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P43 Serum S100A8/A9 concentrations are associated with neuropsychiatric involvement and fatigue in SLE
  1. Kristoffer Alexander Zervides1,
  2. Andreas Jern1,
  3. Jessica Nystedt2,
  4. Petra Nilsson2,
  5. Pia C Sundgren3,
  6. Birgitta Gullstrand4,
  7. Anders A Bengtsson1 and
  8. Andreas Jönsen1
  1. 1Dept. of Clinical Sciences, Rheumatology, Lund University, Skåne University Hospital, Lund
  2. 2Dept. of Clinical Sciences, Neurology, Lund University, Skåne University Hospital, Lund
  3. 3Dept. of Clinical Sciences, Diagnostic Radiology, Lund University, Skåne University Hospital, Lund
  4. 4Dept. of Laboratory Medicine, Clinical Immunology, Lund University, Skåne University Hospital, Lund, Sweden


Background/Purpose Neuropsychiatric (NP) involvement and fatigue are both major problems in SLE. S100A8/A9 is a marker of inflammation, which responds to therapy in SLE patients. S100A8/A9 is expressed in the CNS. We investigated S100A8/A9 in relation to NPSLE and fatigue.

Methods In this cross-sectional study we used ELISA (Bhulmann MRP8/14 ELISA kit, Switzerland) to measure the concentration of S100A8/A9 in serum in 72 SLE patients and 26 healthy controls and in cerebrospinal fluid (CSF) in 33 SLE patients. NP involvement was determined according to ACR case definitions for NPSLE. An MRI was performed in SLE patients and controls assessing white matter abnormalities and cerebral atrophy. Measurements of fatigue were performed using the Fatigue Severity Scale (FSS) and the Visual Analogue Scale (100 mm) (VAS). Statistical calculations were performed using non-parametric methods.

Results In all, 72 female SLE patients (median age 38, range 18–52) and 26 female healthy controls (median age 40, range 23–52) were included in this study. Forty-four (61%) patients had NP involvement. NPSLE patients had higher serum S100A8/A9 concentrations (median 1.40 µg/ml) than the non-NPSLE patients (median 0.92 µg/ml; p=0.011) and the control group (median 0.79 µg/ml; p=0.004). Serum S100A8/A9 correlated with increased VAS fatigue in SLE patients (r=0.311; p=0.008), but not with FSS (r=0.184; p=0.124). Serum S100A8/A9 did not correlate with the extent of white matter lesions, atrophy of brain segments, or disease activity (SLEDAI-2K). S100A8/A9 was not detected in the CSF.

Conclusions Higher serum S100A8/A9 concentrations in NPSLE patients and patients with fatigue may indicate that S100A8/A9 is involved in the pathogenesis of these manifestations, although further investigation is needed.

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