Centro de Biología Celular y Biomedicina (CEBICEM), Facultad de Medicina y Ciencia, Universidad San Sebastián, Carmen Sylva 2444, Providencia, 7510156, Santiago, Chile.
Escuela de Medicina, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.
Clin Rheumatol. 2019 Nov;38(11):3129-3137. doi: 10.1007/s10067-019-04707-x. Epub 2019 Jul 31.
Central nervous system disease occurs in over 20% of patients with systemic lupus erythematosus (SLE) resulting in major morbidity and damage. Cognitive dysfunction is common in SLE, but the cause remains uncertain and treatment options are limited. This study explores the influence of clinical, neuropsychological factors and anti-neuronal antibodies on lupus damage accrual.
A prospective cohort with 99 SLE patients recruited between 2008 and 2013 and followed up in 2016 was established. Baseline evaluations were depression (MINI-Plus), cognitive function evaluating attention, visuospatial memory and executive functions, and anti-neuronal antibodies. Activity index (SLEDAI-2K) and SLICC/ACR Damage Index (SDI) were assessed at baseline and last follow-up.
At baseline, median (interquartile range) age was 36.0 years (27.0-45.0), disease duration 3.7 years (0.4-12.4), SLEDAI-2K 6.0 (3.0-12.0), and SDI score 1.0 (0-1.0). Major depression was present in 23%, cognitive deficit in 18%, and received immunomodulators in 36%. Anti-dsDNA/N-methyl-D-aspartate receptor antibodies were present in 19%, anti-ribosomal P in 12%, and anti-neuronal surface P antigen (NSPA) in 5%. After a median follow-up of 55 months (interquartile range 39-78), 11% had damage accrual. In a multivariate analysis, baseline SDI, SLEDAI-2K, and immunomodulators use were associated with final damage, whereas SLEDAI-2K and immunomodulator use were also associated with accrual damage. Models including anti-NSPA showed impact on final and accrual damage. Cognitive deficit, depression, and other autoantibodies were not predictors.
Disease activity and immunomodulator use associate with lupus damage. Of the anti-neuronal antibodies examined, anti-NSPA emerged as a potential poor prognostic factor, probably related to severe SLE onset requiring elevated corticosteroid doses. Key Points • Anti-NSPA may be a worse prognostic factor in SLE. • Other neuropsychological factors do not influence damage.
中枢神经系统疾病在超过 20%的系统性红斑狼疮 (SLE) 患者中发生,导致严重的发病率和损害。认知功能障碍在 SLE 中很常见,但病因仍不确定,治疗选择有限。本研究探讨了临床、神经心理学因素和抗神经元抗体对狼疮损害积累的影响。
建立了一个前瞻性队列,纳入了 2008 年至 2013 年间招募并于 2016 年随访的 99 例 SLE 患者。基线评估包括抑郁(MINI-Plus)、认知功能评估注意力、视空间记忆和执行功能以及抗神经元抗体。在基线和最后一次随访时评估活动指数 (SLEDAI-2K) 和 SLICC/ACR 损害指数 (SDI)。
基线时,中位数(四分位距)年龄为 36.0 岁(27.0-45.0),病程 3.7 年(0.4-12.4),SLEDAI-2K 为 6.0(3.0-12.0),SDI 评分为 1.0(0-1.0)。23%存在重度抑郁,18%存在认知障碍,36%接受免疫调节剂治疗。19%存在抗 dsDNA/N-甲基-D-天冬氨酸受体抗体,12%存在抗核糖体 P 抗体,5%存在抗神经元表面 P 抗原 (NSPA) 抗体。中位随访 55 个月(四分位距 39-78)后,11%出现损害累积。多变量分析显示,基线 SDI、SLEDAI-2K 和免疫调节剂使用与最终损害相关,而 SLEDAI-2K 和免疫调节剂使用也与损害累积相关。包括抗 NSPA 的模型显示对最终和累积损害有影响。认知障碍、抑郁和其他自身抗体不是预测因素。
疾病活动和免疫调节剂的使用与狼疮损害相关。在所检查的抗神经元抗体中,抗 NSPA 似乎是一个潜在的预后不良因素,可能与需要更高剂量皮质类固醇的严重 SLE 发病有关。
抗 NSPA 可能是 SLE 的一个更差的预后因素。
其他神经心理学因素不会影响损害。