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丙酸氟替卡松吸入对慢性阻塞性肺疾病患者花生四烯酸代谢物水平的影响。

Effects of fluticasone propionate inhalation on levels of arachidonic acid metabolites in patients with chronic obstructive pulmonary disease.

作者信息

Verhoeven G T, Garrelds I M, Hoogsteden H C, Zijlstra F J

机构信息

Department of Pulmonary and Intensive Care Medicine, University Hospital Dijkzigt and Erasmus University, EMCR, Rotterdam, The Netherlands.

出版信息

Mediators Inflamm. 2001 Feb;10(1):21-6. doi: 10.1080/09629350123056.

Abstract

BACKGROUND

In smoking COPD patients the bronchoalveolar lavage (BAL) fluid contains high numbers of inflammatory cells. These cells might produce arachidonic acid (AA) metabolites, which contribute to inflammation and an increased bronchomotor tone.

AIMS

To investigate levels of AA metabolites in BAL fluid, before and after inhaled glucocorticoid therapy: fluticasone propionate (FP) 1 mg per day, or placebo.

METHODS

A double-blind placebo controlled trial lasting six months. COPD patients were selected by clinical criteria and the presence of bronchial hyper-responsiveness (BHR). Lung function was recorded and in BAL fluid we counted cell numbers and measured LTB4, LTC4/D4/E4, PGE2, 6kPGF1alpha, PGF2alpha and TxB2. A control group consisted of asymptomatic smokers (n=6).

RESULTS

Paired data were obtained from 9 FP treated and 11 placebo patients. BAL cells were almost exclusively alveolar macrophages. In patients and controls both cellularity and levels of AA metabolites were equal Cell numbers did not change after treatment. Statistically significant decreases after FP therapy were noticed for PGE2 (30%), 6kPGF1alpha (41%) and PGF2alpha (54%).

CONCLUSIONS

In COPD, the capability of inflammatory cells to produce certain AA metabolites was decreased after inhaled FP treatment. This result is discussed in its relation to clinical effects, the influence of smoking, and the results of an earlier, similar study in asthma patients.

摘要

背景

在吸烟的慢性阻塞性肺疾病(COPD)患者中,支气管肺泡灌洗(BAL)液含有大量炎性细胞。这些细胞可能产生花生四烯酸(AA)代谢产物,其会导致炎症并增加支气管运动张力。

目的

研究吸入糖皮质激素治疗前后BAL液中AA代谢产物的水平:每天1毫克丙酸氟替卡松(FP)或安慰剂。

方法

一项为期6个月的双盲安慰剂对照试验。通过临床标准和支气管高反应性(BHR)的存在来选择COPD患者。记录肺功能,在BAL液中我们计数细胞数量并测量白三烯B4(LTB4)、白三烯C4/D4/E4(LTC4/D4/E4)、前列腺素E2(PGE2)、6-酮-前列腺素F1α(6kPGF1α)、前列腺素F2α(PGF2α)和血栓素B2(TxB2)。一个对照组由无症状吸烟者组成(n = 6)。

结果

从9名接受FP治疗的患者和11名接受安慰剂治疗的患者中获得配对数据。BAL细胞几乎全是肺泡巨噬细胞。在患者和对照组中,细胞数量和AA代谢产物水平均相等。治疗后细胞数量没有变化。FP治疗后,PGE2(30%)、6kPGF1α(41%)和PGF2α(54%)有统计学意义的下降。

结论

在COPD中,吸入FP治疗后炎性细胞产生某些AA代谢产物的能力下降。该结果结合临床效果、吸烟的影响以及早期在哮喘患者中进行的类似研究结果进行了讨论。

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