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Objective. To identify the relative contributions of clinical and laboratory variables, determined at baseline, in predicting the deterioration of radiographic damage 5 years after presentation in patients with inflammatory polyarthritis.Methods. Data from 439 subjects who sought primary care for inflammatory polyarthritis were analyzed. All subjects had paired radiographs, of which the first was obtained within 24 months of presentation and the second at 5 years after presentation. The contribution of baseline clinical and laboratory variables in predicting the degree of radiologic severity as judged by the Larsen score was assessed at both time points. Additionally, the role of these factors in predicting change after adjustment for baseline severity was also measured.Results. By 5 years, 49% of subjects had evidence of erosions. The median Larsen score on the first film was 2 (interquartile range [IQR] 0-10) and the median score on the followup film was 7 (IQR 1-25). These corresponded to a median deterioration of 3 (IQR 0-14) in all subjects, whereas those subjects with evidence of erosions at first film showed a median deterioration of 15 (IQR 6-29) on followup. The rheumatoid factor (RF) status, C-reactive protein levels, the presence of nodules, and number of swollen joints at baseline were all predictive of radiographic severity at first film. Not surprisingly, the baseline radiographic score was a predictor of severity of deterioration. However, after adjusting for baseline severity, a high titer of RF (>1:160) was also an independent predictor of deterioration over 5 years: individuals with an initial RF at that level had a progression in their Larsen score that was 2.3 times (95% confidence interval 1.7-3.2) higher than that in the RF-negative individuals. Apart from this, only age had an independent effect, after adjusting for baseline severity, in predicting increasing radiographic joint damage.Conclusion. High-titer RF is an important variable in predicting continuing severity of radiographic damage during the first 5 years after presentation with inflammatory polyarthritis.

The aims of this study were (i) to determine whether PlGF, VEGF and PlGF/VEGF heterodimers are detected in synovial fluid (SF) and plasma samples from patients with a range of arthropathies; (ii) to describe whether any correlation exists between SF PlGF, VEGF and PlGF/VEGF heterodimer levels and the total and differential SF leucocyte counts; and (iii) to investigate the regulation of peripheral blood mononuclear cell (PBMC) VEGF secretion by stimuli relevant to inflammatory joints. PlGF, VEGF and PlGF/VEGF heterodimer levels were measured in the SF and plasma of patients with a range of arthropathies and normal controls by ELISA. Western blotting for PlGF was performed on SF from three patients with rheumatoid arthritis (RA) and primary inflammatory arthropathies. VEGF was quantified in cell culture supernatants after stimulation with lipopolysaccharide (LPS), PlGF or cobalt ions of PBMC isolated from RA patients and controls. PlGF and VEGF were detected in all SF samples. PlGF/VEGF heterodimers were detected in 10.2% of SF samples, most frequently in RA samples. Western blotting confirmed the presence of PlGF in RA SF. PlGF was detected in 52% of RA and 31% of control plasma samples, and VEGF was detected in 38% of RA and 38% of control plasma samples. PlGF/VEGF heterodimers were detected in 21% of RA samples and none of the control samples. In primary inflammatory arthropathy patients, SF PlGF and VEGF levels correlated significantly with the SF total leucocyte count and the neutrophil count. PlGF was the most potent inducer of PBMC VEGF production in both RA and control subjects. This is the first report of the detection of PlGF and PlGF/VEGF heterodimers in the SF of patients with inflammatory arthropathies, and we have shown for the first time that PlGF up‐regulates PBMC VEGF production. PlGF may therefore play a key role in the production of VEGF in the inflammatory joint.

ObjectiveAnti–cyclic citrullinated peptide (anti-CCP) antibodies are a stronger predictor of the severity of rheumatoid arthritis than is rheumatoid factor (RF). Their role in predicting outcome in unselected patients with new-onset inflammatory polyarthritis (IP) has not been examined. The aims of this study were to examine the role of baseline RF and anti-CCP antibodies in determining the likelihood of patients having erosions at presentation or in predicting future radiologic damage, and to determine whether anti-CCP antibodies or RF is sufficiently robust to be clinically useful in guiding treatment decisions in early IP.MethodsPatients were recruited from the Norfolk Arthritis Register. Logistic regression models were fitted to test the ability of anti-CCP antibodies and RF to predict erosions. Further models were investigated to examine the role of anti-CCP antibodies in patients stratified by RF status.ResultsThe presence of anti-CCP antibodies at baseline was strongly associated with both prevalent erosions (odds ratio [OR] 2.53 [95% confidence interval (95% CI) 1.48–4.30]) and developing erosions at 5 years (OR 10.2 [95% CI 6.2–16.9]). These ORs were higher than those for RF (OR 1.63 [95% CI 0.94–2.82] and OR 3.4 [95% CI 2.2–5.2], respectively). The likelihood ratio (LR) for the prediction of prevalent erosions and erosions at 5 years was highest in the RF−subgroup (LR 2.2 and 5.8, respectively). However, 27% of anti-CCP−patients had developed erosions by 5 years.ConclusionDespite their strong association with the presence, development, and extent of erosions, anti-CCP antibodies alone are not a sufficiently accurate measure upon which to base clinical treatment decisions. Knowledge of anti-CCP antibody status is most informative in RF−negative patients.