PDF(Pubmed)
Abstract：
UNASSIGNED: The immune system is believed to be important in the initiation and maintenance of chronic pain.
UNASSIGNED: The aim was to investigate whether patients with chronic painful polyneuropathy (PP) differ in cytokine profiles of serum and/or cerebrospinal fluid (CSF) compared with pain-free controls.
UNASSIGNED: Thirty-nine patients (16 women and 23 men, mean age, 69.2 ± 12.7 years, range 41-92 years) with PP (mean duration 43 ± 48.3 months) were phenotyped with quantitative sensory testing and electroneurography, and serum and CSF samples were analyzed by 40-multiplexed, bead-based cytokine immunoassays. Results were compared with 36 age- and gender-matched patients with normal pressure hydrocephalus and absence of abnormal CSF findings.
UNASSIGNED: Compared with controls, patients with PP had lower concentrations of several proinflammatory and anti-inflammatory chemokines and cytokines in CSF, and others showed the same tendency, among these were tumor necrosis factor-α (14.1 ± 10.0 vs 23.9 ± 16.4 pg/mL, P < 0.005), interleukin (IL)-2 (0.6 ± 0.4 vs 1.2 ± 0.6 pg/mL, P < 0.0001), IL-6 (4.7 ± 6.8 vs 7.3 ± 9 pg/mL, P = 0.001), and IL-10 (7.5 ± 6.8 vs 16.8 ± 19.2 pg/mL, P < 0.01), whereas no differences were observed in serum.
UNASSIGNED: Results suggest that (1) inflammatory mediators play a minor role in the maintenance of chronic pain in contrast to initiation of acute pain, (2) chemokines/cytokines are downregulated in chronic pain, or (3) chemokines/cytokines have a protective role for nerve regeneration that is disturbed in patients with chronic pain.
UNASSIGNED: The aim was to investigate whether patients with chronic painful polyneuropathy (PP) differ in cytokine profiles of serum and/or cerebrospinal fluid (CSF) compared with pain-free controls.
UNASSIGNED: Thirty-nine patients (16 women and 23 men, mean age, 69.2 ± 12.7 years, range 41-92 years) with PP (mean duration 43 ± 48.3 months) were phenotyped with quantitative sensory testing and electroneurography, and serum and CSF samples were analyzed by 40-multiplexed, bead-based cytokine immunoassays. Results were compared with 36 age- and gender-matched patients with normal pressure hydrocephalus and absence of abnormal CSF findings.
UNASSIGNED: Compared with controls, patients with PP had lower concentrations of several proinflammatory and anti-inflammatory chemokines and cytokines in CSF, and others showed the same tendency, among these were tumor necrosis factor-α (14.1 ± 10.0 vs 23.9 ± 16.4 pg/mL, P < 0.005), interleukin (IL)-2 (0.6 ± 0.4 vs 1.2 ± 0.6 pg/mL, P < 0.0001), IL-6 (4.7 ± 6.8 vs 7.3 ± 9 pg/mL, P = 0.001), and IL-10 (7.5 ± 6.8 vs 16.8 ± 19.2 pg/mL, P < 0.01), whereas no differences were observed in serum.
UNASSIGNED: Results suggest that (1) inflammatory mediators play a minor role in the maintenance of chronic pain in contrast to initiation of acute pain, (2) chemokines/cytokines are downregulated in chronic pain, or (3) chemokines/cytokines have a protective role for nerve regeneration that is disturbed in patients with chronic pain.
摘要：
■免疫系统被认为在慢性疼痛的开始和维持中是重要的。
■目的是研究慢性疼痛性多发性神经病（PP）患者与无痛对照组相比，血清和/或脑脊液（CSF）的细胞因子谱是否存在差异。
■39名患者（16名女性和23名男性，平均年龄,69.2±12.7年，范围41-92年）与PP（平均持续时间43±48.3个月）进行表型定量感官测试和神经电图，血清和CSF样本通过40多重分析，基于珠子的细胞因子免疫测定。结果与36例年龄和性别匹配的正常压力脑积水患者进行了比较，无脑脊液异常发现。
■与对照组相比，PP患者CSF中几种促炎和抗炎趋化因子和细胞因子的浓度较低，其他人也表现出同样的倾向，其中肿瘤坏死因子-α（14.1±10.0vs23.9±16.4pg/mL，P<0.005)，白细胞介素（IL）-2（0.6±0.4vs1.2±0.6pg/mL，P<0.0001),IL-6（4.7±6.8vs7.3±9pg/mL，P=0.001),和IL-10（7.5±6.8vs16.8±19.2pg/mL，P<0.01),而在血清中没有观察到差异。
■结果表明（1）与急性疼痛的开始相比，炎症介质在慢性疼痛的维持中起次要作用，（2）趋化因子/细胞因子在慢性疼痛中下调，或（3）趋化因子/细胞因子对慢性疼痛患者的神经再生具有保护作用。
■目的是研究慢性疼痛性多发性神经病（PP）患者与无痛对照组相比，血清和/或脑脊液（CSF）的细胞因子谱是否存在差异。
■39名患者（16名女性和23名男性，平均年龄,69.2±12.7年，范围41-92年）与PP（平均持续时间43±48.3个月）进行表型定量感官测试和神经电图，血清和CSF样本通过40多重分析，基于珠子的细胞因子免疫测定。结果与36例年龄和性别匹配的正常压力脑积水患者进行了比较，无脑脊液异常发现。
■与对照组相比，PP患者CSF中几种促炎和抗炎趋化因子和细胞因子的浓度较低，其他人也表现出同样的倾向，其中肿瘤坏死因子-α（14.1±10.0vs23.9±16.4pg/mL，P<0.005)，白细胞介素（IL）-2（0.6±0.4vs1.2±0.6pg/mL，P<0.0001),IL-6（4.7±6.8vs7.3±9pg/mL，P=0.001),和IL-10（7.5±6.8vs16.8±19.2pg/mL，P<0.01),而在血清中没有观察到差异。
■结果表明（1）与急性疼痛的开始相比，炎症介质在慢性疼痛的维持中起次要作用，（2）趋化因子/细胞因子在慢性疼痛中下调，或（3）趋化因子/细胞因子对慢性疼痛患者的神经再生具有保护作用。
