Abstract

Objective Systemic lupus erythematosus (SLE) is an immune disease characterized by multiorgan involvement. Neuropsychiatric systemic lupus erythematosus (NPSLE) is one of the most devastating complications of SLE, which lacks efficient diagnostic biomarkers. The recent studies on the anti-GAPDH autoantibodies suggested its potential pathogenic roles in NPSLE. However, the clinical relevance of the anti-GAPDH autoantibodies in patients with SLE is still elusive. In this study, we sought to determine the serum levels of the anti-GAPDH autoantibodies in patients with SLE to investigate the clinical significance of the anti-GAPDH autoantibodies in SLE. Methods Concentrations of the glyceraldehyde 3-phosphate dehydrogenase autoantibodies (anti-GAPDH autoantibodies) in the serum of 130 SLE patients and 55 healthy individuals were determined by enzyme-linked immunosorbent assay (ELISA). Among the 130 SLE patients, 95 were SLE patients without neuropsychiatric symptoms and 35 had NPSLE. White blood cell (WBC) count, hemoglobin (HB), platelet count (PLT), IgG, IgA, IgM, anti-dsDNA, C3, C4, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), RF, anti-cardiolipin (Acl), ANA, AnuA, anti-SSA, anti-SSB, β2-GPI, urinalysis, and 24 h urine protein were measured by standard laboratory techniques. Systemic lupus erythematosus disease activity index 2000 (SLEDAI-2K) and Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) damage index scores were evaluated accordingly. Results The serum levels of the anti-GAPDH autoantibodies were significantly elevated in the SLE patients, especially in the patients with NPSLE (P = 0.0011). Elevated serum anti-GAPDH was correlated with increased SLEDAI-2K (P = 0.017), ESR, IgG, and IgM and associated with increased intracranial pressure and incidence of cerebrovascular lesions, but it was protective for seizure disorder incidence. Conclusions Serum anti-GAPDH autoantibody was increased in both groups of SLE patients with or without neuropsychiatric symptoms and associated with disease severity. It could become an indicator of tissue damages in the brain for the future clinical practice.

Highlights

  • Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by a broad spectrum of autoantibodies and multiorgan involvement, mainly affecting skin, joint, kidney, lung, and nervous system [1, 2].Neuropsychiatric SLE (NPSLE) is one of the most fatal manifestations of SLE [2]

  • The total SLE patients were divided into 2 groups based on the presence of neuropsychiatric symptoms: the non-NPSLE group consisted of 95 SLE patients without neuropsychiatric syndromes and the NPSLE group included all the NPSLE patients

  • When SLE patients were grouped into the anti-GAPDH elevated group (AU ≥ 55 09, n = 86) and anti-GAPDH normal group (AU < 55 09, n = 44) by the cut-off value (AU = 55 09) produced by receiver operating characteristic (ROC) analysis, it was found that the anti-GAPDH autoantibodies were associated with the increased inflammation markers erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) (Table 3). These results suggested that SLE patients with the elevated anti-GAPDH autoantibodies were in more active disease status and the anti-GAPDH autoantibodies might be involved in active inflammation in SLE

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Summary

Introduction

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by a broad spectrum of autoantibodies and multiorgan involvement, mainly affecting skin, joint, kidney, lung, and nervous system [1, 2].Neuropsychiatric SLE (NPSLE) is one of the most fatal manifestations of SLE [2]. Because of lack of specific diagnostic biomarkers, NPSLE is still diagnosed based on a comprehensive conception of clinical observations, laboratory tests, and imaging techniques [6]. Significant correlation has been identified between a series of autoantibodies and NPSLE incidence, such as antiphospholipid antibodies, anti-ribosomal P antibodies, and anti-DNA/NR2 antibodies [5, 8, 9]. None of these NPSLE-related autoantibodies has been widely accepted as a specific biomarker for NPSLE diagnosis [7]

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