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University of Washington, Seattle, WA, USA.
We appreciate M.K. Han's interest in the results of our study 1 and for the extended analyses of our data by calculating the risk for the population with acid gastro-oesophageal reflux (GER) and idiopathic pulmonary fibrosis (IPF). While this interesting observation deserves further study, as emphasised, it is apparent that the calculated risk is based on the number of GER disease+ = 130/number of cases+controls = 179x(OR1)/OR = .498. Since an effective treatment regimen to improve patient outcome is yet to be determined for IPF, M.K. Han argues for patients with IPF to be treated for acid GER.
It is important to reiterate that our study design was not intended to investigate the causal effect of acid GER in IPF. While further studies are needed to clarify this in the pathogenesis of IPF, we have recently reported that some patients with IPF stabilise with adequate control of acid GER 2. Only a double-blind, placebo-controlled, randomised clinical trial, with use of proton pump inhibitors (PPIs), can determine the efficacy of PPI in the treatment for IPF. In designing clinical trials using other agents, it may also be important to stratify randomisation based on the use of PPI at baseline and during the study period.
As more investigators and clinicians are recognising the high association of acid GER in IPF, M.K. Han's suggestion to treat IPF patients empirically with PPI will undoubtedly be raised again. We believe it is imperative to pursue further studies to determine the role of acid GER in the pathogenesis of IPF, and to determine if suppression of acid GER by medical and/or surgical treatment prevents further progression of IPF and/or improves outcome measures for patients with IPF.
We would like to thank M.K. Han for supporting our concepts by further analyses of our data. Hopefully, well-designed prospective clinical studies will be undertaken in the near future and the results will confirm the provocative observations.
REFERENCES
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