Wood-Baker Richard
Royal Hobart Hospital & University of Tasmania, Hobart, Tasmania, Australia.
Am J Respir Med. 2003;2(6):451-8. doi: 10.1007/BF03256672.
COPD, encompassing both chronic bronchitis and emphysema, usually results from exposure to tobacco smoke. Smoking causes infiltration of the airways with leukocytes, an imbalance between proteases and their naturally occurring inhibitors and local cytokine secretion in the lung, which leads to airway inflammation and alveolar destruction. Corticosteroids have a range of anti-inflammatory actions, particularly inhibition of cytokine secretion, which suggests that they may be effective in COPD. However, data from the highest quality studies available do not show any evidence of significant improvement in symptoms of patients with COPD treated with systemic corticosteroids.A meta-analysis found that about 10% of patients with stable COPD showed an improvement in lung function following treatment with short-term systemic corticosteroids compared with placebo. Exercise capacity in patients with COPD was evaluated in four studies, only one of which found a significant improvement with oral corticosteroids compared with placebo. Long-term systemic corticosteroid treatment in patients with stable COPD has not been found to alter the rate of decline in FEV(1). Although systemic corticosteroids are associated with a range of adverse effects, the data do not allow precise quantification of their contribution to morbidity. However, studies show an increased risk of osteoporosis in COPD. Recent studies have also found an association between oral corticosteroid administration and mortality in patients with stable COPD, but it is not clear if this is a cause and effect relationship. Current data do not support long-term administration of systemic corticosteroids to all patients with stable COPD. Results of studies suggest that short-term oral corticosteroid administration may identify a sub-population of patients with COPD who may benefit through a reduction in the decline in FEV(1) and better control of symptoms by long-term administration of inhaled corticosteroids; these findings need to be tested by further research.
慢性阻塞性肺疾病（COPD）包括慢性支气管炎和肺气肿，通常由接触烟草烟雾引起。吸烟会导致气道被白细胞浸润，蛋白酶与其天然存在的抑制剂之间失衡，以及肺部局部细胞因子分泌失调，进而导致气道炎症和肺泡破坏。皮质类固醇具有一系列抗炎作用，尤其是抑制细胞因子分泌，这表明它们可能对COPD有效。然而，现有最高质量研究的数据并未显示接受全身皮质类固醇治疗的COPD患者症状有任何显著改善的证据。一项荟萃分析发现，与安慰剂相比，约10%的稳定期COPD患者在接受短期全身皮质类固醇治疗后肺功能有所改善。四项研究评估了COPD患者的运动能力，其中只有一项研究发现与安慰剂相比，口服皮质类固醇有显著改善。尚未发现对稳定期COPD患者进行长期全身皮质类固醇治疗能改变第一秒用力呼气容积（FEV₁）的下降速率。虽然全身皮质类固醇与一系列不良反应相关，但数据无法精确量化它们对发病率的影响。然而，研究表明COPD患者患骨质疏松症的风险增加。最近的研究还发现稳定期COPD患者口服皮质类固醇与死亡率之间存在关联，但尚不清楚这是否为因果关系。目前的数据不支持对所有稳定期COPD患者长期使用全身皮质类固醇。研究结果表明，短期口服皮质类固醇可能会识别出一部分COPD患者，这些患者可能通过长期吸入皮质类固醇减少FEV₁下降并更好地控制症状而获益；这些发现需要进一步研究来验证。
