Biomarkers to Advance Clinical Phenotypes of Low Back Pain (BACk)

项目摘要/摘要 每年高达25%的人会出现急性下腰痛(LBP)。其中多达63%的人将 患上几个月来几乎每天都会持续的慢性LBP。一些人转型的原因 从急性到慢性LBP的定义都很模糊。我们之前的资助期，以及其他人的工作，已经确定提高了 慢性下腰痛患者体内的炎性细胞因子。炎症持续存在的原因尚不清楚。我们的 长期目标是发现由免疫系统调节的炎症如何预测从急性到 慢性腰痛。确定调节急性LBP炎症反应和慢性LBP发展的机制 LBP可以发现新的治疗靶点，并对疼痛研究领域产生广泛影响。为了实现这一目标，我们将 进行一项观察性队列研究，招募了来自两个不同社区的480名急性LBP参与者 达勒姆和卡巴鲁斯，北卡罗来纳州。在基线、3个月(主要终点)和6个月时，参与者将提供 血液样本、压力痛阈值测试、体能测量、通过活动描记进行体力活动，以及 患者报告的调查问卷。12个月后，将收集基于调查的措施。提出这一建议的理由 研究来自我们强大的试点工作，1)确定免疫细胞图谱和基线炎症的变化 细胞因子可能是预测持续性炎症和慢性LBP的重要生物学因素，以及2)这些反应 免疫系统可能因种族(黑人和白人)而不同，3)急性LBP转变为慢性LBP可能 来自生物、社会、心理领域或这些来源和明确定义的表型的组合 这些领域可以改善慢性LBP的预测。据我们所知，我们将率先全面定义 急性向慢性LBP转化过程中的生化反应、炎症和免疫调节轨迹 多样化的社区。了解急性LBP的免疫反应将导致LBP新的多因素表型 基于表型组成的转变和特定的干预目标。

Project Summary/Abstract Up to 25% of individuals will develop acute low back pain (LBP) each year. As many as 63% of those individuals will develop chronic LBP that persists for most or every day for several months. The reasons why some individuals transition from acute to chronic LBP are poorly defined. Our prior funding period, and work from others, have identified elevated inflammatory cytokines among individuals with chronic LBP. The reasons why inflammation persists are unknown. Our long-term goal is to discover how inflammation, regulated by the immune system, predicts the transition from acute to chronic LBP. Identifying mechanisms that regulate the inflammatory response to acute LBP and the development of chronic LBP could identify novel therapeutic targets and broadly impact the pain research field. To accomplish this goal, we will conduct an observational cohort study enrolling n=480 participants with acute LBP from two diverse communities in Durham and Cabarrus, North Carolina. At baseline, 3 months (primary endpoint), and 6 months, participants will provide a blood specimen, pressure-pain threshold testing, physical performance measurement, physical activity via actigraphy, and patient-reported questionnaires. At 12 months, survey-based measures will be collected. The rationale for this proposed research comes from our strong pilot work in that 1) identifying a change in immune cell profiles and baseline inflammatory cytokines may be important biological factors predicting persistent inflammation and chronic LBP, and 2) these responses from the immune system may be different by race (Black versus White) and 3) acute LBP transition to chronic LBP can result from biological, social, psychological domains or a combination of these sources and well-defined phenotypes from these domains could improve chronic LBP prediction. To our knowledge, we will be the first to comprehensively define the biochemical reaction and inflammatory and immune-regulated trajectories in the transition from acute to chronic LBP in a diverse community. Understanding the immune response to acute LBP would lead to new multifactorial phenotypes of LBP transitions and specific intervention targets based on phenotype composition.