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It is, perhaps, an embarrassment of riches for idiopathic pulmonary fibrosis (IPF) researchers and providers—the approval of pirfenidone and nintedanib for the treatment of IPF and on its heels, an unprecedented interest on the part of pharmaceutical companies to sponsor clinical trials to test new candidates. In addition, large amounts of clinical data from patients with IPF of very diverse genetic and environmental backgrounds accompanied the clinical trials for pirfenidone and nintedanib. And the new studies promise to yield even more data, repositories of blood, cells, DNA and RNA, at an ever-increasing degree of sophistication. With the availability of these biorepositories and data repositories, very provocative questions can be asked—and potentially answered.
It is in this context that we read in Thorax a new post hoc analysis by Professor Kreuter and colleagues of 624 patients with IPF pooled from the placebo arms of the pirfenidone trials (CAPACITY 004 and 006 and ASCEND).1 The authors have previously analysed these patients and have addressed some intriguing questions, including how anticoagulation and acid suppression in IPF for comorbid conditions affected study outcomes.2 ,3 In the present article, they have turned their attention to another question that has dogged clinical researchers previously, namely how the use of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMG coenzyme A) reductase inhibitors, popularly known as ‘statins’, affects outcomes in IPF. The authors employed a shared frailty model, which is an extension of the Cox regression model,1 to determine the effect of statins on study outcomes without adjustment and a multivariate model to adjust for age, …