特发性脊髓硬膜外脂肪瘤病(III 级)中炎症因子的表达及其意义

Neuro endocrinology letters Pub Date : 2024-01-31
Mingkun Yang, Hang Zhang, Minyi Liu, Xindong Jia, Tao Du, Dengpu Wu
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摘要

背景:特发性脊柱硬膜外脂肪瘤病(iSEL)通常与使用类固醇、内分泌失调、肥胖和手术干预有关。然而,人们对 iSEL 的发病机理仍不甚了解。本研究旨在探讨炎症因素对特发性硬膜外脂肪瘤病的影响:方法:选取 2020 年 3 月至 2023 年 4 月期间接受单侧双侧内窥镜检查的 13 例 iSEL(III 级,iSEL 组)患者和 12 例腰椎间盘突出症患者(对照组)作为研究对象。对脂肪组织进行组织学检查,分析血清和硬膜外脂肪细胞中促炎细胞因子(TNF-α、IL-1β)和抗炎因子(精氨酸酶-1、IL-10)的表达:与对照组相比,iSEL 组 HE 染色切片中每视野炎性细胞浸润数明显升高,硬膜外脂肪组织脂肪细胞中 TNF-α 和 IL-1β 的表达明显升高,精氨酸酶-1 和 IL-10 的表达明显降低(均 p <0.001)。然而,两组血清中 TNF-α、IL-1β、精氨酸酶-1 和 IL-10 的水平差异无统计学意义(P = 0.963)。结论:iSEL 显示了硬膜外脂肪组织脂肪细胞中炎性细胞的升高和促炎性细胞因子的失衡,这可能与症状性 iSEL 的发病机制有关。这些数据表明,炎症反应可能是 iSEL 的发病机制之一。然而,要阐明 iSEL 的具体病因,还需要进一步的多中心流行病学调查以及严格的基础和临床研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Expression and Significance of Inflammatory Factors in Idiopathic Spinal Epidural Lipomatosis (Grade III).

Background: Idiopathic spinal epidural lipomatosis (iSEL) is frequently associated with the utilization of steroids, endocrine disorders, obesity, and surgical interventions. Nevertheless, the pathogenesis of iSEL remains inadequately understood. The study aimed to investigate the contribution of inflammatory factors to idiopathic epidural lipomatosis.

Methods: Thirteen patients with iSEL (Grade III, iSEL group) and 12 patients with lumbar disc herniation (control group) who underwent unilateral biportal endoscopy from March 2020 to April 2023 were enrolled. Histological examination of adipose tissue was the performed to analyze expressions of pro-inflammatory cytokines (TNF-α, IL-1β), and anti-inflammatory factors (arginase-1, IL-10) in serum and epidural adipose cells.

Results: Compared with the control group, the number of inflammatory cell infiltrations per field in HE-stained sections was significantly elevated, TNF-α and IL-1β expression in adipocytes of epidural adipose tissue were markedly higher, and arginase-1 and IL-10 expression were significantly lower in the iSEL group (all p < 0.001). However, no statistically significant differences were observed in the serum level of TNF-α, IL-1β, arginase-1, and IL-10 between the two groups (p = 0.963). In addition, there was also no significant disparity in adipocyte size between the two groups (p = 0.739).

Conclusion: iSEL demonstrated elevated inflammatory cells and imbalance towards proinflammatory cytokines in adipocytes of epidural adipose tissue that may be associated with the pathogenesis of symptomatic iSEL. These data suggest that inflammatory response could be one of the mechanisms of iSEL. However, further multicenter epidemiological investigations and rigorous basic and clinical research are warranted to elucidate the specific etiology of iSEL.

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