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http://purl.uniprot.org/citations/25956266http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25956266http://www.w3.org/2000/01/rdf-schema#comment"

Background

Accumulating evidence has demonstrated a pathogenic role of advanced glycation end products (AGEs) and receptors for AGEs (RAGE) in inflammation. Soluble RAGE (sRAGE), with the same ligands-binding capacity as full-length RAGE, acts as a "decoy" receptor. However, there has been scanty data regarding AGEs and sRAGE in adult-onset Still's disease (AOSD). This study aimed to investigate AGEs and sRAGE levels in AOSD patients and examine their association with clinical characteristics.

Methods

Using ELISA, plasma levels of AGEs and sRAGE were determined in 52 AOSD patients, 36 systemic lupus erythematosus(SLE) patients and 16 healthy controls(HC). Their associations with activity parameters and disease courses were evaluated.

Results

Significantly higher median levels of AGEs were observed in active AOSD patients (16.75 pg/ml) and active SLE patients (14.80 pg/ml) than those in HC (9.80 pg/ml, both p < 0.001). AGEs levels were positively correlated with activity scores (r = 0.836, p < 0.001), ferritin levels (r = 0.372, p < 0.05) and CRP levels (r = 0.396, p < 0.005) in AOSD patients. Conversely, significantly lower median levels of sRAGE were observed in active AOSD patients (632.2 pg/ml) and active SLE patients (771.6 pg/ml) compared with HC (1051.7 pg/ml, both p < 0.001). Plasma sRAGE levels were negatively correlated with AOSD activity scores (r = -0.320, p < 0.05). In comparison to AOSD patients with monocyclic pattern, significantly higher AGEs levels were observed in those with polycyclic or chronic articular pattern. With treatment, AGEs levels declined while sRAGE levels increased in parallel with the decrease in disease activity.

Conclusion

The elevation of AGEs levels with concomitant decreased sRAGE levels in active AOSD patients, suggests their pathogenic role in AOSD."xsd:string
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http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/author"Chen Y.M."xsd:string
http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/author"Wu Y.C."xsd:string
http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/author"Lin C.C."xsd:string
http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/author"Chen H.H."xsd:string
http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/author"Chen D.Y."xsd:string
http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/author"Lan J.L."xsd:string
http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/author"Hung W.T."xsd:string
http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/author"Hsieh C.W."xsd:string
http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/name"BMC Musculoskelet Disord"xsd:string
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http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/title"The potential role of advanced glycation end products (AGEs) and soluble receptors for AGEs (sRAGE) in the pathogenesis of adult-onset still's disease."xsd:string
http://purl.uniprot.org/citations/25956266http://purl.uniprot.org/core/volume"16"xsd:string
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