Radiological features of idiopathic interstitial pneumonia: a pictorial review

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1 Radiological features of idiopathic interstitial pneumonia: a pictorial review Poster No.: C-2012 Congress: ECR 2013 Type: Educational Exhibit Authors: M. Piccoli, F. Roccasalva, S. Palmucci, G. Cappello, L. A. Mauro, G. Attinà, S. Puglisi, C. Vancheri, G. C. Ettorre; Catania/IT Keywords: Education and training, Education, CT-High Resolution, Conventional radiography, Thorax, Respiratory system, Lung DOI: /ecr2013/C-2012 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 23

2 Learning objectives To illustrate radiological features of idiopathic interstitial pneumonia according to the American Thoracic Society-European Respiratory Society classification published in 2002; to describe the updates defined in the 2011 evidence-based guidelines. Background Idiopathic interstitial pneumonias (IIP) include a subset of diffuse and restrictive lung diseases, resulting from damage to the parenchyma characterized by inflammation and fibrosis of the interstitium. The interstitium is the space between epithelial and endothelial basement membranes and represents the primary site of injury in IIPs. Nevertheless, these disorders often involve also the airspaces, peripheral airways and vessels. In 2002 The American Thoracic Society-European Respiratory Society published a classification of IIPs. This ATS-ERS classification defines the morphologic patterns of IIPs and classifies them in 7 entities in order of relative frequency: Idiopathic Pulmonary Fibrosis (IPF) or Usual Interstitial Pneumonia (UIP); Nonspecific Interstitial Pneumonia (NSIP); Cryptogenic Organizing Pneumonia (COP); Respiratory Bronchiolitis associated - Interstitial Lung Disease (RB-ILD); Desquamative Interstitial Pneumonia (DIP); Lymphoid Interstitial Pneumonia (LIP); Acute Interstitial Pneumonia (AIP). Imaging findings OR Procedure details The diagnosis of idiopathic pulmonary fibrosis needs to exclude other diffuse lung diseases with well-known causes such as: emphysema or chronic obstructive lung disease (COPD), diffuse lung disease associated with occupational or environmental exposure, collagen vascular disease, granulomatous lung disorder (sarcoidosis), lymphangioleiomyomatosis (LAM), pulmonary Langerhans' cell histiocytosis and eosinophilic pneumonia. Clinical methods like history, physical examination, chest radiology, laboratory studies and pathology, help the clinicians do differential diagnosis. Page 2 of 23

3 Usual interstitial pneumonia (UIP) or Idiopathic pulmonary fibrosis (IPF) IPF is the most common entity of IIPs that indicates a clinical syndrome associated with the morphologic pattern of UIP. IPF has the worst prognosis among all IIPs, with a median survival time ranging from 2 to 4 years. For this reason, a probable diagnosis of UIP is the major pattern to confirm or exclude for the pathologist. Patient's age is typically 50 years old or more. Therefore there is no evident gender predilection, IPF occurs slightly more commonly in men. Cigarette smoking is considered a risk factor for IPF, but seems to have no influence in the course of the disease. Clinically patients present a progressively worsening dyspnoea and non-productive cough refractory to antitussive agents. They can also present clinical signs such as: digital clubbing (25-50% of cases); Velcro-type fine end-inspiratory crackles at the chest auscultation to basal areas, but successively involving the entire lung; right heart failure and peripheral edema found only in the latest stages. Symptoms, generally, occur for more than 6 months before presentation. The clinical course is characterized by gradual deterioration. Occasionally, IPF can present with a period of rapid decline that suggests acute exacerbation, intercurrent viral infection or diffuse alveolar damage. Patients affected by IPF usually are non-responders to high-dose corticosteroid therapy, so they should be considered candidates for lung transplantation soon after diagnosis. Characteristic imaging features of UIP are demonstrated with high-resolution computed tomography (HRCT). A chest radiograph is normal in most patients with early disease, while in advanced disease the radiograph shows decreased lung volumes with subpleural reticular opacities that increase from the apex to the bases. Gold standard is represented by HRCT. The CT scan reveals: subpleural reticular opacities macrocystis honeycombing with traction bronchiectasis basal distribution with apicobasal gradient Page 3 of 23

4 Fig. 1: Pattern of UIP: subpleural reticular opacities (curved arrows), traction bronchiectasis (arrowheads) and peripheral subpleural honeycombing (black arrow). References: Radiodiagnostic and Oncological Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele" - Catania/IT Page 4 of 23

5 Fig. 2: Pattern of UIP-emphysema: large bulla in the upper lung lobes (black arrows), and typical signs of UIP, as showed by traction bronchiectasis (curved black arrows) and diffuse subpleural honeycombing (arrowheads). References: Radiodiagnostic and Oncological Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele" - Catania/IT These signs are highly suggestive of UIP. Ground-glass opacity are present, but limited in extent, in the majority of patients with UIP. In treated patients CT scans commonly show progress to fibrosis with honeycombing and rarely to regression of ground-glass areas. The ATS-ERS has defined some criteria for the diagnosis of IPF in absence of surgical lung biopsy. Page 5 of 23

6 Table 1 References: Radiodiagnostic and Oncological Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele" - Catania/IT When the CT scan shows atypical imaging features (e.g. extensive ground-glass opacities, nodules, consolidation or a predominantly peri-bronchovascular distribution) histologic confirmation is necessary. Histologic features of UIP are characterized by scattered fibroblastic foci with heterogeneous distribution that alternate interstitial inflammation and honeycombing with normal areas. This could explain the presence of discordant histologic pattern from multiple biopsies. So HRCT is required as a guiding tool to choose the correct anatomic location of the biopsy site. Nonspecific Interstitial Pneumonia (NSIP) NSIP is less frequent than UIP but it is still one of the most common IIPs. The diagnosis of NSIP requires an accurate analysis because it is associated with multiple imaging and histologic patterns. Page 6 of 23

7 For this reason NSIP should be considered a transitional diagnosis until determination of this entity. NSIP may be the early manifestation of collagen vascular disease (preceding by several months or several years), the histologic pattern of hypersensitivity pneumonitis or a specific occupational exposure pattern. Therefore it is necessary to search for serological and other markers of connective tissue diseases and for potential occupational exposure. NSIP occurs in patients with median age of between 40 and 50 years. It has no sexual predominance and it is not associated with cigarette smoking. Clinically, symptoms of NSIP are similar to those of IPF but milder. They arise gradually and are represented by dyspnea over several months, cough, fatigue and weight loss (mean. 6 kg). In a minority of patients NSIP presents fever and finger clubbing (less than IPF). Typical signs are basal crackles that become widespread. NSIP shows at lung function tests a restrictive respiratory defect in more than 90% of patients. Clinical course of NSIP is varyiable depending on the extension of fibrosis. The disease in some patients has complete recovery, in other cases it stabilizes or improves on treatment and in a minority of cases it progresses until death. In patients with NSIP a chest radiograph shows normal pattern in early stages and patchy parenchymal opacity in advanced ones. Lower lung areas are more frequently interested but in absence of an apicobasal gradient. HRCT demonstrates typical patchy ground-glass opacities, related to homogeneous interstitial inflammation, combined with irregular linear or reticular opacities and scattered micronodules. Lesions have a characteristic sub-pleural and symmetric distribution. In advanced disease there can be traces of traction bronchiectasis, secondary to fibrosis, consolidation (areas of organising pneumonia) and sub-pleural microcysts (in opposition to macrocysts of UIP). Follow-up CT reveals that ground-glass opacities do not develop to areas of honeycombing. A surgical lung biopsy is necessary when differential diagnosis between NSIP and UIP is not clear. Histologic features of NSIP have a characteristic temporally and spatially homogenous lung involvement. This homogeneity is a key feature in differentiating NSIP patterns from UIP ones. Page 7 of 23

8 NSIP patterns can be classified into cellular and fibrosing subtypes depending on the different amount of inflammation and fibrosis. Cellular NSIP has thickening of alveolar septa Fibrosing NSIP has interstitial fibrosis combined with mild inflammation. Fig. 3: Pattern of NSIP: ground-glass opacifications (black arrowheads) and bronchiectasis (curved arrow). References: Radiodiagnostic and Oncological Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele" - Catania/IT Cellular NSIP is less common than the fibrosing type, but shows a better prognosis due to a positive response to corticosteroids. Fibrosing NSIP and UIP reveal similar patterns that require CT correlation. Cryptogenic organising pneumonia (COP) Page 8 of 23

9 It was first described by Davison to colleagues in 1983 as Bronchiolitis obliterans organizing pneumonia (BOOP). This term was changed to avoid confusion with constructive bronchiolitis obliterans, that is an airway disease. Its histologic pattern is represented by "organizing pneumonia (OP)" that denotes an alveolar inflammation with varied aetiology like OP associated with collagen vascular disease, infectious and drug-induced lung disease. (rheumatoid arthritis or secondary to viral pneumonia, etc.) The idiopathic form of OP is called COP and is classified as an IIP. Mean age of patients affected by COP is 55 years old. There is no gender predilection and no association with cigarette smoking; in fact most patients are nonsmokers or exsmokers. They present with a short duration (less than 2 months) of mild dyspnea, cough and fever. Generally patients are treated with antibiotics for suspected but unconfirmed lower respiratory tracts infection. The arising of weight loss, sweats, chills, intermittent fever and myalgia is common. They often recover completely after administration of corticosteroids and relapse when therapy is stopped. Lung function tests confirm a restrictive ventilator pattern (mild to moderate). However, diagnosis of COP results from exclusion of other possible causes of OP. When chest radiograph is performed, it presents two main aspects: Consolidation (secondary to intraalveolar fibroblast proliferation): bilateral patchy areas usually located in peripheral, sub-pleural and peribronchovascular regions. Nodules: foci of granulation tissue up to 1 cm, occasionally numerous in immunocompromised patients. HRCT features of COP are more extensive than chest radiograph and include: characteristic peripheral or peribronchial patchy consolidation (sometimes with subpleural area spread) with air bronchograms and mild cylindric bronchial dilatation; increasing of consolidation over several weeks after antibiotic therapy ground-glass opacities with tendency to migration, changing location and size rarely mass or nodules that may cavitate, resembling the typical appearance of "atollo sign" (considered highly specific but seen in 20% of patients with COP). Page 9 of 23

10 Fig. 4: Pattern of COP: consolidations (arrowheads) with air bronchograms; diffuse ground-glass opacities (black arrows, patchy distribution). References: Radiodiagnostic and Oncological Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele" - Catania/IT In either case, a clear diagnosis needs surgical lung biopsy confirmation. In recent times, transbronchial lung biopsy is under evaluation. Histologically, it is characterized by granulation tissue polyps (Masson bodies) within the alveolar ducts and alveoli and fibroblast proliferation secondary to extension of inflammatory exudates. These two processes may cause bronchiolar occlusion. Lung involvement is typically patchy with spread of its architecture. Desquamative Interstitial Pneumonia (DIP) DIP is an IIP closely associated with cigarette smoking and is considered the end-stage/ severe RB-ILD. This is called DIP due to the belief that the dominant histologic feature was desquamation of epithelial cells, but actually histologic examinations reveal an accumulation of pigmented macrophages rather than desquamation. Page 10 of 23

11 DIP occurs typically in male patients (2:1). The majority of patients are heavy smokers (90%) with an average smoking history of 18 pack-years; however, DIP can also occur in non-smokers. Other predisposing factors include: systemic disorders, e.g. rheumatoid arthritis, sclerodermia; infection, e.g. HIV; occupational or environmental exposure, e.g. asbestos; drug. Onset of symptoms is between 30 and 40 years of age with incoming dyspnea and dry chronic cough (over weeks or months) that may develop to respiratory failure. At lung functional tests DIP reveals normal volumes or mild restrictive abnormality. Prognosis is good in patients with smoking cessation and corticosteroid therapy. Survival is about 70% after 10 years. Chest radiograph may show bilateral interstitial infiltrates (hazy opacities) but this pattern is non specific for detection of DIP. Pathognomonic radiological features of DIP are revealed by HRCT scan. They are : diffuse ground-glass opacities, correlated histologically with the spatially homogeneous intraalveolar accumulation of macrophages and thickening of alveolar septa: bilateral and symmetric (86%), basal and peripheral (60%), patchy (20%) and diffuse (20%). Irregular linear opacities Microcysts (50% of patients). Page 11 of 23

12 Fig. 5: Pattern of DIP: diffuse subpleural ground-glass consolidation (black arrowheads); small microcystic areas in a peribroncovascular distribution (white arrowheads). References: Radiodiagnostic and Oncological Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele" - Catania/IT Page 12 of 23

13 Fig. 6: Pattern of DIP: ground glass consolidation (blackarrowhead) and small cystic areas (white arrowhead). References: Radiodiagnostic and Oncological Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele" - Catania/IT Because of the similar pattern existing between DIP and RB-ILD, biopsy is required when these entities are suspected. The major histologic pattern of this disease is characterized by alveoli filled with pigmented macrophages and with few alveolar epithelial cells. Unlike RB-ILD, lung involvement is more pronounced in DIP. Respiratory Bronchiolitis- associated Interstitial Lung Disease (RB-ILD) RB-ILD is recognized as a smoking-related interstitial lung disease and seems to be closely related to respiratory bronchiolitis. Because of an overlap in clinical, imaging and histologic features between RB-ILD and DIP, they are considered different degrees of severity of the same disease. In fact, DIP is a more extensive form of RB-ILD that involves larger areas of the lung. Page 13 of 23

14 RB-ILD is usually seen in young middle-aged patients (30-40 years old) with an average smoking history of 30 pack-years or more. Men are more affected than women with a ratio of 2:1 M:F. Onset presents a progressive dyspnea and chronic cough. At clinical examination inspiratory crackles are heard in up to 50% of patients. Digital clubbing is usually absent. Patients with mild symptoms reveal a moderate reduction in carbon monoxide transfer factor and patients with severe symptoms have more significant reduction of it. Lung function tests in patients affected by RB-ILD show both airway obstruction and restriction. Natural history of the disease is not available because of the low number of cases, but progression to dense pulmonary fibrosis has not been described. Nevertheless, smoking cessation determines a clear improvement. The chest radiograph in patients with RB-ILD shows in the majority of cases a normal pattern and in a minority of cases wall thickening of central/peripheral bronchi or reticular opacities. The key HRCT features are: ground-glass opacity (correlated with macrophage accumulation in alveolar ducts and spaces); poorly defined centrilobular nodules (compatible with peribronchial expansion of intraluminal infiltrate) mostly diffuse distribution other features related to smoking : bronchial wall thickening and moderate centrilobular emphysema. Page 14 of 23

15 Fig. 7: Pattern of RB-ILD: small ill-defined centrilobular opacities (white arrowheads). References: Radiodiagnostic and Oncological Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele" - Catania/IT On surgical lung biopsy of RB-ILD the pathognomonic histological pattern is the accumulation of pigment macrophages within alveoli and respiratory bronchioles. Mild peribronchial inflammation and fibrosis are also found. (In respiratory bronchiolitis pigmented macrophages are present within first- and secondorder respiratory bronchioles.) These findings cannot be distinguished from those found in respiratory bronchiolitis. Lymphoid Interstitial Pneumonia (LIP) LIP was introduced by Liebow and Carrington in 1969 to describe a diffuse lymphocytic interstitial infiltrate. The position of LIP within classification has changed thanks to the discovery of the nature of its pulmonary interstitial infiltrates. In the past, it was considered a pulmonary lymphoproliferative disorder because of a high probability of progression to malignant lymphoma. Many supposed cases of LIP were Page 15 of 23

16 non-hodgkin's low-grade B cell MALT lymphomas. In fact, most of these cases were reclassified as lymphoma and a small number of definite LIP cases seems to progress in malignant transformation. It is also considered a secondary disease in association with systemic disorders, particularly with Sjogren syndrome (25% in patients with LIP), human immunodeficiency virus infection (particularly children affected by AIDS), various immunodeficiency syndromes (Castelman disease), Hashimoto's disease. Incidence of LIP is low; it occurs in females typically in the fifth decade. They present mild progressive dyspnea and non productive cough over a period of 3 or more years. Sometimes patients report fever, night sweats and weight loss. The use of corticosteroid revealed an arrest or improvement symptoms in a large range of patients. LIP rarely progress to diffuse fibrosis. Chest radiograph exhibits a non-specific pattern that may include lower areas, predominant bilateral, reticular opacities chronic bilateral airspace opacities. At HRCT scan the panel is more clear but not exclusive to LIP diagnosis. It shows: diffuse and bilateral distribution of abnormalities ground-glass attenuation (more specific) scattered thin-walled perivascular cysts: usually within the lung parenchyma (predominatly in the mid lung zones) and with size of 1-30 mm mediastinal lymphadenopathy small pulmonary nodules : centrilobular or sub-pleural and often ill-defined septal thickening Page 16 of 23

17 Fig. 8: Pattern of LIP (after treatment); small reticular opacities and nodules (black arrowheads). References: Radiodiagnostic and Oncological Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele" - Catania/IT LIP histological pattern is defined by diffuse infiltration of interstitium by lymphocytes, plasma cells and histiocytes. Reactive lymphoid follicles can be found in inflammed peribronchial regions. Disease can also involve airspaces, this is due to the compression by interstitial infiltrates of proteinaceous fluid and macrophages. Acute Interstitial Pneumonia (AIP) Acute interstitial pneumonia (AIP) is a form of interstitial disease with rapid onset and progressive coarse; it occurs equally in men and women. Patients with AIP often refer previous symptoms of a viral upper respiratory infection. The histologic pattern of AIP is the diffuse alveolar damage; it has the same appearance of acute respiratory distress syndrome. Page 17 of 23

18 Radiographically AIP is characterized by alveolar opacifications and ground-glass attenuation areas in the lung, with diffuse bilateral patchy distribution. Typical imaging findings encountered on HRCT are: ground-glass areas of attenuation, predominantly involving the lung bases and diffuse alveolar consolidation traction bronchioloectasis or bronchial dilatation architectural distortion mild bilateral pleural effusion Fig. 9: Pattern of AIP: mild pleural effusion, ground glass opacifications and inhomogeneous consolidations. References: Radiodiagnostic and Oncological Radiotherapy Unit, University Hospital "Policlinico-Vittorio Emanuele" - Catania/IT Differential diagnosis includes several diseases, such as acute exacerbations of idiopathic interstitial fibrosis, NSIP, bronchiolitis organizing obliterans pneumonia (BOOP), infectious diseases, idiopathic acute interstitial pneumonia and collagen-related lung fibrosis. Page 18 of 23

19 Conclusion Updates: the role of HRCT after the statement of the ATS/ERS/JRS/ALAT Committee on IPF The statement of the ATS/ERS/JRS/ALAT Committee on IPF introduces several crucial points about: - diagnosis - treatment - disease progression The diagnosis of IPF is based on HRCT and histopathological criteria. Considering the HRCT appearance, we may have the following 3 situations: 1) UIP pattern, with all four features of disease: - subpleural, basal predominance - reticular abnormality - honeycombing appearance, traction bronchiectasis - no evidence of features inconsistent with UIP pattern 2) possible UIP pattern (all three features) - subpleural, basal predominance - reticular abnormality - no evidence of features inconsistent with UIP pattern 3) inconsistent with UIP pattern (any of these features) - upper or mid-lung predominance - peribronchiovascular predominance - extensive ground-glass abnormality Page 19 of 23

20 - profuse micronodules - discrete cysts - diffuse mosaic attenuation/air-trapping - parenchymal consolidations The reported HRCT features have a great impact on the management of UIP: 1) Typical HRCT UIP pattern (all four criteria mentioned above) - after the exclusion of identifiable causes for ILD - allows to make diagnosis of IPF, even if surgical lung biopsy is possible, probable or non-classificable 2) Possibile UIP pattern - seen on HRCT - need to be correlated with surgical lung biopsy pattern: - Cases with possible UIP pattern on HRCT and UIP or probable histological UIP pattern allows to make the diagnosis of IPF - Cases with possible UIP pattern on HRCT and possibile histological UIP pattern are suggestive of a probable IPF diagnosis 3) Inconsistent UIP pattern seen on HRCT - even with surgical lung biopsy pattern of UIP - do not allow to make diagnosis of IPF!!!; the diagnosis remains of IPF is graded as "possible" Conclusion According to the 2011 evidence-based guidelines, usual interstitial pneumonia can be diagnosed by HRCT when all criteria are fulfilled. The overlap of imaging features among interstitial pneumonia limits the diagnosis; a multidisciplinary approach is recommended. References Mueller-mang C, Grosse C, Schmid K, Stiebellehner L, Bankier AA. What every radiologist should Know about idiopathic interstitial pneumonias. Radiographics, 2007; 27: American Thoracic Society. American thoracic Society/ European Respiratory Society International Multidisciplinary Consensus Classification Page 20 of 23

21 of the Idiopathic Interstitial Pneumonias. American Journal of respiratory and Critical Care Medicine, 2002; 165: Larsen BT, Colby TV. Update for pathologists on idiopathic interstitial pneumonias. Archives of Pathology & Laboratory Medicine Online, 2012; 136: Webb WR, Muller NL, Naidich DP. High-resolution CT of the lung. Lippincott Williams & Wilkins, Lynch DA, Travis WD, Muller NL, Galvin JR, Hansell DM, Grenier PA, King TE. Idiopathic Interstitial Pneumonias: CT features. Radiology, 2005; 236: Souza CA, Muller NL, Flint J, Wright JL, Churg A. Idiopathic pulmonary fibrosis: spectrum of high-resolution CT findings. American J of Roentgenology, 2005; 185: Sverzellati N, Wells AU, Tomassetti S, Desai SR, Copley SJ, Aziz ZA, Zompatori M, Chilosi M, Nicholson AG, Poletti V, Hansell DM. Biopsy-proved idiopathic pulmonary fibrosis: spectrum of nondiagnostic thin-section CT diagnoses. Radiology, 2010; 254: Personal Information Marina Piccoli, MD p.mari4@hotmail.it Radiodiagnostic and Oncological Radiotherapy Unit University Hospital "Policlinico- Vittorio Emanuele" Via Santa Sofia , Catania - Italy Federica Roccasalva, MD f.roccasalva@gmail.com Radiodiagnostic and Oncological Radiotherapy Unit University Hospital "Policlinico- Vittorio Emanuele" Via Santa Sofia , Catania - Italy Stefano Palmucci, MD Page 21 of 23

22 Radiodiagnostic and Oncological Radiotherapy Unit University Hospital "Policlinico- Vittorio Emanuele" Via Santa Sofia , Catania - Italy Giuseppina Cappello, MD giuseppina.cappello@gmail.com Radiodiagnostic and Oncological Radiotherapy Unit University Hospital "Policlinico- Vittorio Emanuele" Via Santa Sofia , Catania - Italy Letizia Antonella Mauro, MD mauroletizia@tiscali.it Radiodiagnostic and Oncological Radiotherapy Unit University Hospital "Policlinico- Vittorio Emanuele" Via Santa Sofia , Catania - Italy Giancarlo Attinà, MD gianco82t@hotmail.it Radiodiagnostic and Oncological Radiotherapy Unit University Hospital "Policlinico- Vittorio Emanuele" Via Santa Sofia , Catania - Italy Silvia Puglisi, MD silviapuglisi@fastwebnet.it Regional Center for Interstitial and Rare Lung Disease, Department of Clinical and Experimental Biomedicine, Section of Respiratory Diseases, University Hospital "Policlinico- Vittorio Emanuele" Page 22 of 23

23 Via Santa Sofia , Catania - Italy Carlo Vancheri, Professor vancheri@unict.it Regional Center for Interstitial and Rare Lung Disease, Department of Clinical and Experimental Biomedicine, Section of Respiratory Diseases, University Hospital "Policlinico- Vittorio Emanuele" Via Santa Sofia , Catania - Italy Giovanni Carlo Ettorre, Professor g.ettorre@unict.it Radiodiagnostic and Oncological Radiotherapy Unit University Hospital "Policlinico- Vittorio Emanuele" Via Santa Sofia , Catania - Italy Page 23 of 23

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