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BackgroundLevels of pentosidine (representative of advanced glycation end-products) in sera of patients with rheumatoid arthritis are increased when compared with sera of other diagnoses or healthy controls. These levels have been reported to correlate with clinical indices of rheumatoid arthritis activity and with laboratory markers of inflammation. The purpose of this study was to find out if these findings pertain to other advanced glycation end-products.MethodsWe have developed two immunoassays based on new monoclonal antibodies to advanced glycation end-products. Antibody 103-E3 reacts with an unidentified antigen, formed in the reaction of proteins with ribose, while antibody 8-C1 responds to Nε-(carboxyethyl)lysine. We have used these monoclonal antibodies to measure levels of advanced glycation end-products in sera of patients with rheumatoid arthritis, systemic lupus erythematosus, osteoarthritis, and healthy controls. We calculated the correlations between advanced glycation end-product levels in rheumatoid arthritis sera and the Disease Activity Score 28 (DAS28), age, disease duration, CRP, anti-CCP, rheumatoid factor and treatment with corticosteroids, respectively.ResultsLevels of both glycation products were significantly higher in sera of patients with rheumatoid arthritis when compared with sera of patients with systemic lupus erythematosus, osteoarthritis, or the healthy controls. Neither the level of Nε-(carboxyethyl)lysine nor the level of the 103-E3 antigen in rheumatoid arthritis sera correlated with the DAS28-scored rheumatoid arthritis activity. The levels of both antigens in rheumatoid arthritis sera did not correlate with age, gender, corticosteroid treatment, or levels of CRP, anti-CCP antibodies, and rheumatoid factor in sera.ConclusionsWe report highly specific increases in the levels of two advanced glycation end-products in sera of patients with rheumatoid arthritis. This increase could be explained neither by rheumatoid arthritis activity nor by inflammation. We propose a working hypothesis that presumes the existence of a link between advanced glycation end-product formation and induction of autoimmunity.

The greatest loss in productivity was in those with psoriatic arthritis; however, it was not significant. In contrast to clinical parameters (DAS28, BSA, and PASI score), PROs (HAQ and BASDAI score) significantly influence loss of productivity. The average annual lost PC per patient was estimated to be €2000.

253 ADA = adenosine deaminase; CCL = CC ligand; CCR = CC receptor; CGRP = calcitonin gene-related peptide; CXCL = CXC ligand; CXCR = CXC receptor; DASH = dipeptidyl peptidase-IV activity and/or structure homologues; DPP = dipeptidyl peptidase; FAP-α = fibroblast-activation protein α/seprase; GLP-1 = glucagon-like peptide-1; GRP = gastrin releasing peptide; HLA = human leukocyte antigens; IFN = interferon; IL = interleukin; IP-10 = IFN-γ inducible protein-10; Mig = monokine induced by interferon-γ; MIP = macrophage inflammatory protein; NAALADase = N-acetylated α-linked acidic dipeptidase; NK = natural killer; NPY = neuropeptide Y; OA = osteoarthritis; PB = peripheral blood; QPP = quiescent cell proline dipeptidase; RA = rheumatiod arthritis; RANTES = regulated upon activation normal T-cell expressed and secreted; SDF = stromal cellderived factor; SF = synovial fluid; SLE = systemic lupus erythematosus; SP = substance P; TGF = transforming growth factor; TNF = tumor necrosis factor; VIP = vasoactive intestinal peptide. Available online http://arthritis-research.com/content/7/6/253 AbstractSeveral of the proinflammatory peptides involved in rheumatoid arthritis pathogenesis, including peptides induced downstream of tumor necrosis factor-α as well as the monocyte/T cell-attracting chemokines RANTES and stromal cell-derived factor (SDF)-1α and the neuropeptides vasoactive intestinal peptide (VIP) and substance P, have their biological half-lives controlled by dipeptidyl peptidase IV (DPPIV). Proteolysis by DPPIV regulates not only the half-life but also receptor preference and downstream signaling. In this article, we examine the role of DPPIV homologs, including CD26, the canonical DPPIV, and their substrates in the pathogenesis of rheumatoid arthritis. The differing specific activities of the DPPIV family members and their differential inhibitor response provide new insights into therapeutic design.

This is the first mapping study conducted in PsA and we hope that our study will encourage further mapping studies in PsA. The results showed that in cases where CRP is absent, cDAPsA provides similar results to DAPsA in predicting QoL.

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Direct costs and productivity costs for patients with RA are closely related to the value of the HAQ score. The annual mean total (direct plus productivity) costs per patient 1) treated with biologics, 2) without biologic treatment, and 3) from the overall cohort were €14,763, €3,559, and €8,882, respectively.

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