Article
Soluble vascular cell adhesion molecule-1 and S100A12 reflect disease activity in patients with rheumatoid arthritis treated with etanercept versus disease-modifying anti-rheumatic drugs
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Published: | August 29, 2016 |
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Background: Markers in rheumatoid arthritis (RA) are warranted to objectively estimate disease activity. Serum soluble vascular adhesion molecules and phagocyte-specific S100A12 (calgranulin C) are excellent candidates. We aimed to compare such markers to C-reactive protein (CRP), disease activity score (DAS 28), health assessement questionaire (HAQ) and visual analogue pain scale (VAS) (pain: 0-100).
Methods: This prospective clinical pilot study compared 10 ACR/EULAR-positive RA patients adequately responding to disease-modifying anti-rheumatic drugs (DMARDs) to 10 RA patients inadequately responding to DMARDs with subsequent etanercept (ETA) therapy, and to age- and gender-matched healthy controls (HC). Soluble serum isoforms of vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1) and E-selectin (sELAM) were measured using commercially available ELISAs at baseline, after four (only ETA) and 12 months following initiation of ETA. S100A12 was measured in parallel by in-house ELISA.
Results: In DMARD-patients, the VAS averaged 21.0±11.3 and 20.2±24.6 (p=0.9). In ETA-patients, the VAS decreased from 46.3±7.9 (baseline) to 23.9±7.1 (p=0.04) and 24.0±6.3 (p=0.04). In DMARD-patients, the DAS28 remained at 2.1±0.6 and 2.9±1.0 (p=0.06). In ETA-patients, it decreased from 3.8±0.4 (baseline) to 2.8±0.3 (p=0.08) and to 2.5±0.3 (p=0.01). CRP levels were not significantly different in both groups. At baseline, sVCAM-1 (pg/ml) was significantly higher in ETA-patients as compared to DMARD-patients and HCs (642.6±124.5 vs. 194.3±90.2; p<0.0001 vs. 344.5±232.8; p=0.003, respectively). After 12 months, sVCAM-1 was still higher in ETA-patients as compared to DMARD-patients (747.0±270.5 vs. 392.9±290.4; p=0.01). sICAM-1 and sELAM-1 were similar in both patient groups and HCs. Serum levels of S100A12 (ng/ml) were significantly higher at baseline in ETA-patients as compared to DMARD-patients and HCs (139.2±91.8 vs. 37.5±17.8; p=0.003 vs. 72.5±32.9; p=0.045, respectively). After 12 months, S100 numerically decreased with ETA treatment compared to baseline and was similar to DMARD-patients (73.3±64.0; p=0.08 vs. 86.3±131.3, p=0.8; respectively). In DMARD-patients, S100 did not change after 12 months.
Conclusion: Similar to collagen diseases, sVCAM-1 was a strong marker for ETA-patients as compared to DMARD-patients. Unlike sVCAM-1, S100A12 numerically decreased after treatment with ETA and DAS remission. sVCAM-1 seems to be a persistent marker for disease severity and high levels may indicate the requirement for anti-TNF-α agents. S100A12 may reflect remission. Higher patient numbers are needed.
Disclosures: In part supported by Pfizer.