Obstructive lung function decline and IPF

Dear Editor,

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease that causes inflammation, scarring, thickening, and stiffening of the lung tissues.¹ The disease is progressive, generally fatal, and causes an irreversible loss of the tissue’s ability to transport oxygen. However, the prognosis is variable and in some cases a great difficult task for pulmonologists.² It is therefore important to determine appropriate determinant factors that may help in predicting the survival and rationale therapeutic interventions.

In this line, we have read with great interest the study by Nishiyama et al. that confirms this poor outcome in IPF.³ In this original observation, Nishiyama et al. hypothesized that the forced expiratory volume in 1 second (FEV₁)/forced vital capacity (FVC) ratio has an impact on prognosis. The results reported have practical implications, however, there are some key aspects on how chronic airway obstruction could impact on IPF.

From a methodology point of view, in order to answer to this question, authors examined retrospectively more than 100 patients and a correlation was found between FEV₁/FVC and survival. Intriguingly, lower FEV₁/FVC was associated with longer survival, making the patients with a lower FEV₁/FVC ratio to have a more favorable prognosis as compared to the patients with higher FEV₁/FVC ratio. In our opinion, it is difficult to find a clear explanation of this observation. The authors speculate that, somehow, smoke may be “good” for the IPF patients (i.e. smoke may inhibit fibroblast proliferation, or decrease the numbers of exacerbations, or determine a slower decrease in lung function). However, it is known that lung fibrosis increases lung elastic recoil. Lung elastic recoil affects the driving pressure that determines the velocity of lung emptying, and we may argue that as the disease progresses, because of the higher elastic recoil of the stiff lungs, the FEV₁/FVC ratio may become higher or higher than normal. Ultimately, a lower FEV₁/FVC ratio may be, somehow, a marker of a less advanced disease.⁴ We consider that to investigate these mechanisms, it would be interesting to measure in these patients transpulmonary pressure and therefore calculate real lung compliance. This approach could give us a more objective and appropriate interpretation of the FEV₁/FVC ratio.

There is a lack of information regarding lung function decline in respiratory symptomatic patients. The real impact of FEV₁,⁴ and other well-known key prognosis factors, as pulmonary artery hypertension should be investigated.⁵ We consider that it is necessary to know whether this variation in FEV₁/FVC is related to the severity of IPF or to other variables. In conclusion, although Nishiyama et al. have made the interesting observation that FEV₁/FVC ratio has an impact on survival in IPF patients, further studies are needed to understand the real physiological mechanisms involved.