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Abstract Number: 2248

Serum Phosphatidylserine-Specific Phospholipase A1 (PS-PLA1) Identified As a Novel Biomarker for Systemic Lupus Erythematosus (SLE)

Tetsuji Sawada1, Kazuhiro Nakamura2, Ryunosuke Ohkawa2, Aki Shoji1, Koichiro Tahara1, Haeru Hayashi1, Eri Kimura1, Koji Igarashi3, Junken Aoki4 and Yutaka Yatomi5, 1Rheumatology, Tokyo Medical University, Tokyo, Japan, 2Department of Clinical Laboratory, The University of Tokyo Hospital, Tokyo, Japan, 3AIA Research Group, TOSOH Corporation, Kanagawa, Japan, 4Department of Molecular and Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Tohoku University, Miyagi, Japan, 5Department of Clinical Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Biomarkers and systemic lupus erythematosus (SLE)

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Session Information

Session Title: Systemic Lupus Erythematosus: Clinical Aspects

Session Type: Abstract Submissions (ACR)

Background/Purpose: Lysophosphatidylserine (LPS), which is a degraded form of phosphatidylserine (PS), is an acidic lyso-glycerophospholipid, similar to lysophosphatidic acid (LPA). LPS is known to mediate a number of biological processes through G protein coupled receptors, and may act as a lipid mediator in autoimmunity. LPS and LPA are generated by lyso-glycerophospholipid producing enzymes, PS-specific phospholipase A1 (PS-PLA1) and phosphatidic acid (PA) selective PLA1, known as autotaxin (ATX), respectively. The purpose of the present study is to determine the serum levels of PS-PLA1 and ATX in sera from patients with systemic lupus erythematosus (SLE), and to investigate their relationship with disease activity.

Methods: Serum levels of PS-PLA1 and ATX of 34 patients with active SLE were quantified by enzyme-linked immunoassay. As for 26 patients with SLE, serum PS-PLA1 levels after corticosteroid treatment were also measured, and their correlation with disease activity and organ damage, as evaluated by SLE Disease Activity Index (SLEDAI) and British Isles Lupus Assessment Group (BILAG) index, were examined. Sera from 40 patients with active rheumatoid arthritis (RA), 23 patients with Sjogren syndrome (SjS), and 23 patients with systemic sclerosis (SSc) were utilized as disease controls.

Results: Serum PS-PLA1 levels were significantly higher in patients with SLE than those in disease controls, while serum levels of ATX were similar among all patients. In SLE patients, serum levels of PS-PLA1 were positively correlated with global SLE activity indices (SLEDAI and BILAG scores) and serum IgG levels, but negatively correlated with complement C3 levels. Regarding individual organ damage, serum PS-PLA1 levels were significantly correlated with the BILAG score for general constitutional symptoms, the mucocutaneous system, and vasculitis. Furthermore, serum PS-PLA1 decreased after immunosuppressive treatment in SLE patients.

Conclusion: The association of serum PS-PLA1 levels with SLE disease activity indicates that measurement of serum PS-PLA1 may be useful for the clinical evaluation of SLE as a novel biological marker. Specific elevation of PS-PLA1 in SLE suggests that lysophosphatidylserine (LPS) generated from PS-PLA1 may be involved in the pathogenesis of SLE.


Disclosure:

T. Sawada,
None;

K. Nakamura,
None;

R. Ohkawa,
None;

A. Shoji,
None;

K. Tahara,
None;

H. Hayashi,
None;

E. Kimura,
None;

K. Igarashi,
None;

J. Aoki,
None;

Y. Yatomi,
None.

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