Department of Orthopaedic Surgery, University of Heidelberg, Schlierbacher Landstrasse 200a, 69118 Heidelberg, Germany.
Arthritis Res Ther. 2010;12(5):R185. doi: 10.1186/ar3155. Epub 2010 Oct 11.
Our previous work showed higher tumour necrosis factor (TNF)-α levels in patients with chronic low back pain (cLBP) compared to healthy controls. However, patients with depression as a comorbidity did not have higher TNF-α levels in comparison to patients without depression. In this study we investigated the influence of depression on therapy outcomes such as TNF-α serum levels, pain intensity and back function in patients with cLBP. Our hypothesis was that patients with both cLBP and depression benefit no less than patients with cLBP alone from the multidisciplinary pain therapy.
A total of 58 patients with cLBP alone or with both cLBP and depression were age- and sex-matched with 29 healthy controls. Serum concentrations of TNF-α were assayed at the beginning of the study (T0) and 10 days (T1), 21 days (T2), and 180 days (T3) later. The clinical outcomes such as pain intensity, as well as back function, sleep, exercise, alcohol and nicotine consumption were documented. In the first three weeks, all patients underwent multidisciplinary therapy based upon biological, psychological, physical and psychosocial components.
Over the whole course there were no differences in TNF-α level between cLBP patients with and without depression. At T0, both cLBP patients with (cLBP+DE) and without (cLBP) depression showed significantly higher TNF-α serum levels (P = 0.002 for cLBP+DE, P = 0.004 for cLBP) than healthy controls (HC) that normalized after 10 days of therapy and remained similar to healthy controls. During the follow-up, the depression scales were normalised and pain intensity was significantly reduced. Both evidences processed parallel to the reduction of TNF-α levels, which correlates neither with depression score nor with pain intensity at any time point.
Depression as a comorbidity to chronic low back pain did not influence the serum TNF-α level in the course of six months, but seemed to affect the success of therapy. cLBP patients with comorbidity of depression benefit from multidisciplinary pain therapy not only to the same extent but also to a greater degree than cLBP patients without depression.
我们之前的研究表明，慢性下背痛（cLBP）患者的肿瘤坏死因子（TNF）-α水平高于健康对照组。然而，与无抑郁的患者相比，患有抑郁症的患者 TNF-α水平并没有更高。在这项研究中，我们研究了抑郁对 cLBP 患者的治疗结果（如 TNF-α 血清水平、疼痛强度和背部功能）的影响。我们的假设是，患有 cLBP 和抑郁症的患者从多学科疼痛治疗中获益不亚于仅患有 cLBP 的患者。
共有 58 例 cLBP 患者（伴或不伴抑郁症）与 29 例健康对照者按年龄和性别匹配。在研究开始时（T0）和 10 天（T1）、21 天（T2）和 180 天（T3）后检测血清 TNF-α浓度。记录疼痛强度、背部功能、睡眠、运动、饮酒和吸烟等临床结果。在前三周，所有患者都接受了基于生物、心理、生理和心理社会因素的多学科治疗。
整个过程中，伴或不伴抑郁的 cLBP 患者的 TNF-α水平没有差异。在 T0，伴抑郁的 cLBP 患者（cLBP+DE）和不伴抑郁的 cLBP 患者（cLBP）的 TNF-α血清水平均显著高于健康对照组（cLBP+DE 为 P = 0.002，cLBP 为 P = 0.004），治疗 10 天后恢复正常，与健康对照组相似。在随访期间，抑郁量表正常化，疼痛强度显著降低。这两个证据与 TNF-α水平的降低平行，而 TNF-α水平与任何时间点的抑郁评分或疼痛强度均无关。
作为慢性下背痛的合并症，抑郁在六个月的病程中并不影响血清 TNF-α水平，但似乎影响治疗的成功。患有抑郁症合并症的慢性下背痛患者不仅受益于多学科疼痛治疗，而且受益程度不亚于没有抑郁症的慢性下背痛患者。
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