprotein metabolism. Finally, baseline GlycA levels predicted poor clinical response upon anti-rheumatic treatment at 6 and 12 months in univariate and multivariate analysis. In sum, increased GlycA levels during the earliest stage of RA can be considered a powerful biomarker for CV risk stratification and treatment response.
Highlights
Rheumatoid arthritis (RA) is a chronic inflammatory condition
The serum levels of glycoprotein signals were assessed in 82 early rheumatoid arthritis (RA) patients, 14 clinically-suspect arthralgia (CSA) individuals, and 28 HCs (Table 1)
GlycA levels were increased in early RA but not individuals with arthralgia, independently of traditional risk factors, and related to serum glycosyltransferase activity
Summary
Rheumatoid arthritis (RA) is a chronic inflammatory condition. Protein post-translational modifications (PTMs) are a common hallmark of RA [1]. The role of protein citrullination is firmly established, less is known about other PTMs, such as glycosylation. Characterizing the human glycoproteome has emerged as a relevant source potential of biomarkers and disease mediators [2]. The use of 1H-nuclear magnetic resonance (H-NMR) has allowed the identification of a prominent signal arising from the highly mobile acetyl groups of the N-acetylglucosamine and N-acetylgalactosamine, called “GlycA” [6]. This signal can be considered a broad surrogate marker of inflammation. Its full clinical implications are to be characterized
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