Holli A. DeVon, PhD, RN, is Associate Professor; and Mariann R. Piano, PhD, RN, is Professor, College of Nursing, University of Illinois at Chicago. Anne G. Rosenfeld, PhD, RN, FAAN, FAHA, is Professor and Associate Dean, College of Nursing, University of Arizona, Tucson. Debra A. Hoppensteadt, PhD, MT (ASCP), is Professor, School of Medicine, Loyola University Chicago, Illinois.
Nurs Res. 2014 Jan-Feb;63(1):51-62. doi: 10.1097/NNR.0000000000000013.
BACKGROUND: Pain is a key diagnostic criterion in many medical conditions. In the absence of self-reported pain, measurement of a proxy for pain, such as an inflammatory biomarker, could aid in diagnosis and disease management. OBJECTIVES: The aim was to determine if there is an association between inflammatory biomarkers and self-reported pain in individuals with medical conditions associated with the symptom of pain and to clarify whether inflammatory biomarkers might aid in the diagnostic process. METHODS: An integrative literature review was conducted. PubMed, CINAHL, and Cochrane databases were searched for articles published between January 2000 and September 2012. Inclusion criteria were original research testing a relationship between inflammatory biomarkers and pain, pain measurement, laboratory measure of inflammatory biomarkers, and a prospective single-group experimental design or comparative nonrandomized or randomized design. Excluded were studies describing an association between inflammatory biomarkers and treatment, risk, and generation; pathophysiology; or genetic polymorphisms/transcripts. Ten studies meeting inclusion criteria were reviewed. RESULTS: In most of the studies, baseline elevations in both proinflammatory and anti-inflammatory cytokines were reported in painful conditions compared with healthy controls. In half of the studies, higher levels of proinflammatory markers (C-reactive protein, tumor necrosis factor-alpha, interleukin-2 [IL-2], IL-6, IL-8, IL-10, and CD40 ligand) were associated with greater pain. Proinflammatory cytokines decreased after treatment for pain in only two studies. DISCUSSION: The association between inflammatory markers varied in the direction and magnitude of expression, which may be explained by differences in designs and assays, disease condition and duration, variations in symptom severity, and timing of measurement. Elevation in anti-inflammatory cytokines in the presence of pain represents a homeostatic immune response. Further study is required to determine the value of cytokines as biomarkers of pain.
背景：疼痛是许多医学病症的关键诊断标准。在没有自我报告的疼痛的情况下，测量疼痛的替代指标，如炎症生物标志物，可能有助于诊断和疾病管理。
目的：本研究旨在确定在伴有疼痛症状的医学病症患者中，炎症生物标志物与自我报告的疼痛之间是否存在关联，并阐明炎症生物标志物是否有助于诊断过程。
方法：进行了综合文献回顾。在 2000 年 1 月至 2012 年 9 月期间，检索了 PubMed、CINAHL 和 Cochrane 数据库中的文章，以寻找测试炎症生物标志物与疼痛之间关系的原始研究、疼痛测量、炎症生物标志物的实验室测量、前瞻性单组实验设计或比较非随机或随机设计。排除描述炎症生物标志物与治疗、风险和生成、病理生理学或遗传多态性/转录本之间关系的研究。有 10 项符合纳入标准的研究进行了综述。
结果：在大多数研究中，与健康对照组相比，疼痛病症患者的基础炎症标志物（促炎细胞因子和抗炎细胞因子）水平升高。在半数研究中，更高水平的促炎标志物（C 反应蛋白、肿瘤坏死因子-α、白细胞介素-2 [IL-2]、IL-6、IL-8、IL-10 和 CD40 配体）与更严重的疼痛相关。只有两项研究报告称，在治疗疼痛后，促炎细胞因子的水平降低。
讨论：炎症标志物与疼痛之间的关联在表达方向和幅度上存在差异，这可能是由于设计和检测、疾病状况和持续时间、症状严重程度的变化以及测量时间的差异所致。在疼痛存在的情况下，抗炎细胞因子的升高代表了一种体内平衡的免疫反应。需要进一步研究以确定细胞因子作为疼痛生物标志物的价值。
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