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类风湿性多肌痛患者在使用肿瘤坏死因子-α阻滞剂依那西普治疗前后神经内分泌轴的活性

Activity of the neuroendocrine axes in patients with polymyalgia rheumatica before and after TNF-α blocking etanercept treatment.

作者信息

Kreiner Frederik Flindt, Galbo Henrik

出版信息

Arthritis Res Ther. 2012 Aug 15;14(4):R186. doi: 10.1186/ar4017.

DOI:10.1186/ar4017
PMID:22894827
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3580582/
Abstract

INTRODUCTION

In this study, we evaluated the activity of the neuroendocrine axes in patients with polymyalgia rheumatica (PMR) before and after tumor necrosis factor (TNF)-α-blocking etanercept treatment, which previously has been shown to reduce interleukin 6 (IL-6) and C-reactive protein (CRP) markedly in PMR.

METHODS

Plasma samples were collected from 10 glucocorticoid-naïve patients with PMR and 10 matched controls before and after etanercept treatment (25 mg biweekly for 2 weeks). The primary end points were pre- and posttreatment levels of adrenocorticotropic hormone (ACTH), cortisol, adrenaline, thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), prolactin, and insulin-like growth factor 1 (IGF-1).

RESULTS

Before TNF-α-blocking treatment, plasma TNF-α, ACTH, and cortisol levels were higher in patients versus controls (P < 0.05 and P < 0.001, respectively); during TNF-α blockade in patients, levels of both hormones decreased (P < 0.05 and P < 0.01, respectively), whereas levels in controls increased (P < 0.05), abolishing the pretreatment differences. Pretreatment adrenaline levels were more than twice as high in patients than in controls (P < 0.01); after treatment in patients, levels had decreased (P < 0.05) but remained higher versus controls (P < 0.05). Levels of the other hormones never differed significantly between groups (P > 0.05).

CONCLUSIONS

In PMR, TNF-α may increase the activities of the hypothalamic-pituitary-adrenal and the hypothalamic-sympthoadrenomedullary axes. Secretion of TSH, FSH, prolactin, and IGF-1 is not clearly changed in PMR.

TRIAL REGISTRATION

ClinicalTrials.gov (NCT00524381).

摘要

引言

在本研究中,我们评估了肿瘤坏死因子(TNF)-α阻断剂依那西普治疗前后风湿性多肌痛(PMR)患者神经内分泌轴的活性,此前已证明依那西普可显著降低PMR患者的白细胞介素6(IL-6)和C反应蛋白(CRP)。

方法

采集10例未使用过糖皮质激素的PMR患者和10例匹配对照在依那西普治疗前及治疗后(每两周25mg,共2周)的血浆样本。主要终点指标为促肾上腺皮质激素(ACTH)、皮质醇、肾上腺素、促甲状腺激素(TSH)、促卵泡激素(FSH)、催乳素和胰岛素样生长因子1(IGF-1)的治疗前及治疗后水平。

结果

在TNF-α阻断治疗前,患者的血浆TNF-α、ACTH和皮质醇水平高于对照组(分别为P < 0.05和P < 0.001);在患者接受TNF-α阻断治疗期间,两种激素水平均下降(分别为P < 0.05和P < 0.01),而对照组水平升高(P < 0.05),消除了治疗前的差异。患者治疗前肾上腺素水平比对照组高出两倍多(P < 0.01);患者治疗后水平下降(P < 0.05),但仍高于对照组(P < 0.05)。其他激素水平在两组之间从未有显著差异(P > 0.05)。

结论

在PMR中,TNF-α可能增加下丘脑-垂体-肾上腺轴和下丘脑-交感-肾上腺髓质轴的活性。PMR中TSH、FSH、催乳素和IGF-1的分泌没有明显变化。

试验注册

ClinicalTrials.gov(NCT00524381)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/74d9ca5e20ef/ar4017-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/3675015cd23f/ar4017-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/7b0dc0626835/ar4017-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/1a660bd6ed70/ar4017-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/5f07f3e08c04/ar4017-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/74d9ca5e20ef/ar4017-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/3675015cd23f/ar4017-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/7b0dc0626835/ar4017-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/1a660bd6ed70/ar4017-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/5f07f3e08c04/ar4017-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f558/3580582/74d9ca5e20ef/ar4017-5.jpg

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