Anti-Ribosomal P Antibody Is a Key Autoantibody Associated with Complications of NP-SLE with High-Levels of CSF IL-8

Hidenaga Kawasumi¹, Takahisa Gono¹, Yasushi Kawaguchi¹, Yasuhiro Katsumata¹, Hisae Ichida¹, Akiko Tochimoto¹, Masanori Hanaoka¹, Yuko Okamoto¹, Sayuri Kataoka¹ and Hisashi Yamanaka², ¹Institute of Rheumatology, Tokyo Women's Medical University, Tokyo, Japan, ²Institute of Rheumatology, Tokyo Women’s Medical University, Tokyo, Japan

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: autoantibodies, cytokines, neuropsychiatric disorders and systemic lupus erythematosus (SLE)

Session Information

Title: Systemic Lupus Erythematosus - Clinical Aspects and Treatment: Central Nervous System and Other Clinical Aspects

Session Type: Abstract Submissions (ACR)

Background/Purpose: Complications of neuropsychiatric systemic lupus erythematosus (NP-SLE) are associated with the morbidity and mortality of patients with SLE. Although the detailed pathophysiology of NP-SLE remains unknown, complements, autoantibodies, and cytokines are involved in the inflammation of the central nervous system (CNS) or the peripheral nervous system (PNS) in SLE. Previous studies have demonstrated that anti-phospholipid (PL), anti-ribosomal P, anti-N-methyl-D-aspartate receptor subunit 2 (NR2), and anti-U1-RNP antibodies are associated with the development of NP-SLE. In addition, cerebrospinal fluid (CSF) proinflammatory cytokines, such as IL-6, are increased in NP-SLE. In this study, we evaluated the associations between several serum autoantibodies and CSF proinflammatory cytokines in NP-SLE.

Methods: In the present study, seventy patients with SLE who had been admitted to our hospital from 2001 to 2013 were enrolled. SLE was diagnosed according to the 1997 ACR revised criteria for the classification of SLE. Disease activity was measured using the SLE disease activity index 2000 (SLEDAI-2k). NP-SLE manifestations were classified according to the 1999 ACR nomenclature and case definitions for NP-SLE syndromes. Serum and CSF samples were obtained from all enrolled patients with SLE. We measured serum autoantibodies, including anti-PL, anti-ribosomal P, anti-NR2, anti-U1-RNP and anti-Sm antibodies, and CSF cytokines (IL-6, IL-8, and IFN-α).

Results: Of the 70 patients with SLE, all patients were female, and their median age was 32 years. The median score on the SLEDAI-2k was 12. NP-SLE was diagnosed in 24 patients. Serum anti-PL, anti-ribosomal P, anti-NR2, anti-U1-RNP, and anti-Sm antibodies were detected in 15, 23, 23, 24, and 13 patients, respectively. The CSF levels of IL-8 were significantly higher in the NP-SLE subset compared with the non-NP-SLE subset (p<0.05). There were no significant differences in the CSF levels of IL-6, IFN-α, total protein, or IgG index between the two subsets. High levels of CSF IL-8 (>30 pg/ml) were significantly (p<0.001) associated with the complications of NP-SLE. No patient was diagnosed with NP-SLE when the CSF levels of IL-8 were less than 30 pg/ml. To identify the specific autoantibodies associated with high levels of CSF IL-8, a multivariate analysis was conducted. Anti-ribosomal P was the most significant autoantibody involved in the high levels of CSF IL-8.

Conclusion: High levels of CSF IL-8 are associated with the complications of NP-SLE. Anti-ribosomal P is a key autoantibody associated with NP-SLE with high levels of CSF IL-8.

Disclosure:

H. Kawasumi,
None;

T. Gono,
None;

Y. Kawaguchi,
None;

Y. Katsumata,
None;

H. Ichida,
None;

A. Tochimoto,
None;

M. Hanaoka,
None;

Y. Okamoto,
None;

S. Kataoka,
None;

H. Yamanaka,
None.

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