AB0201 Association between baseline calprotectin serum levels and response to biological therapy in patients with rheumatoid arthritis. (12th June 2018)

• Record Type: Journal Article
• Authors: Martinez-Feito, A.; Plasencia, C.; Jochems, A.; Navarro-Compan, V.; Pascual-Salcedo, D.; Hernández-Breijo, B.; Nozal, P.; Peiteado, D.; Villalba, A.; Mezcua, A.; Balsa, A.
• Is Part Of: Annals of the rheumatic diseases. Volume 77(2018)Supplement 2
• Page Start: 1286
• Page End: 1286
• Publication Date: 2018-06-12
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2018-eular.5537
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: Calprotectin (CLP) is an important proinflammatory factor of innate immunity released from activated granulocytes and macrophages during inflammation, which has also been identified in synovial fluid. It is a potential pro-inflammatory biomarker reflecting joint damage. CLP levels in synovial fluid are well correlated with levels in plasma, which allows measuring it easily in patients with rheumatoid arthritis (RA). However, the additional value of CLP over other biomarkers is unclear Objectives: To study the association of baseline CLP serum levels with the clinical response and serum drug levels in patients under biological therapy at 6 and 12 months after starting treatment. Methods: Prospective observational study including 109 patients with RA who started biological treatment (Infliximab(Ifx);Adalimumab(Ada);Etanercept(Etn);Certolizumab(Ctz);Golimumab(Glm); Tocilizumab(Tcz) and Rituximab(Rtx) in a tertiary hospital since 1999 to 2016. Serum CLP levels were measured by ELISA with the commercial kit CALPROLAB (Lysaker, Norway). Levels of biological drug and ADA were measured by capture and bridging ELISA respectively, except Certolizumab which was measured by Sanquin Diagnostic Service. Clinical response was assessed by ΔDAS28. Serological and clinical parameters were evaluated at baseline, 6 and 12 months. For analysis, linear regression models adjusted for confounders (age, sex, BMI, DMARDs, smoking status) and with standardised beta as estimate were employed. Results: Out of 109 studied patients, 22% patients received Ifx, 6% Ada, 16% Etn, 18% Ctz, 5% Glm, 25% Tcz and 9% Rtx. Most patients were woman (84%), with a median (IQR) age of 62 (52.3–73.1) and disease duration of 9.5 (4.8–15.3). At baseline, CLP levels directly correlated well with CRP and DAS28(r=0.411;p<0.001 and r=0.308; p<0.001). On the other hand, an inverse correlation between baseline CLP levels and the presence of drug at 6 (β=−0.325;p=0.01) and 12 months (β=−0.397; p<0.001) was also found. Moreover, in the adjusted analyses a trend for this correlation at 6 months (β=−0.199; p=0.07) and a significant correlation at 12 months (β=−0.381; p<0.001) was observed. Additionally, in the non-adjusted models, baseline CLP levels significantly directly correlated with the clinical response at 6 months (β=0.194; p=0.04) while the correlation at 12 months was not significant (β=0.186; p=0.06). However, after adjusting for confounders, no significant correlation was found at any study point (β=0.213; p=0.06 at 6 months and β=0.206; p=0.07 at 12 months). Conclusions: In patients with RA initiating biological therapy, baseline CLP concentrations are inversely correlated with the circulating drug levels along the treatment. However, the additional value of CLP as a predictor of clinical response remains unclear. Acknowledgements: This work has been supported by a SORCOM grant at 2016 Disclosure of Interest: None declared