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OP0090 Serum CD163/Tweak Ratio Predicts Clinical Course of Digital Ulcers in Patients with Systemic Sclerosis
  1. O. Kowal-Bielecka1,
  2. M. Bielecki2,
  3. B. Trzcinska-Butkiewicz3,
  4. M. Michalska-Jakubus4,
  5. M. Brzosko3,
  6. D. Krasowska4,
  7. K. Kowal5
  1. 1Department of Rheumatology and Internal Medicine
  2. 2Department of Orthopedics, Medical University of Bialystok, Bialystok
  3. 3Department of Rheumatology and Internal Medicine, Medical University of Szczecin, Szczecin
  4. 4Department of Dermatology, Medical University of Lublin, Lublin
  5. 5Department of Allergology, Medical University of Bialystok, Bialystok, Poland

Abstract

Background TNF-like weak inducer of apoptosis (TWEAK) regulates inflammation, angiogenesis and tissue remodeling. CD163 molecule, a scavenger receptor and marker of alternatively activated macrophages, modulates TWEAK activity through binding and internalization of TWEAK molecule. We have previously shown that, in a crossectional study, high serum concentrations of soluble CD163 (sCD163) and high CD163/TWEAK ratio were associated with lack of digital ulcers (DU) in patients with systemic sclerosis (SSc) [1].

Objectives To investigate whether serum levels of soluble CD163 (sCD163), soluble TWEAK (sTWEAK) or sCD163/sTWEAK ratio can predict clinical course of DU in patients with (SSc).

Methods 50 patients fulfilling the ACR/EULAR classification criteria of SSc who were followed for at least 1 year were included. Serum levels of sCD163 and sTWEAK were measured using commercially available ELISA kits. Digital ulcers were defined as painful area of loss of tissue on the volar surface of fingertips or around the nail distal to the proximal interphalangeal digital crease, present at the time of assessment. In addition, evaluation of SSc patients included assessment of disease subset (diffuse/limited SSc), modified Rodnan skin score, the presence of interstitial lung disease, pulmonary hypertension, results of pulmonary function tests, echo-Doppler, autoantibody testing (anticentromere antibodies, anti-Scl-70 antibodies) and erythrocyte sedimentation rate.

Results At baseline DU were present in 18 patients. During follow-up DU healed in 12 SSc patients and persisted in the remaining 6. In addition, 5 patients without DU at baseline developed new DU during follow-up. Because of relatively low numbers, patients with recurrent/persistent DU and those with new DU were analyzed together (n=11). In the remaining 27 patients DU were not found at any visit.

There were no significant differences in baseline sCD163 levels between SSc patients in whom DU healed at follow-up, those with persisted/new DU or SSc patients without DU at any visit. In contrast, baseline serum levels of sTWEAK were significantly higher in SSc patients who subsequently experienced healing of DU compared with SSc patients with DU at follow-up and with SSc patients who never had DU (p<0.05 for both comparisons). Accordingly, baseline sCD163/sTWEAK ratio was significantly lower in SSc patients with healed DU as compared with those with persisted/new DU at follow-up and with those who never had DU (p<0.05 for both comparisons).

In univariate analysis baseline DU, anticentromere antibodies (ACA) and sCD163/sTWEAK ratio were significantly associated with outcome of DU. In multivariate analysis including baseline DU, ACA and sCD163/sTWEAK ratio, baseline DUs were the strongest independent predictor of risk of DU at follow-up.

Conclusions Our results suggest that CD163-TWEAK interactions might play a role in the development/healing of DU in SSc and indicate that sCD163–TWEAK serum ratio is a potential biomarker of peripheral vascular disease in SSc.

References

  1. Arthritis Res Ther. 2013; Jun 24;15(3):R69. [Epub ahead of print]

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.5343

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