Arthritis & Rheumatism, Volume 63,
November 2011 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Chicago, Illinois November 4-9, 2011.


EDTA Resistant S100A12 Complexes (ERAC) In Serum of Patients with Coronary Artery Disease (CAD) with and without Inflammatory Rheumatic Disease (IRD).

Hollan1,  Ivana, Kass2,  Anita, Lyberg3,  Torstein, Almdahl4,  Sven M., Forre3,  Øystein T., Mikkelsen5,  Knut, Fagerhol3,  Magne

Lillehammer Hospital for Rheumatic Diseases, Lillehammer, Norway
Betanien Hospital, Skien, Norway
Oslo University Hospital, Oslo, Norway
University Hospital of North Norway, Tromsø, Norway
Lillehammer Hosp for Rheumatic Diseases, Lillehammer, Norway

Background/Purpose:

ERAC is a recently discovered high molecular weight protein fraction containing the leukocyte derived protein S100A12. In contrast to most S100A12 complexes, these complexes do not dissociate after addition of EDTA. The purpose of this study was to compare the occurrence of serum ERAC positivity in patients with CAD with and without IRD, in IRD patients without CAD, and in healthy controls (HC).

Methods:

We examined 4 groups involved in Feiring Heart Biopsy Study: patients with IRD referred to coronary artery bypass graft (CABG) (CAD+IRD), patients without IRD, referred to CABG (CAD-nonIRD), patients with IRD without CAD (IRD-nonCAD), and HC. ERAC was examined in serum by a quantitative rapid test based on monoclonal antibodies and lateral flow principle. ERAC positivity was defined as ERAC>4mg/L.

Results:

There were no significant relationships between ERAC positivity and traditional cardiovascular risk factors, CRP and acute coronary syndromes. The relationship between ERAC and CAD-IRD remained statistically significant after the adjustment for group, age and gender (OR=3.9, 95%CI:1.2–12.9, p=0.024). In age- and sex- adjusted analysis of all patients with IRD, ERAC positivity was related to CAD (OR=9.9, 95%CI:2.4–41.0, p=0.002). Similar relationship, independent of RA activity and duration, was observed also within the RA subgroup. The HC patient with ERAC highly positive (49 years old, ERAC=10000) was diagnosed with CAD (requiring CABG) within 1 year.

Table 1.

 CAD+IRD (n=56)*CAD-nonIRD (n=46)IRD-nonCAD (n=29)**HC (n=26)p
Male sex, no. (%)35 (63)30 (65)8 (28)16 (62)0.006
Age, mean±SD67.7±10.067.5±8.758.2±9.957.3±9.6<0.0005
ERAC positive, no. (%)̂27 (48)5 (11)4 (14)5 (19)<0.0005
* Patients with RA (n=21), giant cell arteritis/polymyalgia rheumatica (17), spondyloarthritis (14), connective tissue diseases (4). There was no significant difference in ERAC positivity between these IRD subgroups.** Patients with RA. ̂ ERAC>100 mg/L occurred in three (5.4%) CAD-IRD patients, in no CAD+IRD patients, and in 1(3.8%)HC.

Conclusion:

Patients with CAD and IRD had higher occurrence of ERAC than patients with CAD or IRD only, and than HC. Within IRD patients, the occurrence of ERAC was related to CAD. Thus, ERAC might be a biomarker of CAD in IRD. Further studies on ERAC may increase insights into the pathogenesis of accelerated CAD in IRD.

To cite this abstract, please use the following information:
Hollan, Ivana, Kass, Anita, Lyberg, Torstein, Almdahl, Sven M., Forre, Øystein T., Mikkelsen, Knut, et al; EDTA Resistant S100A12 Complexes (ERAC) In Serum of Patients with Coronary Artery Disease (CAD) with and without Inflammatory Rheumatic Disease (IRD). [abstract]. Arthritis Rheum 2011;63 Suppl 10 :1052
DOI:

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