Graduate Education and Research Programs.
Research and Clinical Education Programs, Canadian Memorial Chiropractic College, Toronto, ON, Canada.
Clin J Pain. 2019 Oct;35(10):818-825. doi: 10.1097/AJP.0000000000000745.
The pathogenesis of low back pain (LBP) remains unclear. However, recent studies suggest that the inflammatory response may be inherent in spinal pain. The purpose of this study was to discern inflammatory profiles in patients with nonspecific acute and chronic LBP in relation to those in asymptomatic individuals.
Peripheral blood samples were obtained from asymptomatic controls and patients with nonspecific acute and chronic LBP reporting a minimum pain score of 3 on a 10-point Visual Analogue Scale (VAS). The levels of in vitro production of proinflammatory (tumor necrosis factor α [TNFα], interleukin [IL] 1β, IL-6, IL-2, interferon γ) and anti-inflammatory (IL-1 receptor antagonist, soluble receptors of TNF2, and IL-10) mediators were determined by specific immunoassays.
The mean VAS scores were comparable between the acute and chronic LBP patient groups. Compared with asymptomatic group, the production of TNFα, IL-1β, IL-6 and their ratios to IL-10 levels were significantly elevated in both patient groups (P=0.0001 to 0.003). In acute LBP group, the ratio of IL-2:IL-10 was also significantly increased (P=0.02). In contrast, the production of interferon γ was significantly reduced compared with the other study groups (P=0.005 to 0.01), nevertheless, it was positively correlated (P=0.006) with pain scores. In chronic LBP patients, the production of TNFα, IL-1 receptor antagonist, and soluble receptors of TNF2 was significantly increased (P=0.001 to 0.03) in comparison with the control and acute LBP groups, and TNFα and IL-1β levels were positively correlated (P<0.001) with VAS scores.
The inflammatory profiles of patients with acute and chronic LBP are distinct. Nonetheless, in both patient groups, an imbalance between proinflammatory and anti-inflammatory mediator levels favors the production of proinflammatory components.
腰痛（LBP）的发病机制仍不清楚。然而，最近的研究表明，炎症反应可能是脊柱疼痛的固有特征。本研究旨在探讨非特异性急性和慢性 LBP 患者的炎症特征，并与无症状个体进行比较。
从无症状对照组和报告疼痛评分至少为 10 分制 VAS 评分 3 分的非特异性急性和慢性 LBP 患者中获得外周血样本。通过特定的免疫测定法测定体外产生的促炎（肿瘤坏死因子 α [TNFα]、白细胞介素 [IL] 1β、IL-6、IL-2、干扰素 γ）和抗炎（IL-1 受体拮抗剂、TNF2 可溶性受体和 IL-10）介质的水平。
急性和慢性 LBP 患者组的平均 VAS 评分相当。与无症状组相比，两组患者 TNFα、IL-1β、IL-6 及其与 IL-10 水平的比值均显著升高（P=0.0001 至 0.003）。在急性 LBP 组，IL-2:IL-10 的比值也显著升高（P=0.02）。相比之下，与其他研究组相比，干扰素 γ 的产生显著降低（P=0.005 至 0.01），但与疼痛评分呈正相关（P=0.006）。在慢性 LBP 患者中，与对照组和急性 LBP 组相比，TNFα、IL-1 受体拮抗剂和 TNF2 可溶性受体的产生显著增加（P=0.001 至 0.03），并且 TNFα 和 IL-1β 水平与 VAS 评分呈正相关（P<0.001）。
急性和慢性 LBP 患者的炎症特征不同。然而，在两组患者中，促炎和抗炎介质水平之间的失衡有利于促炎成分的产生。
