Rheumatoid arthritis: relation of serum C-reactive protein and erythrocyte sedimentation rates to radiographic changes.

Amos, R S; Constable, T. J.; Crockson, R. A.; Crockson, A. P.; McConkey, B

doi:10.1136/bmj.1.6055.195

Cited by 251 publications

(77 citation statements)

References 5 publications

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“…Those patients with a higher ESR at baseline developed more erosions. Other studies have also identified elevated ESR as being predictive of radiographic progression (24)(25)(26). We were unable to correlate other baseline variables, including duration of arthritis, presence of rheumatoid factor, or clinical variables including the number of painful or swollen joints, with a worsening of the erosion score.…”

Section: Discussionmentioning

confidence: 99%

The effects of drug therapy on radiographic progression of rheumatoid arthritis. results of a 36‐week randomized trial comparing methotrexate and auranofin

Weinblatt

Polisson

Blotner

et al. 1993

Arthritis & Rheumatism

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Objective. To determine the effects of drug therapy (methotrexate [MTX] versus auranofin [AUR]) onradiographic progression in patients with active rheumatoid arthritis (RA).Methods. We conducted a 9-month randomized, multicenter, double-blind trial comparing MTX and AUR. Standardized radiographs of the hands and wrists were obtained at baseline and at completion of the study. Four experienced bone radiologists graded the radiographs for erosions, joint space narrowing, erosion healing, and reparative bone formation. Conclusion. The rate of radiographic progression in patients with RA, as measured by erosion score and joint space narrowing score, was demonstrated to be lower in those treated with MTX, as compared with AUR, over a 36-week period.The rate of radiographic progression is considered to be an important parameter of the efficacy of second-line therapy in rheumatoid arthritis (RA). Whether any second-line therapy in current use, including methotrexate (MTX), slows radiographic progression is uncertain (1,2). The clinical efficacy profile of MTX is, however, favorable, based on data from short-term randomized placebo-controlled trials (3-3, comparative studies with other second-line therapies ( 6 4 , and long-term prospective studies (9,lO). In a previously published report we described the clinical results of a 36-week multicenter study comparing MTX and auranofin (AUR) (11). The effect of treatment on radiographic activity has now been evaluated PATIENTS AND METHODSPatients. Two hundred eighty-one patients with active RA were enrolled in a multicenter double-blind trial comparing MTX and AUR (1 1). All patients had had inadequate disease response to at least 2 nonsteroidal antiinflammatory drugs (NSAIDs). Patients who had received prior treatment, of any duration, with gold salts, MTX, D-penicillamine, or cytotoxic agents were excluded from the study.Patients were randomized to receive either AUR (n = 143) or MTX (n = 138) for 9 months. (At 1 of the sites, only 1 patient was enrolled in the AUR group, and that patient was excluded from the efficacy analysis.) The initial dosage of AUR was 6 mg/day; this could be increased to 9 mg/day after 24 weeks of treatment, if there was a lack of a beneficial response with the lower dosage. The initial dosage of MTX was 7.5 mg/week, which could be increased to 15 mg/week between weeks 6 and 12 in patients who had not shown a clinical response. Patients were allowed to continue taking stable maintenance doses of background NSAIDs and/or prednisone (at a maximum dosage of 10 mg/day). Standard clinical assessments of arthritis activity were performed during the trial.Radiographic evaluation. Radiographs of the hands and wrists were obtained at baseline and at completion of the 9-month trial. A standardized protocol was used for obtaining these radiographs. All radiographs were taken on a single 30 X 35-cm cassette, with the patient in a posteroanterior position with the fingers slightly separated and the forearms flat. Each study center was provided with a Kodak (Ea...

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Section: Discussionmentioning

confidence: 99%

The effects of drug therapy on radiographic progression of rheumatoid arthritis. results of a 36‐week randomized trial comparing methotrexate and auranofin

Weinblatt

Polisson

Blotner

et al. 1993

Arthritis & Rheumatism

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“…In addition, rabbits treated with the antagonist exhibited a significant reduction in ESR (Fig. 8), a clinical measurement that correlates with the severity of RA (48).…”

Section: The Cxcr2 Antagonist Inhibits Lps-induced Joint Inflammationmentioning

confidence: 99%

A Potent and Selective Nonpeptide Antagonist of CXCR2 Inhibits Acute and Chronic Models of Arthritis in the Rabbit

Podolin

Bolognese

Foley

et al. 2002

The Journal of Immunology

146

112

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Much evidence implicates IL-8 as a major mediator of inflammation and joint destruction in rheumatoid arthritis. The effects of IL-8 and its related ligands are mediated via two receptors, CXCR1 and CXCR2. In the present study, we demonstrate that a potent and selective nonpeptide antagonist of human CXCR2 potently inhibits 125I-labeled human IL-8 binding to, and human IL-8-induced calcium mobilization mediated by, rabbit CXCR2 (IC50 = 40.5 and 7.7 nM, respectively), but not rabbit CXCR1 (IC50 = >1000 and 2200 nM, respectively). These data suggest that the rabbit is an appropriate species in which to examine the anti-inflammatory effects of a human CXCR2-selective antagonist. In two acute models of arthritis in the rabbit induced by knee joint injection of human IL-8 or LPS, and a chronic Ag (OVA)-induced arthritis model, administration of the antagonist at 25 mg/kg by mouth twice a day significantly reduced synovial fluid neutrophils, monocytes, and lymphocytes. In addition, in the more robust LPS- and OVA-induced arthritis models, which were characterized by increased levels of proinflammatory mediators in the synovial fluid, TNF-α, IL-8, PGE2, leukotriene B4, and leukotriene C4 levels were significantly reduced, as was erythrocyte sedimentation rate, possibly as a result of the observed decreases in serum TNF-α and IL-8 levels. In vitro, the antagonist potently inhibited human IL-8-induced chemotaxis of rabbit neutrophils (IC50 = 0.75 nM), suggesting that inhibition of leukocyte migration into the knee joint is a likely mechanism by which the CXCR2 antagonist modulates disease.

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“…These extraarticular changes include constitutional symptoms, such as malaise, fatigue, weight loss, and fever, an elevated erythrocyte sedimentation rate (ESR), decreased serum levels of iron and zinc, and an increase in hepatic synthesis of acute-phase proteins (APP), such as C-reactive protein (CRP) and serum amyloid A (SAA) protein. In clinical practice, levels of serum CRP are used to monitor the severity of joint inflammation in patients with RA (2), and several studies have found a positive correlation between persistently elevated CRP levels and progression of radiographic changes in the joints (3)(4)(5). It is now known that systemically active inflammatory cytokines are produced abundantly within the joints of patients with RA, released into the circulating blood, and consequently stimulate CRP production by the liver.…”

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confidence: 99%

The synovial expression and serum levels of interleukin‐6, interleukin‐11, leukemia inhibitory factor, and oncostatin m in rheumatoid arthritis

Okamoto

Yamamura

Morita

et al. 1997

Arthritis & Rheumatism

212

146

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Objective. To determine the expression of interleukin‐6 (IL‐6), IL‐11, leukemia inhibitory factor (LIF), and oncostatin M (OSM) and their major cellular sources in the joints of rheumatoid arthritis (RA) patients, as well as the correlation of circulating levels of these IL‐6‐type cytokines and C‐reactive protein (CRP). Methods. Messenger RNA (mRNA) and protein levels for IL‐6, IL‐11, LIF, and OSM were determined by using reverse transcription‐polymerase chain reaction and enzyme‐linked immunosorbent assay, respectively. Results. Cells isolated from the synovium of RA patients expressed mRNA for IL‐6, IL‐11, LIF, and OSM at higher levels than did synovial cells from osteoarthritis (OA) patients, and spontaneously released greater quantities of these proteins in culture. Fibroblast cell lines derived from RA synovium were able to produce IL‐6, IL‐11, and LIF, but not OSM, when stimulated with IL‐1 and tumor necrosis factor α. OSM was found to be produced spontaneously by synovial tissue macrophages. IL‐6, IL‐11, LIF, and OSM were present in synovial fluid from the RA patients; levels of IL‐6, LIF, and OSM were present in significantly greater quantities in RA patients than in OA patients. However, only IL‐6 was significantly elevated in the serum of RA patients and correlated with the serum CRP level, while other IL‐6‐type cytokines were not detected. Conclusion. IL‐6, IL‐11, LIF, and OSM are all produced in large amounts at the site of disease activity, but IL‐6 derived from synovial fibroblasts may be the major hormone‐like mediator that induces the hepatic synthesis of acute‐phase proteins in RA.

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Rheumatoid arthritis: relation of serum C-reactive protein and erythrocyte sedimentation rates to radiographic changes.

Cited by 251 publications

References 5 publications

The effects of drug therapy on radiographic progression of rheumatoid arthritis. results of a 36‐week randomized trial comparing methotrexate and auranofin

The effects of drug therapy on radiographic progression of rheumatoid arthritis. results of a 36‐week randomized trial comparing methotrexate and auranofin

A Potent and Selective Nonpeptide Antagonist of CXCR2 Inhibits Acute and Chronic Models of Arthritis in the Rabbit

The synovial expression and serum levels of interleukin‐6, interleukin‐11, leukemia inhibitory factor, and oncostatin m in rheumatoid arthritis

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