Nakamura Y, Hoshino M, Sim J J, Ishii K, Hosaka K, Sakamoto T
Second Department of Internal Medicine, Toho University School of Medicine, Tokyo, Japan.
Thorax. 1998 Oct;53(10):835-41. doi: 10.1136/thx.53.10.835.
It has been reported that pranlukast reduces the antigen induced immediate and late phase asthmatic responses, airway hyperreactivity to acetylcholine, and pulmonary eosinophil accumulation in guinea pigs. A study was undertaken to test the hypothesis that pranlukast may reduce the number of inflammatory cells in the bronchial mucosa of patients with asthma.
A double blind, placebo controlled study was performed in 17 mild to moderate asthmatic subjects to examine changes in inflammatory cell infiltration in response to pranlukast (225 mg orally twice per day for four weeks). Comparisons of the mean daily beta 2 agonist use, symptom score, FEV1 percentage predicted, and airway methacholine responsiveness were made before and after treatment. Using fibreoptic bronchoscopy, bronchial biopsy specimens were obtained before and after treatment with either pranlukast (n = 10) or placebo (n = 7). Immunohistology was performed using monoclonal antibodies for CD3, CD4, CD8, CD68, NP57, AA1, EG1, EG2, gamma GTP and CD19.
When the pranlukast and placebo treated groups were compared there were decreases in beta 2 agonist use, symptom score, and airway methacholine responsiveness after pranlukast but no increase in FEV1 was seen. The clinical response in patients treated with pranlukast was accompanied by a reduction in CD3 (median difference -37, 95% confidence interval (CI) -69 to -1; p < 0.05), CD4 (median difference -28, 95% CI -49 to -8; p < 0.01), AA1 (median difference -15, 95% CI -26 to 0; p < 0.05) and EG2 positive cells (95% CI -35 to 0; p < 0.05), but not in EG1 positive eosinophils, gamma GTP positive cells, and CD19 positive plasma cells.
These results support the view that pranlukast may act by inhibition of bronchial inflammation in patients with asthma.
据报道，普仑司特可减轻豚鼠抗原诱导的速发和迟发性哮喘反应、气道对乙酰胆碱的高反应性以及肺部嗜酸性粒细胞聚集。本研究旨在验证普仑司特可能减少哮喘患者支气管黏膜炎症细胞数量这一假说。
对17例轻至中度哮喘患者进行了一项双盲、安慰剂对照研究，以观察普仑司特（每日口服225mg，分两次服用，共四周）治疗后炎症细胞浸润的变化。比较了治疗前后每日β2激动剂的使用量、症状评分、预测的FEV1百分比以及气道对乙酰甲胆碱的反应性。使用纤维支气管镜，在普仑司特（n = 10）或安慰剂（n = 7）治疗前后获取支气管活检标本。使用针对CD3、CD4、CD8、CD68、NP57、AA1、EG1、EG2、γGTP和CD19的单克隆抗体进行免疫组织学检查。
比较普仑司特治疗组和安慰剂治疗组，普仑司特治疗后β2激动剂使用量、症状评分和气道对乙酰甲胆碱的反应性均降低，但FEV1未见增加。普仑司特治疗患者的临床反应伴随着CD3（中位数差异-37，95%置信区间（CI）-69至-1；p < 0.05）、CD4（中位数差异-28，95%CI -49至-8；p < 0.01）、AA1（中位数差异-15，95%CI -26至0；p < 0.05）和EG2阳性细胞（95%CI -35至0；p < 0.05）数量减少，但EG1阳性嗜酸性粒细胞、γGTP阳性细胞和CD19阳性浆细胞数量未减少。
这些结果支持普仑司特可能通过抑制哮喘患者支气管炎症发挥作用的观点。
