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Objective There is evidence that autoimmunity plays a significant role in the pathogenesis of relapsing polychondritis (RP). This study was designed to investigate circulating levels of various cytokines in relation to the etiology of this rare disorder, and to compare the pattern of cytokine elevations in RP with that in another autoimmune disease, rheumatoid arthritis (RA). Methods Serum from 22 patients with active RP and an equal number of age- and sex-matched healthy controls and RA patients were available for analysis. The following cytokines were measured: interleukin-1β (IL-1β), IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-17, interferon-γ (IFNγ), tumor necrosis factor α, granulocyte colony-stimulating factor (G-CSF), granulocyte–macrophage colony-stimulating factor (GM-CSF), monocyte chemoattractant protein 1 (MCP-1), and macrophage inflammatory protein 1β (MIP-1β). Results were analyzed by nonparametric Mann-Whitney test with Holm stepdown adjustment for multiple testing. Results The levels of 3 of these cytokines showed significant differences between RP patients and controls. Compared with controls, mean serum levels of MCP-1, MIP-1β, and IL-8 were all much higher in patients with active RP. In contrast, RA patients showed a more general increase in all cytokines measured, with much higher levels of IL-2, IL-4, IL-5, IL-6, IL-7, IL-10, IL-13, IFNγ, G-CSF, GM-CSF, MCP-1, and MIP-1β compared with controls. Conclusion Levels of 3 serum cytokines were significantly higher in RP patients than in age- and sex-matched controls. One of these 3 cytokines, IL-8, was not significantly elevated in RA samples. Overall, in RP, a more discrete group of cytokines exhibited significantly increased levels than was found in RA. Each of the 3 cytokines that were elevated in RP is a proinflammatory chemokine, characteristic of activation of the monocyte and macrophage lineage, and in the case of IL-8, also of neutrophils. These data suggest a major role for a cell-mediated immune response in the pathophysiology of RP.

A 60-year-old woman with rheumatoid arthritis had 4 pulmonary rheumatoid nodules with unchanged size since 1999 that appeared during methotrexate (MTX) treatment (Figure 1A). MTX was stopped. Because of persistent inflammatory joint pain with functional impairment, etanercept monotherapy (25 mg twice a week) was started in February 2003. After 21 months of treatment, in November 2004, the joint …

Relapsing polychondritis (RP) is a rare and severe disease which may lead to destruction of elastic cartilages. Until now, no reliable biomarker of disease activity in RP has been available. This study was designed to measure serum levels of cartilage biomarkers during both active and inactive phases of the disease.Serum levels of cartilage oligomeric matrix protein (COMP), chondroitin sulfate 846 epitope (CS846) of proteoglycan aggrecan and collagen type II collagenase cleavage neoepitope (C2C) were measured retrospectively in 21 subjects with RP. The Wilcoxon matched-pairs signed-rank test was used for statistical comparisons of biomarker levels in active and inactive phases of RP.Only the serum level of COMP was significantly increased during disease flares. Steroids did not alter the serum cartilage-related biomarker levels. However, during the active phase, C2C levels were significantly higher in steroid treated patients compared with non-steroid treated patients.This study suggests that serum COMP level may be useful for monitoring disease activity of RP. Further prospective studies are required to confirm this result.

To report early experience of switching anti-tumor necrosis factor-a (TNF-alpha) therapy from infliximab to etanercept in patients with spondyloarthropathy (SpA) and psoriatic arthritis (PsA).Thirteen patients with various SpA (7 with ankylosing spondylitis and 6 with undifferentiated SpA) and 2 patients with PsA were receiving infliximab. Because they were experiencing inadequate response or adverse events, therapy was changed to etanercept. Patients were evaluated for response to the change in anti-TNF-alpha therapy at baseline, after 3 months, and then every 6 months.During the mean 10-month followup after the change in therapy, 9 of 13 patients with SpA and both patients with PsA responded to etanercept and none experienced intolerance to this agent.These data suggest that switching between anti-TNF-alpha drugs may be useful for patients with SpA who are unresponsive or intolerant to a first anti-TNF-alpha agent.