Relationship between systemic inflammation and recovery over 12 months after an acute episode of low back pain
Relationship between systemic inflammation and recovery over 12 months after an acute episode of low back pain
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DOI：
10.1016/j.spinee.2021.09.006
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发表时间：
2022-01-20
期刊：
影响因子：
4.5
通讯作者：
Hodges, Paul W.
中科院分区：
文献类型：
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作者：
Klyne, David M.;Barbe, Mary F.;Hodges, Paul W.
背景背景：个体特征可以影响损伤后的结果。我们以前在患有早期急性下腰痛(LBP)的患者中所做的工作确定了具有特定生物心理社会特征的亚群(群)，这些群在6个月后恢复得很差或很好。PURPOSE：这项研究通过揭示这些参与者群的短期和长期恢复和全身炎症的轨迹来扩展这项工作：(1)“炎症性睡眠不良”(群1)，“高肿瘤坏死因子和抑郁”(群2)，“高疼痛和高疼痛相关恐惧”(群3)，和“低疼痛和低疼痛相关恐惧”(第4组)。研究设计/环境：纵向队列研究。患者样本：83名LBP急性发作后2周内的个体-被分组到他们的先验定义的组中。OUTCOME测量：一般参与者特征(性别、年龄、体重指数、吸烟史、既往LBP病史)；自报LBP(0-10数字评定量表)、LBP相关残疾(罗兰-莫里斯残疾问卷)、抑郁症(流行病学研究中心)、抑郁量表、疼痛灾害化(疼痛灾害化问卷)、恐惧回避(恐惧回避信念问卷)、疼痛自我效能(疼痛自我效能问卷)和睡眠(匹兹堡睡眠质量指数)；全身炎性生物标志物(C-反应蛋白[CRP]、白介素6[IL-6]、白介素1β(IL-1β)、肿瘤坏死因子[TNF])。方法：受试者提供血液用于测定CRP/细胞因子，并完成与疼痛/残疾、心理和睡眠状况相关的问卷。连续9个月重复3个月的血液测量，并在12个月内每两周自我报告疼痛/残疾。恢复情况(疼痛变化)和C反应蛋白/细胞因子使用混合模型进行纵向比较。结果：第1组和第2组与12个月后的恢复情况相关，但与之相反。组1每隔3个月报告的恢复最多，而组2报告的恢复最少。第1组在基线时CRP(和IL-6)升高，从3个月到9个月持续下降。结论：研究结果支持C反应蛋白(可能还有IL-6)在炎症和恢复中的早期作用，以及持续性的肿瘤坏死因子过度表达的病理作用，这种作用可能因抑郁样行为而延续。(C)2021 Elsevier Inc.保留所有权利。
BACKGROUND CONTEXT: Individual characteristics can influence outcomes after injury. Our previous work in individuals with early-acute low back pain (LBP) identified subgroups (clusters) with specific biopsychosocial features that recovered poorly or well by 6 months.PURPOSE: This study extends on that work by revealing the short- and long-term trajectories of recovery and systemic inflammation of these participant clusters: (1) "inflammatory & poor sleep" (Cluster 1), "high TNF & depression" (Cluster 2), "high pain & high pain-related fear" (Cluster 3), and "low pain & low pain-related fear" (Cluster 4).STUDY DESIGN/SETTING: Longitudinal cohort study.PATIENT SAMPLE: Eighty-three individuals within 2 weeks of an acute episode of LBP - grouped into their a priori-defined cluster.OUTCOME MEASURES: General participant characteristics (sex, age, body mass index, smoking history, previous LBP history); self-reported LBP (0-10 numerical rating scale, LBP-related disability (Roland-Morris Disability Questionnaire), depression (Center for Epidemiological Studies Depression Scale, pain catastrophizing (Pain Catastrophizing Scale), fear avoidance (Fear Avoidance Beliefs Questionnaire), pain self-efficacy (Pain Self-Efficacy Questionnaire), and sleep (Pittsburgh Sleep Quality Index); systemic inflammatory biomarkers (C-reactive protein [CRP], interleukin-6 [IL-6], interleukin-1 beta, tumor necrosis factor [TNF]).METHODS: Participants provided blood for the measurement of CRP/cytokines, and completed questionnaires related to their pain/disability, psychological and sleep status. Blood measures were repeated 3-monthly for 9 months, and pain/disability were self-reported fortnightly for 12 months. Recovery (change in pain) and CRP/cytokines were longitudinally compared between clusters using mixed-models. Associations between baseline factors and follow-up CRP/cytokines levels were assessed with multiple regression.RESULTS: Clusters 1 and 2 were associated, but oppositely, with recovery over the 12-months. Cluster 1 reported most recovery at every 3-monthly interval, whereas Cluster 2 reported least recovery. Cluster 1 had elevated CRP (and IL-6) at baseline that continued to decrease from 3 to 9 months. TNF was elevated early and persistently in Cluster 2. Baseline factors other than inflammation generally failed to predict follow-up inflammation.CONCLUSIONS: Findings support the early role of CRP (and perhaps IL-6) in control of inflammation and recovery, and a pathological role of persistent TNF overexpression, which may be perpetuated by depressive-like behaviors. (C) 2021 Elsevier Inc. All rights reserved.