Rheumatology 2000; 39: 1082-1088
© 2000 British Society for Rheumatology
Association of rheumatoid factors and anti-filaggrin antibodies with severity of erosions in rheumatoid arthritis
Division of Rheumatology, Department of Internal Medicine, University Hospital, Geneva,
1 Quality of Care Unit and Institute of Social and Preventive Medicine, University Hospital, Geneva,
2 Department of Rheumatology and Clinical Immunology/Allergology, Inselspital, Bern,
3 Transplantation Immunology Unit, Department of Internal Medicine, University Hospital, Geneva and
4 Division of Immunology and Allergology, Department of Internal Medicine, University Hospital, Geneva, Switzerland
Objectives. To evaluate and to compare the association of two types of autoantibodies—rheumatoid factors (RF) and anti-filaggrin antibodies (AFA)—with clinical severity and joint damage progression in rheumatoid arthritis (RA) patients.
Methods. In a cross-sectional study, we determined RF and AFA titres in 199 RA patients and 65 controls. Erosions apparent on X-rays were quantified using the Larsen score in 143 patients, and the distribution of these scores was studied according to disease duration in patients who were positive and negative for RF and AFA.
Results. RF were detected in 72% and AFA in 47% of RA patients. AFA were highly specific for RA (100%). RF positivity was correlated with the presence of subcutaneous nodules, sicca syndrome and the severity of erosions for a given disease duration. AFA positivity was correlated only with the presence of the HLA-DRB1 shared epitope.
Conclusions. Since no significant correlation was observed between joint damage progression and AFA positivity, the determination of AFA does not appear to be useful in assessing the prognosis of RA. However, AFA, which appear early in RA, could be helpful for the diagnosis of RA in patients who do not fulfil four American College of Rheumatology criteria.
KEY WORDS: Rheumatoid factors, Anti-filaggrin antibodies, Rheumatoid arthritis, Erosion, Larsen score, Prognosis.
Correspondence to: S. Bas, Research Laboratory, Division of Rheumatology, University Hospital, 1211 Geneva 14, Switzerland.
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