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THU0112 Utility of Calprotectin Levels as a Marker of Remission in Rheumatoid Arthritis
  1. S. Garcia-Carazo1,
  2. E. de Miguel1,
  3. A. Martinez-Feito2,
  4. D. Pascual-Salcedo2,
  5. M. Arribas-Arribas2,
  6. T. Jermann3,
  7. M. Diaz4,
  8. E. Martin-Mola1,
  9. A. Balsa1
  1. 1Rheumatology
  2. 2Inmunology, la Paz University Hospital., Madrid, Spain
  3. 3Bühlman Laboratories AG, Schönenbuch, Switzerland
  4. 4Biostatistic, la Paz University Hospital., Madrid, Spain


Background Current treatment strategies in rheumatoid arthritis (RA) aim to remission or low disease activity. Composite indexes used in clinical practice to assess RA disease activity have good correlation with joint ultrasonography (US), but some patients clinically classified as in remission have subclinical synovitis which cannot be detected by clinical examination or acute phase reactants. We have previously shown that calprotectin correlates with disease activity (1) but it is not known if can be useful to detect patients who have achieved the therapeutic target in whom active synovitis is still present.

Objectives To investigate in RA patients who have achieved the therapeutic target (remission or low disease activity) if plasma calprotectin levels can be useful to classify patients in clinical remission or low disease activity using US as gold standard.

Methods RA patients taking DMARD or biological agents in clinical remission or low disease activity (DAS28-ESR<3,2) were included. Disease activity was also assessed by SDAI and CDAI. US examination was done by an US expert rheumatologist, in mode B and Power Doppler (PD) in 42 joints according to OMERACT definitions of pathology. Mode B evaluation combined the presence or absence of synovial hypertrophy and/or joint effusion (SH). Both SH and PD were graded using a semiquantitative scoring method (0-3). Calprotectin levels in plasma were determined by ELISA. Data were analysed using parametric or nonparametric test depending on variable distribution.

Results 82 patients, age 53.9±12.1 years, 69 (84%) female with a disease duration of 7.5±3.9 years were studied. 72 (87%) and 73 (89%) were anti-CCP and RF positive respectively. Mean DAS28 was 2.47±0.5 and 43 (52%) were in remission by DAS28 (DAS28<2.6) and 39 (48%) in low activity disease. Mean SDAI was 4.8±3.1, 26 (32%) were in remission by SDAI (SDAI<3.3) and 53 (65%) in low activity. 81 patients (99%) showed SH in US with a mean number of joints with SH of 9.02±7.7. PD was observed in 65 patients (64%) with a mean number of joints with PD of 3.5±2.8.

Calprotectin levels correlated with SDAI (r=0.34; p=0.001) and CDAI (r=0.34; p=0.002), but not with DAS28 (r=0.17; p=0.1). No correlation was observed between calprotectin and ESR (r=-0.08; p=0.9) or CRP (r=0.02; p=0.8). A significant correlation was found between Calprotectin levels and US PD in 42 joints (r=0.23; p=0.03), that was not found between Calprotectin and SH.

If we consider remission the absence of joints with PD signal, no differences were found by DAS28 between patients in remission and low disease activity (p=0.3), although differences were present by SDAI (p=0.007) and CDAI (p=0.003).

No differences in calprotectin levels were found between patients in US remission vs no US remission (0.9±0.7 vs 2.6±7.4; p=0.4).

Conclusions In patients in low disease activity or remission, calprotectin levels correlate with SDAI and CDAI but not with DAS28-ESR. Although, calprotectin levels correlate with the number of joints with PD signal it was not possible to accurately classify patients in US remission.


  1. García-Arias M. Calprotectin in rheumatoid arthritis: association with disease activity in a cross-sectional and a longitudinal cohort. Mol Diagn Ther. 2013 Feb;17(2):49-56

Disclosure of Interest S. Garcia-Carazo Grant/research support from: This work was supported by an unrestricted grant from UCB, E. De Miguel: None declared, A. Martinez-Feito: None declared, D. Pascual-Salcedo: None declared, M. Arribas-Arribas: None declared, T. Jermann: None declared, M. Diaz: None declared, E. Martin-Mola: None declared, A. Balsa Grant/research support from: This work was supported by an unrestricted grant from UCB

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