Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Division of Advanced Medicine, Nagoya University Hospital, Nagoya, Japan.
Muscle Nerve. 2022 Aug;66(2):175-182. doi: 10.1002/mus.27636. Epub 2022 Jun 1.
INTRODUCTION/AIMS: The mechanism of complement-mediated neurological injury in vasculitic neuropathy associated with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) is unknown. The current study aimed to investigate the local activation of the complement system in vasculitic neuropathy associated with SLE and RA.
We analyzed sural nerve biopsy specimens collected from patients with SLE (n = 12) and RA (n = 12). The deposition of complement components comprising the classical and lectin pathways was assessed via immunohistochemistry.
The disease duration was longer in the RA group than in the SLE group (median [interquartile range]: 11.5 [5.5-31.0] and 4 [2-10] y, respectively). Complement components were found in the epineurial blood vessel walls in patients with SLE and RA, but not in controls. Deposition of the classical pathway component C1q in the blood vessel wall was more commonly observed in the SLE group (71.3% [25.6-85.8]) than in the RA group (20.1% [10.5-35.6]). As for the lectin pathway component, the incidence of ficolin-3 deposition in the blood vessel wall was higher in the SLE group (42.3% [25.7-51.3]) than in the RA group (17.2% [10.3-26.8]). On the contrary, the mannose-binding lectin level was higher in the RA group (37.5% [21.7-51.4]) than in the SLE group (17.8% [11.4-31.0]).
The classical and lectin pathways of the complement system may be involved in vasculitic neuropathy associated with SLE and RA.
简介/目的：红斑狼疮（SLE）和类风湿关节炎（RA）相关血管炎性神经病中补体介导的神经损伤机制尚不清楚。本研究旨在探讨 SLE 和 RA 相关血管炎性神经病中补体系统的局部激活情况。
我们分析了来自 SLE（n=12）和 RA（n=12）患者的腓肠神经活检标本。通过免疫组织化学评估补体成分（包括经典途径和凝集素途径）的沉积。
RA 组的疾病病程长于 SLE 组（中位数[四分位距]：11.5[5.5-31.0]和 4[2-10]年）。SLE 和 RA 患者的神经外膜血管壁中有补体成分沉积，但对照组没有。SLE 组血管壁中经典途径成分 C1q 的沉积更为常见（71.3%[25.6-85.8]），而 RA 组为 20.1%[10.5-35.6]。对于凝集素途径成分，SLE 组血管壁中 ficolin-3 沉积的发生率较高（42.3%[25.7-51.3]），而 RA 组为 17.2%[10.3-26.8]。相反，RA 组甘露聚糖结合凝集素水平较高（37.5%[21.7-51.4]），而 SLE 组为 17.8%[11.4-31.0]。
补体系统的经典途径和凝集素途径可能参与了 SLE 和 RA 相关的血管炎性神经病。
