T. Falasinnu, PhD, Department of Epidemiology and Population Sciences, Stanford University School of Medicine, and Department of Anesthesiology, Perioperative, and Pain Medicine, Stanford University School of Medicine, Stanford, California;
C. Drenkard, MD, PhD, S.S. Lim, MD, MPH, Department of Medicine, Division of Rheumatology, Emory University, and Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia.
J Rheumatol. 2021 Aug;48(8):1279-1289. doi: 10.3899/jrheum.200595. Epub 2020 Dec 1.
To define biopsychosocial mechanisms of pain that go above and beyond disease activity and organ damage in systemic lupus erythematosus (SLE).
We conducted a cross-sectional analysis of patient-reported data in a population-based registry of 766 people with SLE. Predictors of pain intensity and interference were examined using hierarchical linear regression. We built 2 main hierarchical regression models with pain intensity and interference as outcomes, both regressed on disease activity and organ damage. For each model, we sought to establish the relationship between pain outcomes and the primary exposures using sequential steps comprising the inclusion of each construct in 6 stages: demographic, socioeconomic, physical, psychological, behavioral, and social factors. We also conducted sensitivity analyses eliminating all overt aspects of pain in the disease activity measure and reestimated the models.
Disease activity and organ damage explained 32-33% of the variance in pain intensity and interference. Sociodemographic factors accounted for an additional 4-9% of variance in pain outcomes, whereas psychosocial/behavioral factors accounted for the final 4% of variance. In the sensitivity analyses, we found that disease activity and organ damage explained 25% of the variance in pain outcomes.
Disease activity only explained 33% of the variance in pain outcomes. However, there was an attenuation in these associations after accounting for psychosocial/behavioral factors, highlighting their roles in modifying the relationship between disease activity and pain. These findings suggest that multilevel interventions may be needed to tackle the negative effect of pain in SLE.
确定系统性红斑狼疮（SLE）中超越疾病活动和器官损伤的疼痛的生物心理社会机制。
我们对基于人群的 766 例 SLE 患者注册登记处的患者报告数据进行了横断面分析。使用分层线性回归分析了疼痛强度和干扰的预测因素。我们建立了 2 个主要的分层回归模型，将疼痛强度和干扰作为因变量，均回归于疾病活动和器官损伤。对于每个模型，我们试图通过以下 6 个阶段中的每个阶段来建立疼痛结果与主要暴露因素之间的关系：人口统计学、社会经济学、身体、心理、行为和社会因素。我们还进行了敏感性分析，消除了疾病活动测量中所有明显的疼痛方面，并重新估计了模型。
疾病活动和器官损伤解释了疼痛强度和干扰的 32-33%的方差。社会人口因素解释了疼痛结果的额外 4-9%的方差，而心理社会/行为因素则解释了最后的 4%的方差。在敏感性分析中，我们发现疾病活动和器官损伤解释了疼痛结果的 25%的方差。
疾病活动仅解释了疼痛结果的 33%。然而，在考虑到心理社会/行为因素后，这些关联有所减弱，突出了它们在改变疾病活动与疼痛之间关系中的作用。这些发现表明，可能需要多层次的干预措施来解决 SLE 中疼痛的负面影响。
