Title: Interstitial Lung Abnormality: Recognition and Perspectives
Abstract: HomeRadiologyVol. 291, No. 1 Next Reviews and CommentaryFree AccessPerspectivesInterstitial Lung Abnormality: Recognition and PerspectivesHiroto Hatabu , Gary M. Hunninghake, David A. LynchHiroto Hatabu , Gary M. Hunninghake, David A. LynchAuthor AffiliationsFrom the Department of Radiology (H.H.) and Pulmonary and Critical Care Division (G.M.H.), Brigham and Women’s Hospital and Harvard Medical School, 75 Francis St, Boston, MA 02215; and Department of Radiology, National Jewish Medical and Research Center, Denver, Colo (D.A.L.).Address correspondence to H.H. (e-mail: [email protected]).Hiroto Hatabu Gary M. HunninghakeDavid A. LynchPublished Online:Dec 18 2018https://doi.org/10.1148/radiol.2018181684MoreSectionsPDF ToolsImage ViewerAdd to favoritesCiteTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinked In IntroductionThere is increasing awareness of the clinical importance of incidentally detected interstitial lung abnormalities (ILAs) on noncontrast chest CT scans. Both at the American Thoracic Society meeting in San Diego, Calif, and the Fleischner Society meeting in Dublin, Ireland, in the early summer of 2018, the emerging concept of ILAs was a highly discussed topic among researchers, pathologists, radiologists, pulmonologists, and industry representatives. An ILA refers to a subtle or mild parenchymal abnormality identified in more than 5% of lungs on CT scans in patients in whom interstitial lung disease was not previously clinically suspected (Fig 1). ILAs are currently reported on CT examinations as follows: (a) incidental findings of no significance, (b) findings of uncertain clinical significance, (c) age-related changes of no clinical significance, (d) findings are appreciated but not mentioned, or (e) findings not observed by the reporting radiologist (1). Most often, even if observed, these changes fall below the reporting threshold. Recent evidence has shown that an ILA is not a benign finding. Thus, observing these changes and reporting their presence on CT scans of the chest has prognostic value.Figure 1a: Images in 73-year-old female participant in the COPDGene Study. (a) Baseline noncontrast CT scan of chest shows mild ground-glass abnormalities with interlobular septal thickening with subpleural distribution. (b) CT scan obtained 5½ years later demonstrates reticular and ground-glass opacities with mild traction bronchiectasis and architectural distortion indicating progression. During this time period, the participant experienced an increase in respiratory symptoms and a decrease in total lung capacity.Figure 1a:Download as PowerPointOpen in Image Viewer Figure 1b: Images in 73-year-old female participant in the COPDGene Study. (a) Baseline noncontrast CT scan of chest shows mild ground-glass abnormalities with interlobular septal thickening with subpleural distribution. (b) CT scan obtained 5½ years later demonstrates reticular and ground-glass opacities with mild traction bronchiectasis and architectural distortion indicating progression. During this time period, the participant experienced an increase in respiratory symptoms and a decrease in total lung capacity.Figure 1b:Download as PowerPointOpen in Image Viewer ILAs have been defined as nondependent changes affecting more than 5% of any lung zone, including nondependent ground-glass or reticular abnormalities, diffuse centrilobular nodularity, nonemphysematous cysts, honeycombing, and traction bronchiectasis (2,3). It is a common finding in older individuals and, hence, the reason this had been attributed to “normal aging.” In a study of 2416 CT scans of cigarette smokers obtained to evaluate chronic obstructive pulmonary disease (COPD), the Genetic Epidemiology of COPD (COPDGene) Study (3), ILA was found in 8% of subjects. Among 194 subjects with ILA, 37 ILAs were centrilobular, 107 were subpleural, 38 were mixed centrilobular and subpleural, and 12 were thought to have abnormality severe enough to represent more advanced interstitial lung disease (3). Subjects with ILA were found to have reduced total lung capacity and were less likely to meet criteria for COPD compared with those without ILA (3). Similarly, in a study of 884 subjects enrolled in the National Lung Screening Trial at a single site, ILA was found in 86 (9.7%) (4).In 2011, a single-nucleotide polymorphism (SNP) (rs35705950) in the promoter region of the gene encoding mucin 5B (MUC5B) was reported to be associated with both familial and sporadic idiopathic pulmonary fibrosis (5). The minor allele of SNP rs35705950, located 3 kb upstream of the MUC5B transcription start site, was present at a frequency of 34% among subjects with familial interstitial pneumonia, 38% among subjects with idiopathic pulmonary fibrosis, and 9% among control subjects. The minor allele of SNP rs35705950 is relatively common, is present in approximately 20% of the European population, and confers an approximately sixfold increase in the risk of idiopathic pulmonary fibrosis per copy of the minor allele (6). To test the hypothesis that subjects with the MUC5B variant in the general population would have an increased prevalence of ILA and interstitial lung disease, we examined 2633 CT scans obtained as part of the Framingham Heart Study (7). Of these, 177 (7%) had ILA, 1086 (41%) had indeterminate findings, and 1370 (52%) did not have ILA. Compared with subjects without ILA, the subjects with ILA were found to be older, had increased exposure to tobacco smoke, and were twice as likely to report having a chronic cough and shortness of breath. The prevalence of ILA was 2% in subjects who were 50 years of age or younger and 9% in subjects who were older than 50 years. In subjects with ILA, diffusion capacity for carbon monoxide was decreased by 12% and total lung capacity was decreased by 9% compared with those without ILA. The minor allele frequency of the MUC5B promoter SNP rs3570950 was 10.5%. After adjustment for covariates, for each copy of the MUC5B promoter polymorphism, the odds of ILA were 2.8 times greater (7). Of 177 subjects with ILA, 42 (27%) could be classified as having architectural distortion, and, similarly, after adjustment for covariates, for each copy of the MUC5B promoter polymorphism the odds of ILA with architectural distortion were 6.3 times greater (7).To evaluate the relationship between ILA and mortality, CT scans from four different prospective cohort studies, including the Framingham Heart Study (n = 2633), the Age, Gene/Environment Susceptibility–Reykjavik, or AGES-Reykjavik, Study (n = 5320), the COPDGene Study (n = 2068), and the Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-Points, or ECLIPSE, Study (n = 1670), were systematically reviewed. In all four cohorts, ILA was associated with a greater risk of all-cause mortality (8) (Fig 2). In the AGES-Reykjavik cohort, the higher rate of mortality could be explained by a higher rate of death due to respiratory disease, in particular due to pulmonary fibrosis (8). In a study of 172 National Lung Screening Trial subjects who died of respiratory illnesses other than lung cancer, interstitial lung abnormality was found on baseline CT scans in 18.6% of subjects, compared with 0.6% of control subjects, further supporting the concept of ILA as a risk factor for death (9). The increased risk of mortality with ILA may in part be related to an increased risk of developing acute respiratory distress syndrome (ARDS). In a study of 227 patients with systemic inflammatory response syndrome or sepsis who underwent CT at least 7 days before admission to the intensive care unit, ILA was present in 8% (19 of 227). Of those 19 patients, 14 (74%) were subsequently diagnosed with ARDS. ARDS was diagnosed in only 17 of the 113 patients (15%) without ILA (P < .0001) (10).Figure 2: Graph shows survival rates according to interstitial lung abnormality (ILA) status for the Age Gene/Environment Susceptibility–Reykjavik, or AGES-Reykjavik, study. The x-axis indicates duration of follow-up in years up to 12 years, and the y-axis indicates survival range from 0% to 100%. Hazard ratio was 1.3 (95% confidence interval: 1.2, 1.4; P < .001) between participants with and participants without ILA with use of the adjusted Cox proportional hazards model including adjustments for age, sex, body mass index, pack-years of smoking, and current or former smoking status. Created from data published in reference 8.Figure 2:Download as PowerPointOpen in Image Viewer ILA has been shown to progress over time. In 79 subjects with ILA detected at lung cancer screening CT, progression was identified at 2-year follow-up in 16 (20%), primarily in those with a fibrotic component (4). In 1867 subjects from the Framingham Heart Study who underwent serial CT examinations at a 6-year interval, 37 (2%) had stable to improving ILA and 118 (6%) had progression of ILA, indicating that up to three-quarters of subjects with ILA (6% out of 8%) had progression (11) (Fig 1). ILA progression was associated with a more rapid decrease in pulmonary function and an increased risk of death (hazard ratio: 3.9; 95% confidence interval: 1.3, 10.9; P = .01) (11).ILA has also been shown to correlate with histologic evidence of pulmonary fibrosis. In a study of 424 patients who underwent lung nodule resection and who underwent CT within 3 months before surgery, ILA was present in 26 (6%) (12). At histologic evaluation, the patients with ILA had increased rates of pulmonary fibrosis in general and of specific features including subpleural interstitial fibrosis, fibroblastic foci, honeycombing and/or usual interstitial pneumonia, and atypical adenomatous hyperplasia (12).Despite remarkable advances in our understanding of this entity, several uncertainties remain in the radiologic evaluation of ILA. Because ILA is usually found on supine chest CT scans obtained for other reasons, it can be difficult to differentiate between dependent lung atelectasis and ILA. This is a major reason why a substantial proportion of CT scans in the studies mentioned earlier have been read as indeterminate for ILA. In addition, it is often not possible for a radiologist to differentiate between asymptomatic ILA and clinically significant interstitial lung disease; this will usually require clinical evaluation. Finally, the terminology for categorizing patterns of ILA is not standardized, although most investigators believe it important to differentiate between inflammatory-appearing abnormalities (ground-glass attenuation and centrilobular nodules) and fibrotic-appearing abnormalities (subpleural irregularity, reticular abnormality, traction bronchiectasis, and honeycombing) (4).In summary, ILA is increasingly recognized as a common feature of CT of the lung in older individuals, occurring in 4%–9% of smokers and 2%–7% of nonsmokers. Subjects with ILA have increased symptoms of chronic cough and shortness of breath, decreased total lung capacity, decreased diffusion capacity, reduced exercise capacity, and increased all-cause mortality (3,4,7,8,13). ILA often progresses and may represent a subclinical or early phase of pulmonary fibrosis. Practicing radiologists now live in an era where there are new therapies for fibrotic lung disease with positive clinical trial outcomes in idiopathic pulmonary fibrosis (14–16). Researchers and clinicians have started to consider the possibility of including subjects with early stages of pulmonary fibrosis as potential candidates for early treatment or prevention of developing pulmonary fibrosis. The exact relationship between ILA and fibrotic lung disease necessitating treatment is not elucidated and is currently under active investigation (17,18). For these reasons, we believe that radiologists should systematically record the presence and pattern of ILA on CT scans. It is likely that some imaging patterns of ILA (eg, ILA with a prominent subpleural distribution) are more likely to represent an underlying early stage of pulmonary fibrosis than are others. Appropriate recommendations for evaluation and follow-up remain to be determined, but, until further evidence emerges, it is probably reasonable to recommend clinical evaluation to identify any physiologic impairment and to assess for an underlying cause of interstitial lung disease. The Fleischner Society is moving toward creation of a multidisciplinary consensus on standardization of definition and terminology, understanding of clinical significance, preliminary guidelines for management, and outline of future research needs for ILA. In the near future, it is hoped that quantitative techniques, such as hyperpolarized xenon 129 spectroscopy, and machine learning may assist with evaluation and follow-up of ILA (19–24). It is time for radiologists to stop attributing ILA to a benign age-related finding, as these changes have been clearly shown to be associated with increased mortality, increased risk of ARDS, and a decrease in pulmonary function over time.Disclosures of Conflicts of Interest: H.H. Activities related to the present article: disclosed no relevant relationships. Activities not related to the present article: is a paid consultant for Toshiba Medical and Mitsubishi Chemical; has grants/grants pending from Toshiba Medical, Konica Minolta, and Canon. Other relationships: disclosed no relevant relationships. G.M.H. Activities related to the present article: disclosed no relevant relationships. Activities not related to the present article: is a paid consultant for Genentech, Boehringer-Ingelheim, and Gerson Lehrman Group. Other relationships: disclosed no relevant relationships. D.A.L. Activities related to the present article: disclosed no relevant relationships. Activities not related to the present article: is paid to be on the board at Siemens; is a paid consultant for Parexel, Boehringer Ingelheim, Acceleron, and Veracyte; has grants/grants pending from Siemens and Veracyte; receives payment for lectures including service on speakers bureaus from France Foundation; receives payment for development of educational presentations from France Foundation. Other relationships: institution has a patent pending.AcknowledgmentsWe are grateful to Tetsuro Araki, MD, PhD, Rachel Putman, MD, MPH, Mizuki Nishino, MD, MPH, and Tomoyuki Hida, MD, PhD, for their excellent collaboration and contributions to our work.References1. Oldham JM, Adegunsoye A, Khera S, et al. Underreporting of interstitial lung abnormalities on lung cancer screening computed tomography. Ann Am Thorac Soc 2018;15(6):764–766. Crossref, Medline, Google Scholar2. Washko GR, Lynch DA, Matsuoka S, et al. 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Publication Year: 2019
Publication Date: 2019-04-01
Language: en
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Indexed In: ['crossref', 'pubmed']
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