Mechanisms of transition from acute to chronic pain in Non-Hispanic Black and White injury patients

非西班牙裔黑人和白人损伤患者从急性疼痛转变为慢性疼痛的机制

• 批准号: 10703490
• 负责人: Matthew C. Morris
• 金额: $ 66.41万
• 依托单位: UNIVERSITY OF MISSISSIPPI MED CTR
• 依托单位国家: 美国
• 财政年份: 2022
• 资助国家: 美国
• 起止时间: 2022-09-11 至 2027-04-30
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10703490
• 关键词: Accounting; Acute; Address; Adult; Age; Biological Markers; Black race; Buffers; Characteristics; Chronic; Cognition; Development; Disease susceptibility; Disparity; Early Intervention; Elements; Emergency department visit; Fracture; Gender; Health Care Visit; Healthcare; Hospitalization; Hospitals; Individual; Inflammation; Inflammatory; Injury; Interleukin-1 beta; Interleukin-6; Knowledge; Life; Measures; Mediation; Medical; Methods; Modeling; Neighborhoods; Not Hispanic or Latino; Orthopedics; Pain; Pain Measurement; Pain intensity; Pain interference; Pathway interactions; Patients; Perception; Prospective Studies; Psychopathology; Race; Reporting; Research Personnel; Risk; Risk Assessment; Risk Factors; Sensory; Severities; Shapes; Social support; Socioeconomic Status; Stress; Stressful Event; Surveys; TNF gene; Testing; Traumatic injury; Work; biobehavior; biopsychosocial; black patient; chronic pain; chronic painful condition; clinical pain; cost effective; depressive symptoms; expectation; experience; functional disability; improved; inflammatory marker; injured; innovation; low socioeconomic status; minority stress; multidisciplinary; novel; pain chronification; pain outcome; pain sensitivity; post-traumatic stress; post-traumatic symptoms; predictive modeling; protective factors; racial difference; racial disparity; recruit; sample fixation; skills; social; social factors; social health determinants; social influence; theories; trauma centers

Current understanding of how and why race influences the transition from acute to chronic pain following traumatic injury remains limited. Traumatic injuries result in over 30 million emergency department visits and 2.5 million hospitalizations each year in the U.S. Risk for developing post-injury chronic pain is significantly greater for non-Hispanic Black (NHB) patients compared to non-Hispanic White (NHW) patients with similar injuries. Although NHB patients experience higher levels of acute post-injury pain and are more likely to transition to chronic pain than NHW patients, the biobehavioral and social factors that influence this transition are not well understood. The overall aim of this proposal is to improve understanding of the factors that influence the transition to post-injury chronic pain and shape racial pain disparities. To address our aims, we will recruit 150 NHB and 150 NHW adults with traumatic orthopedic injuries from a level 1 trauma center and assess pain outcomes during hospitalization and across monthly follow-ups. First, we will identity similarities and differences in the extent to which biobehavioral factors explain post-injury chronic pain in NHB and NHW patients. We hypothesize that greater pain sensitivity (assessed in hospital via quantitative sensory testing), elevated acute inflammatory biomarkers (hsCRP, TNFα, IL1β, IL-6), more negative cognitions (catastrophizing, pain/treatment expectations), and higher depressive/posttraumatic stress symptoms will predict post-injury chronic pain (i.e., higher odds of chronic pain onset, greater pain intensity and interference) in both NHB and NHW patients. If chronic pain risks are moderated by race, we hypothesize that worse post-injury chronic pain in NHB relative to NHW patients will be explained, in part, by higher biobehavioral risk factors. Second, we will identify similarities and differences in the extent to which social factors explain post-injury chronic pain in NHB and NHW patients. We hypothesize that social risk factors (greater life and neighborhood stress, lower socioeconomic status) will predict post-injury chronic pain in both NHB and NHW patients, and that social protective factors (higher social support) will buffer against in the influence of social risk factors. If chronic pain risks are moderated by race, we hypothesize that worse post-injury chronic pain in NHB relative to NHW patients will be explained, in part, by higher levels of social risk factors. The comprehensive assessment of risk and protective factors across multiple levels of the biopsychosocial model will advance understanding of the pathways that contribute to post-injury chronic pain for both NHB and NHW adults, including factors implicated in racial differences in transition to chronic pain. Evaluating in-hospital evoked pain sensitivity as a predictor of post-injury chronic pain development represents a major innovation. This knowledge could spur the development of cost-effective, scalable screens for hospital settings to redress racial disparities in pain. The investigators assembled for this multidisciplinary team possess complementary skill sets in traumatic injury, chronic pain, quantitative sensory testing, inflammation, pain-relevant biobehavioral and social factors, and racial disparities in chronic pain.

当前对如何以及为什么影响从急性到慢性疼痛的过渡之后的理解 创伤性伤害仍然有限。 美国每年在美国每年的住院数百万次住院，发生伤害后慢性疼痛的风险大大增加 与非西班牙裔白人（NHW）患者相比，非西班牙裔黑人（NHB）患者的损伤相似。 尽管NHB患者经历了更高水平的急性伤害后疼痛，并且更多地过渡到 慢性疼痛患者，影响过渡的生物核心和社会因素不好 理解。 过渡到伤害后的慢性疼痛和形状的种族疼痛差异，我们将招募150 NHB和150名NHW成年人患有1级创伤中心的创伤性骨科伤害并评估疼痛 首先，在杂货期间的结果和每月随访。 在多大程度上，生物性因素解释了NHB和NHW患者的伤害后慢性疼痛 假设较高的疼痛敏感性（通过定量感觉测试在Hosspital评估），急性升高 炎性生物标志物（HSCRP，TNFα，IL1β，IL-6），更多的负认知（灾难性，疼痛/治疗） 期望），较高的抑郁/创伤后压力症状将预测伤害后慢性疼痛（即 NHB和NHW患者的慢性疼痛发作的几率，更大的疼痛强度和干扰 种族调节了慢性疼痛风险 NHW患者将部分通过更高的生物行为风险因素来解释。 在社会因素解释NHB和NHW患者中innjury慢性疼痛的程度上的差异和差异。 我们假设社会风险因素 预测NHB和NHW患者的伤害后慢性疼痛，以及社会保护因素（更高的社交因素 支持）将在社会风险因素的影响下进行缓冲。 假设将在NHB相对于NHW患者的NHB后遭受更严重的后慢性疼痛，部分地解释了 较高的社会风险因素。 生物心理社会模型的水平将提高对有助于伤害后的途径的理解 NHB和NHW成年人的慢性疼痛，包括与种族差异过渡到的因素 慢性疼痛评估院内诱发疼痛敏感性 压制主要创新。 用于纠正痛苦中种族差异的医院环境。 团队拥有创伤性损伤，慢性疼痛，定量感觉测试的互补技能， 炎症，疼痛与疼痛相关的生物无害和社会因素以及慢性疼痛的种族差异。