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吸入性糖皮质激素治疗哮喘四个月的安慰剂对照免疫病理学研究

Placebo-controlled immunopathologic study of four months of inhaled corticosteroids in asthma.

作者信息

Trigg C J, Manolitsas N D, Wang J, Calderón M A, McAulay A, Jordan S E, Herdman M J, Jhalli N, Duddle J M, Hamilton S A

机构信息

Department of Respiratory Medicine and Allergy, St. Bartholomew's Hospital, London, United Kingdom.

出版信息

Am J Respir Crit Care Med. 1994 Jul;150(1):17-22. doi: 10.1164/ajrccm.150.1.8025745.

Abstract

The effect of prolonged inhaled corticosteroid treatment on bronchial immunopathology was assessed in 25 nonsmoking mildly asthmatic subjects previously receiving intermittent inhaled beta 2-agonist alone. Inhaled beclomethasone dipropionate (BDP), 500 micrograms twice per day or placebo was administered for 4 mo in a double-blind parallel group study. Histamine bronchial provocation, fiberoptic bronchoscopic biopsy, and bronchoalveolar lavage (BAL) were performed before and after treatment. There was no difference in bronchial responsiveness or lung function between groups. In patients treated with BDP compared with placebo, there was a significant reduction in toluidine blue-staining mast cells (p = 0.028) and total (p = 0.005) and activated eosinophils (p = 0.05) in biopsies but no difference in eosinophils or eosinophil cationic protein in BAL. Granulocyte-macrophage colony-stimulating factor expression was significantly reduced in the bronchial epithelium, and the thickness of Type III collagen deposition in the bronchial lamina reticularis reduced from 29.7 +/- 4.4 to 19.8 +/- 3.4 microns (mean +/- 95% confidence interval) (p = 0.04). No change in helper or activated helper T cells occurred. Prolonged BDP treatment reduces inflammatory infiltration, proinflammatory cytokine expression, and subepithelial collagen deposition, a recognized abnormality in asthma.

摘要

在25名此前仅接受过间歇性吸入β2激动剂治疗的非吸烟轻度哮喘患者中,评估了长期吸入皮质类固醇治疗对支气管免疫病理学的影响。在一项双盲平行组研究中,给予500微克二丙酸倍氯米松(BDP),每日两次,或安慰剂,持续4个月。在治疗前后进行组胺支气管激发试验、纤维支气管镜活检和支气管肺泡灌洗(BAL)。两组之间支气管反应性或肺功能无差异。与安慰剂治疗的患者相比,接受BDP治疗的患者活检中甲苯胺蓝染色肥大细胞(p = 0.028)、总嗜酸性粒细胞(p = 0.005)和活化嗜酸性粒细胞(p = 0.05)显著减少,但BAL中的嗜酸性粒细胞或嗜酸性粒细胞阳离子蛋白无差异。支气管上皮中粒细胞巨噬细胞集落刺激因子表达显著降低,支气管网状板中III型胶原沉积厚度从29.7±4.4微米降至19.8±3.4微米(平均值±95%可信区间)(p = 0.04)。辅助性或活化辅助性T细胞无变化。长期BDP治疗可减少炎症浸润、促炎细胞因子表达和上皮下胶原沉积,这是哮喘中公认的异常情况。

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