AB0497 SERUM CALPROTECTIN IN SYSTEMIC LUPUS ERYTHEMATOSUS: IS IT A GOOD ACTIVITY BIOMARKER?

Background Clinical manifestations of systemic lupus erythematosus (SLE) and infections sometimes are difficult to distinguish. In clinical practice low complement and anti(ds)DNA levels are used to assess lupus activity but its determination usually requires some days. Leukocyte count, CRP and ESR cannot discriminate SLE from infectious processes. Calprotectin could be a good biomarker to assess lupus activity since it is more specific than CRP and ESR and faster to analyse than anti(ds)DNA. Objectives Our aim is to determine serum calprotectin levels in patients with SLE, and its correlation with analytical and clinical manifestations, especially with disease activity. Methods A total of 148 patients were included. All patients included fulfilled the SLE criteria (SLICC 2012). A quantitative ELISA analysis was performed to assess levels of serum calprotectin (CALPRO AS, Norway). Other biomarkers of lupus disease activity were also assessed (levels of anti(ds)DNA, hypocomplementemia, ESR and CRP). Clinical variables and activity/damage index (SLEDAI/SLICC) were also evaluated. The study was approved by the Clinical Research Ethics Committee of the hospital and all patients signed an informed consent. The results were compared with a healthy control group of similar age and sex (n=20). Results 134 patients (92%) were women with a mean age of 46±12 years and an average SLE evolution of 12±7 years. Mean SLEDAI was 2±2 (105 inactive [ 13]). Mean SLICC was 0.31±0.70. No significant differences were observed in serum calprotectin levels between patients with SLE and healthy controls (2.93±2.35 vs 2.17±1.49 µg/mL, p=0.160). Calprotectin was positively correlated with CRP (r=0.447, p= 100UI/mL) had higher calprotectin compared to patients with lower anti(ds)DNA (3.20±2.63 vs 2.42±1.57 µg/mL; p=0.027), however this pattern was not observed with hypocomplementemia. Contrary to what we expected, we did not observe significant differences on calprotectin levels depending on SLEDAI index classification (cutoff at 4 and 12). Moreover, no differences were observed on calprotectin levels between those patients with/without clinical manifestations such as serositis, arthritis or glomeruloneprhitis. Patients with antiphospholipid antibodies had higher calprotectin levels (3.75±2.04 vs 2.77±2.38 µg/mL;p=0.045). Conclusion Serum calprotectin levels were positively correlated with CRP levels and leukocyte count. Patients with higher anti(ds)DNA levels had higher calprotectin levels, however we did not observe significant differences depending on SLEDAI index or the presence of arthritis, serositis neither glomerulonephritis. Even that calprotectin determination is faster than anti(ds)DNA levels and could be helpful in assessing inflammatory activity. There is an interesting relation between antiphospholipid antibodies and calprotectin. This study should be continued in a larger sample of active SLE patients to assess its utility in clinical practice as a discriminating biomarker for flares and even infection Disclosure of Interests None declared