Abstract
Rheumatoid arthritis (RA) is a common autoimmune disease in which a heterogeneous course and different pathogenic mechanisms are implicated in chronic inflammation and joint destruction. Despite the diagnostic contribution of anti-citrullinated protein/peptide antibodies (ACPAs) and rheumatoid factors, about one-third of RA patients remain seronegative. ACPAs belong to a heterogeneous family of autoantibodies targeting citrullinated proteins, including myelin-basic protein, several histone proteins, filaggrin and fibrin, fibrinogen or vimentin. In addition to ACPAs, antibodies directed against other post-translationally modified-carbamylated proteins (anti-CarP) were detected in up to 30% of ACPA-negative patients. Using phage display technology, further autoantibodies were recently discovered as candidate biomarkers for seronegative RA patients. Furthermore, in clinical practice, ultrasound may reveal subclinical synovitis and radiographically undetected bone erosions. To improve diagnostic certainty in undifferentiated arthritis and seronegative patients, ultrasound imaging and several new biomarkers may help to identify at risk patients and those with early disease. In this commentary we summarize recent advances in joint ultrasound and future potential of serological biomarkers to improve diagnosis of RA.
Highlights
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation and joint damage with a heterogeneous course and different pathogenic mechanisms leading to common signs and symptoms [1]
The other group of novel serological markers identified by proteomic approach represents antibodies to Peptidyl arginine deiminase 4 (PAD4) and BRAF (v raf murine sarcoma viral oncogene homolog B1) catalytic domain open new avenues to further pinpoint anti-citrullinated protein/peptide antibodies (ACPAs)-negative RA patients [3]
Despite many unanswered questions in the understanding of the mechanisms driving the immunological changes seen during the development of RA, there is evidence that systemic abnormalities defined as the presence of RA-related autoantibodies can occur several years before clinical symptoms appear
Summary
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation and joint damage with a heterogeneous course and different pathogenic mechanisms leading to common signs and symptoms [1]. It is not easy to summarize the wide range of US findings that may be candidates for the role of useful diagnostic and prognostic biomarkers in patients with arthritis [7] These include: fluid collections, synovial hypertrophy, cartilage abnormalities, bone erosions, crystal aggregates, tendon damage, entesophytes, increased soft tissue perfusion (Figures 1 and 2). The persistence of intensely perfused areas of synovial hypertrophy inside the joint is a reliable indicator of inadequate response to therapy Patients with this type of active synovitis should be carefully monitored and their treatment schedules modified, even if clinical response appears encouraging. Special attention should be paid to identifying areas where the perfused synovial pannus is in close contact with bone or cartilage In these areas, early signs of circumscribed anatomical damage can be seen (Figure 3). The other group of novel serological markers identified by proteomic approach represents antibodies to PAD4 (peptidyl arginine deiminase 4) and BRAF (v raf murine sarcoma viral oncogene homolog B1) catalytic domain open new avenues to further pinpoint ACPA-negative RA patients [3]
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