Associations between sickness behavior, but not inflammatory cytokines, and psychiatric comorbidity in chronic pain

IF 3.4 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Jenny L.M. Åström Reitan , Bianka Karshikoff , Linda Holmström , Mats Lekander , Mike K. Kemani , Rikard K. Wicksell
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Abstract

Objectives

Approximately one in five adults experiences chronic pain, often in co-occurrence with depression, insomnia, anxiety, and lower self-rated health. Elevated levels of cytokines, e.g. tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), interleukin 8 (IL-8), and interleukin 10 (IL-10), have been identified in patients with chronic pain. Depression, insufficient sleep, poor self-rated health, and pain intensity have also been associated with inflammatory biomarkers. This study aimed to investigate the interrelationships between inflammatory biomarkers and depression, insomnia, anxiety, self-rated health, sickness behavior, and pain intensity in patients with chronic pain.

Methods

Self-report questionnaires and blood samples analyzed for plasma levels of inflammatory biomarkers were collected from 80 adult patients with chronic pain. Associations between inflammatory biomarkers (TNF-α, IL-6, IL-8, IL-10, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR)) and depression, insomnia, anxiety, self-rated health, sickness behavior, and pain intensity, were analyzed using bivariate Spearman rank correlation coefficients and regression analyses.

Results

Participants were mainly women (72.5 %), with a mean age of 50.8 years, and a reported mean pain duration of 16.7 years. There were significant correlations between insomnia and CRP (rs =.26, p <.05); sex and ESR (rs =.29, p <.05); age and IL-6 (rs =.29, p <.05) and IL-8 (rs =.30, p <.05); BMI and IL-6 (rs =.50, p <.001), CRP (rs =.63, p <.001) and ESR (rs =.42, p <.001). Ratings of depression were positively and significantly related to ratings of sickness behavior and anxiety (β =.32 and β =.40, respectively), explaining 49 % of the total variance in depression ratings. Insomnia was positively and significantly related to sickness behavior (β =.37) explaining 31 % of the total variance in insomnia ratings. Inflammatory biomarkers, however, did not contribute significantly to the models.

Conclusions

Participants reported high levels of symptoms, yet the associations between these ratings and the inflammatory biomarkers were either absent or weak. Also, despite high levels of self-reported sickness behavior, overall the inflammatory status remained within the normal range. Ratings of sickness behavior contributed more than inflammatory markers in explaining ratings of depression and insomnia. The present results point to the complexity of chronic pain, and the challenges of identifying biomarkers that explain symptomatology.

慢性疼痛患者的病态行为(而非炎性细胞因子)与精神病合并症之间的关系
目标大约每五个成年人中就有一人有慢性疼痛的经历,而且往往同时伴有抑郁、失眠、焦虑和自我健康评价较低等症状。慢性疼痛患者体内的细胞因子水平升高,如肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、白细胞介素8(IL-8)和白细胞介素10(IL-10)。抑郁、睡眠不足、自评健康不良和疼痛强度也与炎症生物标志物有关。本研究旨在调查慢性疼痛患者的炎症生物标志物与抑郁、失眠、焦虑、自评健康状况、疾病行为和疼痛强度之间的相互关系。结果参与者主要为女性(72.5%),平均年龄为 50.8 岁,报告的平均疼痛持续时间为 16.7 年。失眠与 CRP(rs =.26,p <.05)、性别与血沉(rs =.29,p <.05)、年龄与 IL-6 (rs =.29,p <.05)和 IL-8(rs =.30,p <.05);体重指数与 IL-6(rs =.50,p <.001)、CRP(rs =.63,p <.001)和 ESR(rs =.42,p <.001)。抑郁评分与疾病行为和焦虑评分呈显著正相关(分别为 β =.32 和 β =.40),占抑郁评分总方差的 49%。失眠与生病行为呈显著正相关(β=.37),占失眠评分总方差的 31%。然而,炎症生物标志物对模型的贡献不大。结论参与者报告的症状水平很高,但这些评分与炎症生物标志物之间的关联要么不存在,要么很弱。此外,尽管自我报告的疾病行为水平较高,但总体炎症状态仍在正常范围内。在解释抑郁和失眠的评分时,对疾病行为的评分比炎症标志物的贡献更大。本研究结果表明了慢性疼痛的复杂性,以及确定能解释症状的生物标志物所面临的挑战。
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来源期刊
Psychoneuroendocrinology
Psychoneuroendocrinology 医学-精神病学
CiteScore
7.40
自引率
8.10%
发文量
268
审稿时长
66 days
期刊介绍: Psychoneuroendocrinology publishes papers dealing with the interrelated disciplines of psychology, neurobiology, endocrinology, immunology, neurology, and psychiatry, with an emphasis on multidisciplinary studies aiming at integrating these disciplines in terms of either basic research or clinical implications. One of the main goals is to understand how a variety of psychobiological factors interact in the expression of the stress response as it relates to the development and/or maintenance of neuropsychiatric illnesses.
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