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SAT0181 CXCL4 Is Not A Biomarker in Rheumatoid Arthritis Patients Treated with Abatacept and Tocilizumab
  1. V. D'abrosca,
  2. S. Vettori,
  3. G. Cuomo,
  4. D. Iacono,
  5. G. Valentini
  1. Rheumatology Section Departement of Clinical and Experimental Medicine, Second University of Naples, Naples, Italy


Background CXCL4 (platelet factor4, PF4) is a pleiotropic α-granules chemokine, produced by platelets, dendritic cells, macrophages and neutrophils. Recently, CXCL4 levels have been found to increase under treatment with infliximab, in unresponsive Rheumatoid Arthritis (RA) patients [1]. At present, the influence of non TNFalfa blockers biological DMARDs (Abatacept and Tocilizumab) on CXCL4 serum levels not have been investigated in RA.

Objectives To investigate CXCL4 serum levels in RA patients naïve for biological disease-modifying anti-rheumatic drugs (bDMARDs) at baseline and after 1-year treatment and look for associations with disease features at baseline and distinct biological therapy overtime.

Methods Fifty-six RA were enrolled in the study at the time of initiating a treatment with a biological DMARD. CXCL4 serum levels were investigated by a multiplex suspension immunoassay at baseline and after 1 year and compared with those detected in 30 healthy controls. Epidemiological, clinical and serological features of RA patients at baseline are showed in table 1.

Results Out 56 RA patients, 39 (70%) were assigned to an anti-TNF-α treatment (3 patients to Infliximab, 12 to Etanercept, 24 to Adalimumab); 10 to Abatacept and 7 to Tocilizumab.

At baseline, CXCL4 serum levels were found to be increased in RA patients as compared to controls but the difference was not significant (1,538 ng/ml vs 1.26 ng/ml, p=0.082). Moreover, CXCL4 levels were not found to be related to any disease feature. At baseline, 6 (10%) RA patients presented serum CXCL4 levels exceeding the 95th percentile of the values detected in controls (4.569 ng/ml). These patients did not differed from the remaining RA patients in any feature. After 1 year of treatment, CXCL4 levels increased with respect to basal values in the whole series (3.280 ng/ml vs 1.538 ng/ml, p<0.0001). However, a different trend was detected in patients undergoing distinct treatments: CXCL4 serum levels were found to increase after 1 year in patients treated with anti-TNF agents (3.595 ng/ml, vs 1,241 ng/ml, p<0.0001); on the contrary, CXCL4 levels at 1-year remained unchanged in patients treated with Abatacept (4.160 ng/ml vs 2.030 ng/ml, p=0.21) and with Tocilizumab (3.310 ng/ml, vs 3.290 ng/ml, p=0.6). At 1-year follow-up, 32 patients could be considered responsive to the treatment (R); 24 (43%) were non-responder (NR). No difference was detected in the change of CXCL4 over time, comparing the 32 responsive to treatment with the 24 unresponsive patients.

Conclusions Similarly to previous studies (1) we found an increase in CXCL4 serum levels in patients undergoing an antiTNFa agent, but we failed to find differences between responsive and unresponsive patients. Moreover, we found that treatment with Abatacept and Tocilizumab did not modify CXCL4 serum level. Finally, we failed to detect any correlation between CXCL4 levels and any disease feature both at baseline and during follow-up.

  1. Trocmé C., et al. Ann Rheum Dis. Aug 2009; 68(8): 1328–1333

Disclosure of Interest None declared

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