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SAT0200 Clinical Application of the Soluble Lectin-Like Oxidized LDL Receptor-1 (SLOX-1) in Rheumatoid Arthritis: from Bench to Bedside
  1. M. Ishikawa1,2,
  2. H. Ito1,2,
  3. M. Furu1,2,
  4. M. Hashimoto2,
  5. T. Fuji2,3,
  6. S. Matsuda1,
  7. T. Mimori2,3
  1. 1Dept. of Orthopedic Surgery, Graduate school of Medicine, Kyoto University
  2. 2Dept. of the Control for Rheumatic Diseases
  3. 3Dept. of Rheumatology and Clinical Immunology, Kyoto University, Kyoto, Japan

Abstract

Background Previously, we have reported that levels of sLOX-1 (soluble Lectin-like oxidized LDL receptor 1) in the plasma of RA patients were significantly higher than those in healthy controls, and the anti-cytokine therapies decreased the sLOX-1 level in plasma.

Objectives Then, we investigated whether sLOX-1 levels are associated with RA disease activity or remission using a cohort study

Methods The study examined 278 RA patients (female 84.9%) in the cohort. Levels of sLOX-1 in plasma were measured by ELISA. To evaluate the correlation with sLOX-1, VAS, CRP, ESR, MMP-3, autoantibody status, the number of swollen and tender joints, DAS-ESR, SDAI, and Boolean-based remission were measured in all patients.

Results The levels of sLOX-1 in RF-positive or ACPA-positive RA were significantly higher than that in RF-negative or ACPA-negative RA. Levels of sLOX-1 in the patients with remission significantly lower than those with moderate disease activity. In the subgroup of patients who were not achieving Boolean-based remission, sLOX-1 level in RF-positive or ACPA-positive RA were significantly higher than that in RF-negative or ACPA-negative RA. In contrast, in the subgroup of patients who were achieving Boolean-based remission, the levels of sLOX-1 in ACPA-positive RA were not significantly higher than that in ACPA-negative RA.

Conclusions These results suggest that the levels of sLOX-1 in the patients who are not achieving remission, especially ACPA-positive RA, increase to reflect disease activity. Therefore, sLOX-1 levels may be useful to evaluate the therapeutic effects of the anti-cytokine therapies.

References

  1. Sawarura T, et al. Nature 1997; 386

  2. Nakagawa T, et al. Arthritis Rheum 2002; 46, 2486-94.

  3. Kakimuma T, et al. Arthritis Rheum 2004; 50, 3495-503.

  4. Ishikawa M, et al. Arthritis Rheum 2012; 64, 1024-34.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.2628

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