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Acute-Phase Serum Amyloid A Regulates Tumor Necrosis Factor alpha and Matrix Turnover and Predicts Disease Progression in Patients With Inflammatory Arthritis Before and After Biologic Therapy

St. Vincent's University Hospital, Dublin Academic Medical Centre, The Conway Institute of Biomolecular and Biomedical Research, Dublin, Ireland.
Arthritis & Rheumatology (Impact Factor: 7.87). 04/2012; 64(4):1035-45. DOI: 10.1002/art.33455
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ABSTRACT In this study, we demonstrated a specific relationship between A-SAA and clinical disease activity in inflammatory arthritis, as measured by the SJC. Hepatic induction of acute-phase proteins including CRP is a nonspecific feature of systemic inflammation in response to diverse causes, including trauma, infection, and autoimmune disease (36). In contrast to other hepatic-derived acute-phase proteins, A-SAA at concentrations of up to 1,000 μg/ml has previously been reported in RASFs, which may exceed serum levels obtained in the same subjects (37). Measurement of serum A-SAA levels, which may be partly SF-derived, may therefore be a more accurate indicator of radiographic progression in clinical practice, although further direct comparison with high-sensitivity CRP may be useful. Although heterogeneous by diagnosis, the patients with RA and the patients with PsA in this cohort were indistinguishable in terms of disease duration and baseline radiographic damage prior to biologic therapy. The relatively high incidence of radiographic progression observed in both patients with RA and patients with PsA prior to biologic therapy is likely to be due to a combination of factors, including the high incidence of baseline structural damage, the long history of DMARD-resistant disease, incomplete adherence to therapy, and a relatively high rate of biologic monotherapy, which has been shown to be associated with worse radiographic outcomes (38).

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