Merlin Jessica S, Westfall Andrew O, Heath Sonya L, Goodin Burel R, Stewart Jesse C, Sorge Robert E, Younger Jarred
*Division of Infectious Diseases, University of Alabama at Birmingham, Birmingham, AL; †Division of Gerontology, Geriatrics, and Palliative Care, University of Alabama at Birmingham, Birmingham, AL; ‡Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL; §Department of Psychology, University of Alabama at Birmingham, Birmingham, AL; ‖Division of Pain Medicine, University of Alabama at Birmingham, Birmingham, AL; and ¶Department of Psychology, Indiana University-Purdue University Indianapolis (IUPUI), Indianapolis, IN.
J Acquir Immune Defic Syndr. 2017 Aug 1;75(4):e99-e103. doi: 10.1097/QAI.0000000000001377.
The pathophysiology of chronic pain experienced by people living with HIV (PLWH) in the current antiretroviral treatment era is poorly understood. We sought to investigate the relationship between inflammation and chronic pain in PLWH. We hypothesized that, among PLWH who have undetectable HIV viral loads, those with chronic multisite pain (CMP) would have higher levels of circulating pain-related inflammatory markers than those without chronic pain.
This study was conducted at the University of Alabama at Birmingham's Center for AIDS Research Network of Integrated Clinical System site.
We compared inflammatory markers in 70 PLWH with CMP and 70 PLWH without chronic pain. Custom multiplex human inflammatory assays were completed on banked plasma specimens to measure cytokines commonly associated with chronic inflammatory pain: interleukin 1β (IL-1β), eotaxin, IL-15, IL-6, tumor necrosis factor α, and leptin. Logistic regression models were built using group status (CMP vs no pain) as the outcome variable, with each cytokine as independent variables and age, sex, substance use, and prescribed opioid medications as covariates.
Participants were mostly men (71%); 53% were 50 years or older. The most common sites of pain were low back (86%), hands/feet (81%), and knee (66%). Median CD4 T-cell count was 676 cells per milliliter. IL-1β was significantly higher in the CMP group than in the individuals without chronic pain (odds ratio: 1.35, 95% confidence interval: 1.01 to 1.82, P < 0.05). Eotaxin, IL-15, IL-6, tumor necrosis factor α, and leptin were not significantly different between groups.
We found that PLWH who also have CMP have significantly higher levels of IL-1β than PLWH who do not have any pain. Future work on the role of IL-1β on chronic pain pathogenesis in this population may inform novel approaches to chronic pain management.
在当前抗逆转录病毒治疗时代，人们对感染艾滋病毒者（PLWH）所经历的慢性疼痛的病理生理学了解甚少。我们试图研究PLWH中炎症与慢性疼痛之间的关系。我们假设，在艾滋病毒病毒载量无法检测到的PLWH中，患有慢性多部位疼痛（CMP）的人比没有慢性疼痛的人具有更高水平的循环疼痛相关炎症标志物。
本研究在阿拉巴马大学伯明翰分校综合临床系统艾滋病研究网络中心进行。
我们比较了70名患有CMP的PLWH和70名没有慢性疼痛的PLWH的炎症标志物。对储存的血浆样本进行定制的多重人类炎症检测，以测量通常与慢性炎症性疼痛相关的细胞因子：白细胞介素1β（IL-1β）、嗜酸性粒细胞趋化因子、IL-15、IL-6、肿瘤坏死因子α和瘦素。使用组状态（CMP与无疼痛）作为结果变量建立逻辑回归模型，将每种细胞因子作为自变量，年龄、性别、物质使用情况和处方阿片类药物作为协变量。
参与者大多为男性（71%）；53%的人年龄在50岁及以上。最常见的疼痛部位是下背部（86%）、手/脚（81%）和膝盖（66%）。CD4 T细胞计数中位数为每毫升676个细胞。CMP组的IL-1β显著高于没有慢性疼痛的个体（比值比：1.35，95%置信区间：1.01至1.82，P<0.05）。嗜酸性粒细胞趋化因子、IL-15、IL-6、肿瘤坏死因子α和瘦素在两组之间无显著差异。
我们发现，患有CMP的PLWH的IL-1β水平显著高于没有任何疼痛的PLWH。未来关于IL-1β在该人群慢性疼痛发病机制中作用的研究可能为慢性疼痛管理的新方法提供依据。
