Early rheumatoid arthritis: can we predict its outcome?

Abstract

The continuing trend towards more aggressive treatment of rheumatoid arthritis (RA) has seen an increasing interest in the early phase of this chronic inflammatory disease. Optimal benefit from present and emerging therapies is limited by our prognostic abilities during this period. The present review attempts to outline first the many methodological issues encountered in studies of early RA, and second the extent to which each major outcome measure can be explained, both by readily available clinical variables and by HLA-DR genotyping. The evidence supporting the clinical usefulness of genotyping is discussed separately. Based on this information, a clinically appropriate approach to the management of early RA and the identification of patients suitable for experimental therapies is suggested.

Preparation and properties of conductive polyaniline/poly‐ω‐aminoundecanoyle fibers

“…RA disease activity and inflammation have been associated with progression of cardiovascular disease and increased mortality rates in previous studies (1). An important observation is the discordance between high levels of hsCRP and low values for clinical markers (swollen joint count, modified Health Assessment Questionnaire, and patient's assessments of pain and well‐being) and for traditional biochemical markers (ESR and CRP) of disease activity (8). Unlike the first‐generation CRP assay (which was not suitable for predicting CAD), the high‐sensitivity assay has not been assessed as a disease activity marker in RA and may be more sensitive to subclinical disease.…”

“…All study subjects completed a questionnaire to assess smoking status, family history of vascular events, education level, and current medication use. The activity and extent of RA were measured with the swollen joint count (28 joints counted), the modified Health Assessment Questionnaire (calculated score between 0 and 3), average duration of early morning stiffness (in minutes, as estimated by the patient), and patient's assessment of pain and global well‐being (on 10‐cm linear visual analog scales) (8).…”

“…The pathogenic events in atherosclerosis share many similarities with synovial inflammation in RA: activation of inflammatory cells and increased expression of adhesion molecules and cytokines (7). C‐reactive protein (CRP) is a well‐established disease activity marker in RA (8), and when measured by high‐sensitivity assay (hsCRP), it is predictive of atherosclerosis in the general population (9). Hence, inflammation may contribute to increased vascular disease risk in RA by promoting endothelial and vascular wall damage.…”

The Integration of Molecular Diagnostics With Therapeutics

“…A number of groups have studied patients with rheumatoid arthritis to learn whether germline-based SNP detection or biomarker assays performed on serum or synovial fluid could predict the development of erosive disease and guide the selection of therapy. 77,78 Patients with inflammatory bowel disease have been tested for biomarkers of disease severity as a method of selecting local vs systemic drug therapy. 79,80 In addition to classic measurements of known risk factors, new strategies for predicting the risk of early-onset coronary atherosclerosis have emerged that use well-established traditional biomarkers such as serum C-reactive protein levels in new ways 81 and novel biomedical imaging and molecular diagnostic tests.…”

Tumour necrosis factor inhibitors: risks and benefits in patients with rheumatoid arthritis

“…Best evidence-based practice involves early diagnosis, risk stratification, and aggressive treatment in patients with poor prognostic factors (Table 1). 3,4 Disease modifying anti-rheumatic drugs (DMARD) are the mainstay of early treatment. In patients at risk of erosive disease, combination DMARD therapy is superior to monotherapy without a measurable increase in toxicity.…”