Arthritis & Rheumatism, Volume 60,
October 2009 Abstract Supplement

The 2009 ACR/ARHP Annual Scientific Meeting
Philadelphia October 16-21, 2009.


A-SAA Levels in Inflammatory Arthritis Patients Prior to Biologic Therapy Are Associated with Increased Cardiovascular Events in Longterm Follow-up

Ng,  Chin Teck, Mullan,  Ronan, Connolly,  Mary, FitzGerald,  Oliver, Bresnihan,  Barry, Fearon,  Ursula, Veale,  Douglas J.

Purpose:

The acute phase apoprotein Serum Amyloid A (A-SAA) is elevated in serum and is the best marker to correlate with disease activity in inflammatory arthritis. Several studies show that atherosclerotic cardiovascular (CV) disease is the primary cause of premature death in RA patients. A-SAA has been proposed as a potential prognostic biomarker for RA disease activity, however it may also be relevant as a biomarker for cardiovascular disease, possibly comparable to hs-CRP. The collagen cleavage neo-epitopes, C2C and C1–2C are specific for the destruction of type I and II collagens by the collagenases MMP-1, MMP-8 and MMP-13 and are elevated in arthritis and may be associated with CV remodelling. Aim: To determine serial serum A-SAA levels, collagen neoepitopes and CV events in a follow-up cohort of inflammatory arthritis patients, 4 years after starting on biologic therapy.

Method:

Patients were assessed at baseline, 1, 3, 6, 9, 12 and 48-months (m) after commencing anti-TNFa therapy. Twenty eight tender and swollen joint count (28-TJC, -SJC), CRP, DAS28-CRP score, and HAQ were measured at each assessment. Cardiovascular (CV) events were recorded at 48m. A-SAA levels were measured by ELISA at baseline, 1m and 3m. C2C and C1–2C were measured at baseline, 1, 3, 6, 9, and 12m. Statistical analysis was performed using SPSS 12 statistical software.

Results:

RA (n=45) and PSA (n=17) were followed up. At 48m, 8 patients developed one or more cardiovascular events since starting on anti-TNF therapy. Baseline A-SAA levels were significantly higher in patients with new CV events (CV+) at 48m follow-up compared to patients without CV events (CV-) [927.01ug/ml (285.88–3524.67) vs. 137.51ug/ml (2.44–1648.29), p< 0.05]. High A-SAA levels persisted at 1m and 3m post therapy in CV+ compared to CV-, where A-SAA levels decreased significantly after treatment at 1m and 3m (p<0.05). In contrast, there was no significant difference in CRP at baseline between the two groups. In addition, C2C and C1–2C levels remained higher at all time points in CV+ patients, and were associated with lower clinical responses (DAS28-CRP and HAQ) to anti-TNF therapy.

Conclusion:

High A-SAA levels at baseline, but not CRP, were associated with CV events in this long-term follow-up cohort. A-SAA may be a biomarker, but may also reflect a mechanism of action of CV disease in inflammatory arthritis.

To cite this abstract, please use the following information:
Ng, Chin Teck, Mullan, Ronan, Connolly, Mary, FitzGerald, Oliver, Bresnihan, Barry, Fearon, Ursula, et al; A-SAA Levels in Inflammatory Arthritis Patients Prior to Biologic Therapy Are Associated with Increased Cardiovascular Events in Longterm Follow-up [abstract]. Arthritis Rheum 2009;60 Suppl 10 :949
DOI: 10.1002/art.26028

Abstract Supplement

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