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Anti-N-methyl-D-aspartate receptor antibodies are associated with fibromyalgia in patients with systemic lupus erythematosus: a case-control study
D.-J. Park1, Y. Takahashi2, J.-H. Kang3, Y.-R. Yim4, J.-E. Kim5, J.-W. Lee6, K.-E. Lee7, J.-K. Lee8, S.-S. Lee9
- Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea.
- Department of Paediatrics, Shizuoka Institute of Epilepsy and Neurological Disorders, Shizuoka, Japan.
- Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea.
- Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea.
- Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea.
- Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea.
- Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea.
- Department of Neurosurgery, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea.
- Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea. shinseok@chonnam.ac.kr
CER10039
2017 Vol.35, N°3 ,Suppl.105
PI 0054, PF 0060
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PMID: 28339361 [PubMed]
Received: 23/10/2016
Accepted : 06/02/2017
In Press: 10/03/2017
Published: 29/06/2017
Abstract
OBJECTIVES:
The high concordance between systemic lupus erythematosus (SLE) and fibromyalgia (FM) suggests common underlying mechanisms related to pain and distress in both patient groups. Increasing evidence indicates that N-methyl-D-aspartate receptors (NMDARs) play a major role in the induction and maintenance of central sensitisation with chronic pain. In this study, we evaluated the role of anti-NMDAR antibodies in the development of FM in patients with SLE.
METHODS:
Sera from 104 patients with SLE, 112 patients with FM, and 110 healthy controls were analysed to detect antibodies to the N-terminus of the 2B subunit of NMDARs (GluN2B). Subjects underwent clinical examination and neuropsychiatric evaluation, and completed a questionnaire regarding FM and neuropsychiatric symptoms.
RESULTS:
Of the 104 patients with SLE, 18 (17.3%) had FM. The anti-GluN2B antibody titer was significantly higher in patients with SLE (p<0.001). Among patients with SLE, those with concomitant FM had higher anti-GluN2B antibody titers (p<0.05). The anti-GluN2B antibody titer was associated positively with the tender point count (p=0.016) and the widespread pain index (p=0.005), but not with other symptom measurements. Anti-GluN2B antibody–positive patients with SLE were more likely to have neuropsychiatric systemic lupus erythematosus (NPSLE) and concomitant FM (p<0.05). Multivariate analysis showed that the anti-GluN2B antibody was an independent predictor of concomitant FM and NPSLE.
CONCLUSIONS:
To our knowledge, this report is the first to suggest that anti-NMDAR antibodies are associated with the pathogenesis of FM with SLE.
