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Poster session 2: Autoantibodies, biomarkers and imaging (2), Environmental, epigenetics and genomics
PS2:26 Sle patients with secondary sjÖgren´s syndrome are characterised by typical autoantibodies and a pro-inflammatory state
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  1. M Kvarnström1,
  2. G Ruacho2,
  3. J Gustafsson1,
  4. A Zickert1,
  5. V Oke1,
  6. J Rönnelid3,
  7. K Elvin4,
  8. I Gunnarsson1 and
  9. E Svenungsson1
  1. 1Unit of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden
  2. 2Centre for Clinical Research Sörmland, Uppsala University, Uppsala, Sweden
  3. 3Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden
  4. 4Unit of Clinical Immunology, Department of Clinical Immunology and Transfusion Medicine, Karolinska Institutet, Karolin, Stockholm, Sweden

Abstract

Background Sjögren´s syndrome occurs in isolation (primary Sjögren´s syndrome, pSS), but it is also often secondary (sSS) to, and sometimes difficult to delineate from systemic lupus erythematosus (SLE). Consequently there is a need to investigate similarities and differences between SLE patients with (SLE-sSS) and without sSS (SLE-noSS).

Objective To investigate the occurrence of sSS in a large cohort of SLE patients and to explore clinical and laboratory characteristics associated with SLE-sSS as compared to SLE-noSS and controls.

Methods We included 504 consecutive SLE patients and 322 population controls, matched for age and gender. All patients fulfilled the 1982 revised ACR criteria for SLE. SLE-sSS was defined according to the American-European consensus criteria (AECC). Subjective and objective quantifications of sicca symptoms were recorded. All underwent a thorough clinical investigation. SLE-associated autoantibodies, (ANA screening by BioPlex 2200 system, Bio-Rad) and Rheumatoid factor (Rf, Phadia Immunocap 250) were determined, Routine laboratory workup and a panel of cytokines (MSD 30-plex cytokine assays, performed on samples from 433 consecutive SLE patients and 319 controls) were measured.

Results SLE-sSS, occurred in 23% of the SLE patients. Compared to SLE-noSS the SLE-sSS group was older, both at inclusion (55 vs 43 years, p<0.0001) and at disease onset (40 vs 32 yrs p<0.0001), and more enriched in females (96 vs 83%, p=0.0007), Leucopenia (57 vs 45%, p=0.02) and peripheral neuropathy (15 vs 7%, p=0.01) were more common and nephritis less common (32 vs 43%, p=0.03). Higher levels of total IgG, positivity for anti-SSA/Ro52, anti-SSA/Ro60, anti-SSB antibodies, Rf IgM and Rf IgA characterised the SLE-sSS group. 19/20 levels of detected cytokines were higher in SLE than in controls. 6/20 cytokines (TNF-a, IL-6, MCP-4, MIP-1β, IL12/IL-23p40 and IP-10) were upregulated in SLE-sSS vs SLE-noSS (see table for figures).

Conclusion Frequency of SLE-sSS increases with age and affects roughly ¼ of SLE patients. Nephritis was less common while leucopenia and peripheral neuropathy were more common. We report higher levels of six pro-inflammatory. These findings demonstrate that, though often regarded as a milder version of SLE, patients with SLE-sSS are characterised by a state of chronic systemic inflammation.

View this table:
Abstract PS2:26 Table 1

Immunoglobulins autoantibodies and pro-inflammatory cytokines in SLE-SS, SLE-noSS and population controls

  • Secondary Sjögren’s Syndrom
  • Clinical Characteristics
  • Cytokines

https://doi.org/10.1136/lupus-2018-abstract.74

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