[Autoantibodies, diagnostic and prognostic markers of rheumatoid polyarthritis].
AN IMPORTANT CLINICAL TOOL: A sensitive and specific marker allowing the diagnosis of rheumatoid arthritis, and even more importantly an early assessment of severity, would be a highly valuable clinical tool. Autoantibodies have been found to be quite useful in clinical practice for diagnosis and assessing prognosis. EARLY-STAGE RHEUMATOID ARTHRITIS: Ideally, the marker should be sensitive and specific when the first signs of the disease develop. To date, only the rheumatoid factor and anti-filaggrin antibodies (including anti-stratum comeum or "anti-keratin" and anti-perinuclear factors) have been used with sufficiently acceptable standards. IgM rheumatoid factors can be detected in about 80% of patients with rheumatoid arthritis but they lack specificity since they are also found in other auto-immune conditions (lupus, Sjögren's syndrome), in chronic infections, and in certain lymphoproliferative syndromes (with or without cryoglobulinemia). Anti-filaggrin antibodies are more specific (70 to 100% depending on the study) but can only be detected in 30 to 50% of the patients. High titers of rheumatoid factors (IgM and/or IgA) and anti-filiggrin antibodies are factors of poor prognosis because they are associated with destructive polyarthritis, sometimes complicated with extra-articular signs (nodules, vasculitis). Among the new autoantibodies being studied, only anti-Sa appears to have real diagnostic and prognostic value. The recent data must be confirmed. STRATEGIES FOR OVERT DISEASE: Systematic and repeated assay of autoantibody levels is not warranted in patients with overt disease. Anti-Ro-SS/A, ANCA can however, in some cases, detect unusual complications. THREE STRATEGIES WOULD BE PARTICULARLY INTERESTING: The first is to search for highly specific markers with the aim of identifying a subgroup of rheumatoid arthritis patients as early as possible who have specifically defined clinical, biological and disease-progression criteria. The second is to validate composite scores integrating autoantibodies to achieve early definition of disease severity. The third is to search for markers of progression, particularly autoantibodies, that could modulate inflammatory processes and osteo-cartilaginous degeneration.
Sibilia
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Service de Rhumatologie, CHU Hautepierre, Strasbourg.
D019268:Antibodies, Antineutrophil Cytoplasmic / Q000276:immunology; D000918:Antibody Specificity; D001172:Arthritis, Rheumatoid / Q000175:diagnosis* / Q000276:immunology; D001323:Autoantibodies / Q000032:analysis*; D015415:Biomarkers; D004797:Enzyme-Linked Immunosorbent Assay; D004817:Epidermis / Q000276:immunology; D000091344:Filaggrin Proteins; D005455:Fluorescent Antibody Technique; D006801:Humans; D007075:Immunoglobulin M / Q000032:analysis; D007381:Intermediate Filament Proteins / Q000276:immunology; D007633:Keratins / Q000276:immunology; D009195:Peroxidase / Q000276:immunology; D011379:Prognosis; D012217:Rheumatoid Factor / Q000032:analysis; D012261:Ribonucleoproteins / Q000276:immunology; D012680:Sensitivity and Specificity
D019268:Antibodies, Antineutrophil Cytoplasmic; D001323:Autoantibodies; D015415:Biomarkers; C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D007075:Immunoglobulin M; D007381:Intermediate Filament Proteins; D012261:Ribonucleoproteins; D007633:Keratins; D012217:Rheumatoid Factor; D009195:Peroxidase