Anti-acid treatment and disease progression in idiopathic pulmonary fibrosis: an analysis of data from three randomised controlled trials.
Anti-acid treatment and disease progression in idiopathic pulmonary fibrosis: an analysis of data from three randomised controlled trials.
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DOI：
10.1016/s2213-2600(13)70105-x
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发表时间：
2013-07
影响因子：
76.2
通讯作者：
Raghu, Ganesh
中科院分区：
文献类型：
--
作者：
Lee, Joyce S.;Collard, Harold R.;Anstrom, Kevin J.;Martinez, Fernando J.;Noth, Imre;Roberts, Rhonda S.;Yow, Eric;Raghu, Ganesh
异常酸性胃食管反流在特发性肺纤维化中很常见，被认为是其发展的危险因素。回顾性研究表明，抗酸治疗患者的结局有所改善。本研究的目的是确定抗酸治疗与特发性肺纤维化疾病进展之间的关系。从3项IPFnet随机临床试验的安慰剂组中确定IPF患者。病例报告表旨在前瞻性地收集有关胃食管反流诊断和治疗的数据。使用纵向重复测量模型分析这些数据，以确定抗酸治疗（即质子泵抑制剂和组胺-2阻滞剂）的使用与用力肺活量变化之间的关系。分析的次要结局包括急性加重、全因住院和全因死亡。242例特发性肺纤维化患者随机接受安慰剂治疗。51%的患者在入组时正在接受抗酸治疗。服用和未服用抗酸治疗的患者在人口统计学和肺生理学方面没有显著差异。校正性别、基线用力肺活量%预测值和基线一氧化碳弥散量%预测值后，基线时接受抗酸治疗的患者用力肺活量下降较慢（30周内的估计变化为-0.06升vs-0.12升，p值= 0.05）。基线时接受抗酸治疗的患者在研究期间的急性加重较少（无事件vs 9起事件，p值<0.01）。使用抗酸治疗与特发性肺纤维化患者的用力肺活量随时间下降较慢以及急性加重较少有关。这些发现支持了异常酸性胃食管反流促进疾病进展的假设，并表明抗酸治疗可能对特发性肺纤维化患者有益。
Abnormal acid gastroesophageal reflux is common in idiopathic pulmonary fibrosis and is considered a risk factor for its development. Retrospective studies have suggested improved outcomes in patients treated with anti-acid therapy. The aim of this study was to determine the association between anti-acid therapy and disease progression in idiopathic pulmonary fibrosis. Patients with IPF were identified from the placebo arms of the three IPFnet randomized clinical trials. Case report forms were designed to prospectively capture data regarding gastroesophageal reflux diagnosis and treatment. These data were analyzed to determine the relationship between use of anti-acid therapy (i.e. proton pump inhibitors and histamine-2 blockers) and change in forced vital capacity using a longitudinal repeated-measures model. Secondary outcomes analyzed included acute exacerbation, all-cause hospitalization, and all-cause mortality. Two hundred and forty-two patients with idiopathic pulmonary fibrosis were randomized to receive placebo therapy. Fifty-one percent were taking anti-acid therapy upon enrollment. There were no significant differences in demographics and pulmonary physiology between patients taking and not taking anti-acid therapy. After adjustment for sex, baseline forced vital capacity %predicted, and baseline diffusing capacity for carbon monoxide %predicted, patients taking anti-acid therapy at baseline had a slower decline in forced vital capacity (estimated change over 30-weeks of -0.06 liters vs. -0.12 liters, p-value = 0.05). Patients taking anti-acid therapy at baseline had fewer acute exacerbations (no events versus nine events, p-value <0.01) during the study period. The use of anti-acid therapy was associated with a slower decline in forced vital capacity over time and fewer acute exacerbations in patients with idiopathic pulmonary fibrosis. These findings support the hypothesis that abnormal acid gastroesophageal reflux contributes to disease progression and suggest that anti-acid therapy may be beneficial in patients with idiopathic pulmonary fibrosis.