Patients with systemic lupus erythematosus with high plasma levels of sFas risk relapse

T van Lopik*, M Bijl, M Hart, L Boeije, T Gesner, AA Creasy, CGM Kallenberg, LA Aarden, RJT Smeenk, JT Smeenk

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

21 Citations (Scopus)

Abstract

Objective. We related soluble Fas (sFas) levels to the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) in a longitudinal series of plasma samples of patients with SLE to evaluate the relation between excessive production of sFas and disease activity.

Methods. We generated 21 monoclonal antibodies against Fas. Two Of these were used to develop and validate a sensitive sandwich ELISA for the longitudinal analysis of sFas levels in plasma of 30 patients and 25 controls.

Results. At the start of followup, a significant elevation (p <0.0001) was found in sFas levels in SLE (1167 +/- 337 pg/ml sFas) compared to controls (618 +/- 98 pg/ml sFas). Also, at the start of the followup a significant difference (p = 0.0028) existed between patients who were going to have a relapse (1236 +/- 402 pg/ml sFas) during followup and patients who were not (809 +/- 276 pg/ml sFas). While sFas did not fluctuate with disease activity in individual patients, we found a strong correlation (r = 0.75, p <0.0001) between sFas and SLEDAI, but only at the time of relapse, when we analyzed the patients as a group.

Conclusion. In individual patients with SLE, sFas does not fluctuate with disease activity. However, patients with high plasma levels of sFas are at risk of relapse.

Original languageEnglish
Pages (from-to)60 - 67
Number of pages8
JournalJournal of Rheumatology
Volume26
Issue number1
Publication statusPublished - Jan-1999

Keywords

  • soluble Fas
  • CD95
  • monoclonal antibodies
  • apoptosis
  • Systemic Lupus Erythematosus
  • TUMOR-NECROSIS-FACTOR
  • CONGESTIVE-HEART-FAILURE
  • INDUCED CELL-DEATH
  • SOLUBLE FAS
  • SERUM LEVELS
  • T-CELLS
  • RHEUMATOID-ARTHRITIS
  • MULTIPLE-SCLEROSIS
  • MOLECULAR-CLONING
  • INDUCED APOPTOSIS

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