Autoantibodies predicting the outcome of rheumatoid arthritis: evaluation in two subsets of patients according to severity of radiographic damage

Abstract

Objective-Autoantibodies such as rheumatoid factor (RF), antikeratin antibodies (AKA), antiperinuclear factor (APF), and anti-RA 33 antibodies are considered of value for the diagnosis of RA. The purpose of this study was to evaluate these autoantibodies as predictors of severe radiographic damage in rheumatoid arthritis (RA). Patients and methods-Eighty six patients with RA (70 women, 16 men) fulfilling 1987 ACR criteria were selected from a cohort of 469 patients followed up since the first year of RA onset because they could be divided in two groups according to the severity of the radiographic damage. These 86 patients had a mean (SD) disease duration of eight (four) years: 43 patients had severe radiographic damage (Larsen score >2) and 43 had limited radiographic damage (Larsen score < 2). The two groups were matched by disease duration and sex. The following autoantibodies were looked for: RF, ANA, AKA, APF, and anti-RA 33 antibodies. In addition, HLA class II DR alleles and standard inflammatory parameters (erythrocyte sedimentation rate, C reactive protein) were determined. Results-Patients with severe radiographic damage diVered from those with limited radiographic damage in that they had higher RF (p=0.01), APF (p<0.02), and AKA (p=0.001) titres. Stepwise regression analysis was done to calculate the odds ratios (OR) for each clinical and laboratory variable; only presence of cutaneous nodules (OR: 14.9; 95% CI: 7, 128), HLA DRB1*04 or DRB1*01 (OR: 7.53; 95% CI: 1.32, 42.9), AKA (OR: 3.11; 95%, CI: 0.58, 16.8 ), a high erthrocyte sedimentation rate (OR: 2.66; 95% CI: 0.60, 11.9), and a high C reactive protein value (OR: 7.4; 95% CI : 1.43, 38.1) were predictive of severe radiographic damage. Conclusion-These data suggest that the risk of severe radiographic damage in RA patients is higher when cutaneous nodules, HLA DRB1*04 or DRB1*01, and/or AKA are present. The other autoantibodies of diagnostic significance are of little help for predicting joint destruction.

The Major Synovial Targets of the Rheumatoid Arthritis-Specific Antifilaggrin Autoantibodies Are Deiminated Forms of the α- and β-Chains of Fibrin

“…Their presence and titer are related to the disease activity and severity (1,2,17), their ratio to global IgG is increased in the synovial membrane interstitium with regard to the serum or the synovial fluid, and they are synthesized by plasmocytes of the rheumatoid pannus (18). The above points strongly suggest that AFA are implicated in the pathophysiology of RA.…”

How to diagnose rheumatoid arthritis early: A prediction model for persistent (erosive) arthritis

“…In doing this, the models can be considered to be overall diagnostic tests, and the estimated probabilities for each patient are then the test results. The discriminative abilities of the different diagnostic models were compared with each other and with a diagnostic model formed by the list version of the ACR 1987 classification criteria (22). In the diagnostic model formed by the ACR 1987 classification criteria, all individual criteria had the same weight.…”

Autoimmune Response to Post‐Translationally Modified (Citrullinated) Proteins: Prime Suspect in the Pathophysiology of Rheumatoid Arthritis

“…More directly concerning ACPA, and suggesting that they are not neutral to the disease course, is the notion that the presence of ACPA in the serum is not a consequence of chronic synovitis since it occurs early in the disease course [57][58][59][60][61][62][63][64][65][66][67][68][69] and, further, frequently predates for several years the appearance of clinical signs of RA, a fact acknowledged in the early 1990s when the antibodies were still called AKA [70], and confirmed later with the first commercially available ACPA assays [71][72][73]. In addition a positive association of their presence and/or titre with the intensity of radiologically observed joint damage has been reported in numerous not only cross-sectional [74][75][76][77][78][79][80][81][82][83], but also longitudinal [64,68,[84][85][86][87][88][89][90][91][92][93][94][95][96][97] studies, unravelling the high prognostic value of these powerful diagnostic markers.…”