IMAGES IN PULMONARY, CRITICAL CARE, SLEEP MEDICINE AND THE SCIENCES A Case of Amiodarone-induced Acute Fibrinous and Organizing Pneumonia Mimicking Mesothelioma Sara Piciucchi1, Alessandra Dubini 2, Sara Tomassetti 3, Gianluca Casoni 3, Claudia Ravaglia 3, and Venerino Poletti 3 1
Department of Radiology, 2Department of Pathology, and 3Department of Diseases of the Thorax, Morgagni Pierantoni Hospital, Forl`ı, Italy
Figure 1. Multiple bilateral pleural plaques (A and B; blue arrow) associated with bilateral round atelectasis (C; yellow arrows) and huge bilateral basal calcified plaques (D).
A 79-year-old man who was a nonsmoker, ex–truck driver, and metalworker (20 years) was admitted to our hospital. He had a diagnosis of pleural and parenchymal asbestos-related lesions with bilateral, partly calcified, pleural plaques (Figure 1B, blue arrow) and bilateral round atelectasis in both lower lobes (Figure 1C, yellow arrows). He had already undergone bronchoalveolar lavage (BAL) that did not show any asbestos bodies. Treatment with amiodarone (200 mg four times daily for 5 d/wk) was started 8 months before for a paradoxical atrial fibrillation. He was admitted to the hospital for recent appearance of dyspnea, dry cough, and low-grade fever persisting despite antibiotics treatment. A computed tomography scan detected unilateral, circumferential right pleural effusion, pleural thickening, and right upper lobe ground glass attenuation (Figures 2A and 2B). Moreover, right hemithorax volume was reduced. Mediastinal adenopathies, right lower lobe consolidation (Figure 2C), and peripheral consolidation in the left lower lobe were also observed (Figure 2C). A neoplastic lesion (mesothelioma, adenocarcinoma) was considered. Vacuolated macrophages and asbestos bodies were not identified in BAL fluid (Figure 2D). In the transbronchial lung biopsy specimens (Figures 3A and 3B), intraalveolar fibrin balls (arrow), chronic inflammatory interstitial infiltrate, and myofibroblasts embedded in the alveolar proteinaceous exudate and extracellular matrix were observed (acute fibrinous and organizing pneumonia [AFOP] pattern) (1). The patient was treated with methylprednisolone 40 mg twice daily, and amiodarone was withdrawn. Three months later, computed tomography scan showed complete remission of the pleural effusion and of alveolar consolidations (Figures 4A and 4B).
Am J Respir Crit Care Med Vol 191, Iss 1, pp 104–106, Jan 1, 2015 Copyright © 2015 by the American Thoracic Society DOI: 10.1164/rccm.201405-0844IM Internet address: www.atsjournals.org
104
American Journal of Respiratory and Critical Care Medicine Volume 191 Number 1 | January 1 2015
IMAGES IN PULMONARY, CRITICAL CARE, SLEEP MEDICINE AND THE SCIENCES
Figure 2. Right circumferential pleural effusion associated to a moderate volume reduction of the hemithorax (A). The lung window shows a moderate ground glass attenuation in the right upper lobe (B) associated with bilateral consolidations, particularly in the right lower lobe (C). Bronchoalveolar lavage shows multiple vacuolated macrophages (D).
Figure 3. Transbronchial lung biopsy specimen shows proteinaceous exudation in some airspaces (low magnification) (A). At higher magnification, intraalveolar balls of fibrin, chronic interstitial inflammatory cells, and intraalveolar fibroblasts embedded in extracellular matrix are evident (acute fibrinous and organizing pneumonia) (B).
Figure 4. Complete disappearance of the right pleural effusion (A). The lung window shows a moderate residual interlobular septal thickening with perilobular pattern likely caused by a mild residual organizing pneumonia (B).
Rate of amiodarone pulmonary toxicity is reported to be between 0 and 8% (1–4). Its clinical-radiologic and pathologic manifestations are pleomorphic (5, 6). Association of the AFOP pattern and amiodarone is not described in literature, with the exception of one case of the series, described by Beasley and colleagues (1). Lung injury (AFOP pattern) resulting from amiodarone superimposed to the asbestos-related pleuroparenchymal lesions might explain the peculiar computed tomography features observed in this case. n Author disclosures are available with the text of this article at www.atsjournals.org.
Images in Pulmonary, Critical Care, Sleep Medicine and the Sciences
105
IMAGES IN PULMONARY, CRITICAL CARE, SLEEP MEDICINE AND THE SCIENCES References 1. Beasley MB, Franks TJ, Galvin JR, Gochuico B, Travis WD. Acute fibrinous and organizing pneumonia: a histological pattern of lung injury and possible variant of diffuse alveolar damage. Arch Pathol Lab Med 2002;126: 1064–1070. 2. Jackevicius CA, Tom A, Essebag V, Eisenberg MJ, Rahme E, Tu JV, Humphries K, Behlouli H, Pilote L. Populationlevel incidence and risk factors for pulmonary toxicity associated with amiodarone. Am J Cardiol 2011;108: 705–710.
106
3. Doval HC, Nul DR, Grancelli HO, Perrone SV, Bortman GR, Curiel R. Randomised trial of low-dose amiodarone in severe congestive heart failure. Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiaca en Argentina (GESICA). Lancet 1994;344:493–498. 4. Yamada Y, Shiga T, Matsuda N, Hagiwara N, Kasanuki H. Incidence and predictors of pulmonary toxicity in Japanese patients receiving lowdose amiodarone. Circ J 2007;71:1610–1616. 5. Camus P, Fanton A, Bonniaud P, Camus C, Foucher P. Interstitial lung disease induced by drugs and radiation. Respiration 2004;71:301–326. 6. Ruangchira-Urai R, Colby TV, Klein J, Nielsen GP, Kradin RL, Mark EJ. Nodular amiodarone lung disease. Am J Surg Pathol 2008;32: 1654–1660.
American Journal of Respiratory and Critical Care Medicine Volume 191 Number 1 | January 1 2015
Department of Radiology, 2Department of Pathology, and 3Department of Diseases of the Thorax, Morgagni Pierantoni Hospital, Forl`ı, Italy
Figure 1. Multiple bilateral pleural plaques (A and B; blue arrow) associated with bilateral round atelectasis (C; yellow arrows) and huge bilateral basal calcified plaques (D).
A 79-year-old man who was a nonsmoker, ex–truck driver, and metalworker (20 years) was admitted to our hospital. He had a diagnosis of pleural and parenchymal asbestos-related lesions with bilateral, partly calcified, pleural plaques (Figure 1B, blue arrow) and bilateral round atelectasis in both lower lobes (Figure 1C, yellow arrows). He had already undergone bronchoalveolar lavage (BAL) that did not show any asbestos bodies. Treatment with amiodarone (200 mg four times daily for 5 d/wk) was started 8 months before for a paradoxical atrial fibrillation. He was admitted to the hospital for recent appearance of dyspnea, dry cough, and low-grade fever persisting despite antibiotics treatment. A computed tomography scan detected unilateral, circumferential right pleural effusion, pleural thickening, and right upper lobe ground glass attenuation (Figures 2A and 2B). Moreover, right hemithorax volume was reduced. Mediastinal adenopathies, right lower lobe consolidation (Figure 2C), and peripheral consolidation in the left lower lobe were also observed (Figure 2C). A neoplastic lesion (mesothelioma, adenocarcinoma) was considered. Vacuolated macrophages and asbestos bodies were not identified in BAL fluid (Figure 2D). In the transbronchial lung biopsy specimens (Figures 3A and 3B), intraalveolar fibrin balls (arrow), chronic inflammatory interstitial infiltrate, and myofibroblasts embedded in the alveolar proteinaceous exudate and extracellular matrix were observed (acute fibrinous and organizing pneumonia [AFOP] pattern) (1). The patient was treated with methylprednisolone 40 mg twice daily, and amiodarone was withdrawn. Three months later, computed tomography scan showed complete remission of the pleural effusion and of alveolar consolidations (Figures 4A and 4B).
Am J Respir Crit Care Med Vol 191, Iss 1, pp 104–106, Jan 1, 2015 Copyright © 2015 by the American Thoracic Society DOI: 10.1164/rccm.201405-0844IM Internet address: www.atsjournals.org
104
American Journal of Respiratory and Critical Care Medicine Volume 191 Number 1 | January 1 2015
IMAGES IN PULMONARY, CRITICAL CARE, SLEEP MEDICINE AND THE SCIENCES
Figure 2. Right circumferential pleural effusion associated to a moderate volume reduction of the hemithorax (A). The lung window shows a moderate ground glass attenuation in the right upper lobe (B) associated with bilateral consolidations, particularly in the right lower lobe (C). Bronchoalveolar lavage shows multiple vacuolated macrophages (D).
Figure 3. Transbronchial lung biopsy specimen shows proteinaceous exudation in some airspaces (low magnification) (A). At higher magnification, intraalveolar balls of fibrin, chronic interstitial inflammatory cells, and intraalveolar fibroblasts embedded in extracellular matrix are evident (acute fibrinous and organizing pneumonia) (B).
Figure 4. Complete disappearance of the right pleural effusion (A). The lung window shows a moderate residual interlobular septal thickening with perilobular pattern likely caused by a mild residual organizing pneumonia (B).
Rate of amiodarone pulmonary toxicity is reported to be between 0 and 8% (1–4). Its clinical-radiologic and pathologic manifestations are pleomorphic (5, 6). Association of the AFOP pattern and amiodarone is not described in literature, with the exception of one case of the series, described by Beasley and colleagues (1). Lung injury (AFOP pattern) resulting from amiodarone superimposed to the asbestos-related pleuroparenchymal lesions might explain the peculiar computed tomography features observed in this case. n Author disclosures are available with the text of this article at www.atsjournals.org.
Images in Pulmonary, Critical Care, Sleep Medicine and the Sciences
105
IMAGES IN PULMONARY, CRITICAL CARE, SLEEP MEDICINE AND THE SCIENCES References 1. Beasley MB, Franks TJ, Galvin JR, Gochuico B, Travis WD. Acute fibrinous and organizing pneumonia: a histological pattern of lung injury and possible variant of diffuse alveolar damage. Arch Pathol Lab Med 2002;126: 1064–1070. 2. Jackevicius CA, Tom A, Essebag V, Eisenberg MJ, Rahme E, Tu JV, Humphries K, Behlouli H, Pilote L. Populationlevel incidence and risk factors for pulmonary toxicity associated with amiodarone. Am J Cardiol 2011;108: 705–710.
106
3. Doval HC, Nul DR, Grancelli HO, Perrone SV, Bortman GR, Curiel R. Randomised trial of low-dose amiodarone in severe congestive heart failure. Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiaca en Argentina (GESICA). Lancet 1994;344:493–498. 4. Yamada Y, Shiga T, Matsuda N, Hagiwara N, Kasanuki H. Incidence and predictors of pulmonary toxicity in Japanese patients receiving lowdose amiodarone. Circ J 2007;71:1610–1616. 5. Camus P, Fanton A, Bonniaud P, Camus C, Foucher P. Interstitial lung disease induced by drugs and radiation. Respiration 2004;71:301–326. 6. Ruangchira-Urai R, Colby TV, Klein J, Nielsen GP, Kradin RL, Mark EJ. Nodular amiodarone lung disease. Am J Surg Pathol 2008;32: 1654–1660.
American Journal of Respiratory and Critical Care Medicine Volume 191 Number 1 | January 1 2015
