慢性阻塞性肺病的氣道發炎與重塑：長效型支氣管擴張劑的角色

慢性阻塞性肺病是常見且重要的呼吸道疾病，主要因為長期吸菸或空氣汙染的刺激造成氣道的發炎與重塑，造成支氣管收縮、肺功能下降等後果。治療方面除了擴張支氣管緩解症狀以及延緩肺功能惡化之外，如何降低氣道發炎與重塑亦是重要課題。抗發炎的藥物例如類固醇、巨環內酯、第四型磷酸二酯酵素抑制劑等仍有阻抗性或副作用等缺點，亦無法有效抑制氣道重塑。目前主要的支氣管擴張劑包括長效抗膽鹼製劑及長效乙二型交感神經興奮劑兩類，除了擴張支氣管之外，在細胞與動物實驗中，均有研究顯示其有對抗氣道發炎與重塑的效果。然而，這樣的效果對於臨床病人而言目前仍具爭議性，期待未來可藉由分析慢性阻塞性肺病患者的不同分型、合併多種藥物、或更大規模的臨床試驗等方式取得更有力的證據。

關鍵字

慢性阻塞性肺病；長效型支氣管擴張劑；長效抗膽鹼製劑；長效乙二型交感神經興奮劑；氣道發炎與重塑

並列摘要

Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality and morbidity worldwide. The etiology of COPD is mainly due to chronic exposure of cigarette smoke or air pollutants, causing airway inflammation and remodeling with the consequence of airflow limitation and emphysema. In addition to symptomatic treatment, numerous studies focused on how to inhibit airway inflammation and remodeling of COPD. Anti-inflammatory agents such as corticosteroid, macrolides or phosphodiesterase-4 inhibitor have limitations such as cigarette-smoke related corticosteroid resistance, concerns of major adverse effects, or failure of showing significant anti-remodeling activity. Bronchodilators including long acting muscarinic antagonist, LAMA, and long acting β2-adrenergic receptor agonist, LABA, are mainstay pharmacological choices of COPD. Recent studies have shown that both LAMA and LABA had the abilities to inhibit cigarette smoke-induced airway inflammation and remodeling in vitro and in vivo. However, these anti-inflammatory and anti-remodeling effects remain controversial in the clinical setting. Future studies may be focused on combining different agents, analyzing these effects in different phenotype of COPD patients or larger numbers of study population.

並列關鍵字

Chronic Obstructive Pulmonary Disease, COPD ； Long acting bronchodilators ； Long acting muscarinic antagonist ； Long acting β2-adrenergic receptor agonist ； Airway inflammation and remodeling

國際替代計量

慢性阻塞性肺病的氣道發炎與重塑：長效型支氣管擴張劑的角色

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