Abstract
BackgroundIdiopathic Pulmonary Fibrosis (IPF) is a progressive and irreversible disease leading to terminal respiratory insufficiency. Fluorodeoxyglucose ([18F]-FDG) PET/CT has been proposed to track the activity of the disease. However, IPF is characterized by regional changes in lung density that affects the FDG uptake, a factor generally not taken into account in previous studies. In this work, we studied the relationship between severity of IPF and lung uptake of [18F]-FDG, evaluated by mean and maximum standardized uptake value (SUV), corrected (SUVmean-corr; SUVmax-corr) and uncorrected for lung density (SUVmean-uncorr; SUVmax-uncorr).Methods[18F]-FDG PET/CT was performed in 31 IPF patients between 2013 and 2017. Lung density was determined on CT. SUV values were correlated with lung function tests, carbon monoxide diffusion (DLCO) and 6-min walking test (6MWT) at baseline and at 1 year. Correlation with the GAP index, a well-validated prognostic score in IPF, was also determined.ResultsAt baseline, SUVmean-uncorr was highly correlated with lung density (r = 0.755; p < 0.001). SUVmean-uncorr and lung density were correlated with lung function tests (vital capacity (VC): p = 0.013 and p = 0.003; forced vital capacity (FVC): p = 0.004 and p = 0.001; total lung capacity (TLC): p = 0.001 and p = 0.001, respectively), while SUVmean-corr was not (VC: p = 0.733; FVC: p = 0.667; TLC: p = 0.382). Interestingly, SUVmean-corr was significantly higher in patients with a GAP index of 3 (p = 0.005), and negatively correlated with DLCO (r = − 0.398; p = 0.026) and desaturation during the 6MWT (r = − 0.401; p = 0.024). But no correlation was found with changes in lung function tests, walk distance and DLCO at 1 year.ConclusionTo evaluate the role of ([18F]-FDG) PET/CT in IPF, correction for lung density appears necessary. As suggested by the correlation with DLCO, density-corrected SUV seems related to the intrinsic disease activity and particularly to the integrity of the alveolar-capillary barrier. However, ([18F]-FDG) PET/CT has probably a limited prognostic value as no correlation was found between SUVmean-corr and the clinical evolution at 1 year. Further studies with a longer follow-up are warranted.
Highlights
Idiopathic Pulmonary Fibrosis (IPF) is a progressive and irreversible disease leading to terminal respiratory insufficiency
If [18F]-FDG Positron emission tomography with computed tomography (PET/CT) is used to assess the intrinsic activity of the disease, the influence of lung density should be taken into consideration in the [18F]-FDG uptake evaluation (Lambrou et al, 2011; Holman et al, 2015)
Mean pulmonary density, as well as uncorrected SUVmean and SUVmax, were negatively correlated with lung volumes (VC, forced vital capacity (FVC), total lung capacity (TLC)) measured at the time of PET/CT. This is explained by the fact that with the development of fibrotic tissue, density increases while pulmonary compliance decreases, resulting in a reduction in lung volumes. These results are consistent with a pilot study showing that SUVmean uncorrected for density is negatively correlated with FVC (Lee et al, 2014) and other studies in which CTmean values were correlated with pulmonary physiological variables (FVC, TLC) (Ohkubo et al, 2016; Best et al, 2003)
Summary
Idiopathic Pulmonary Fibrosis (IPF) is a progressive and irreversible disease leading to terminal respiratory insufficiency. IPF is characterized by regional changes in lung density that affects the FDG uptake, a factor generally not taken into account in previous studies. Idiopathic pulmonary fibrosis (IPF) is a chronic, irreversible, and progressive fibrosing interstitial lung disease leading to a terminal respiratory insufficiency (Raghu et al, 2011). Apart from an ineluctable evolution towards respiratory failure, IPF is associated with an increased incidence of lung cancer (Archontogeorgis et al, 2012). Its clinical course is unpredictable with the majority of patients experiencing a slow progression over many years, while others show an accelerated decline with or without acute exacerbations (Raghu et al, 2011). Identification and validation of predictive markers of the clinical evolution are crucial
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