- Email: [email protected]
Bad for Breathing: A Pictorial of Drug-Induced Pulmonary Disease
Author's Accepted Manuscript
Bad for Breathing: A Pictorial of Drug Induced Pulmonary Disease Amy C. Taylor MD, Nupur Verma MD, Roberta Slater MD, Tan-Lucien H. Mohammed MD, FCCP
www.cpdrjournal.com
PII: DOI: Reference:
S0363-0188(15)30005-0 http://dx.doi.org/10.1067/j.cpradiol.2015.10.002 YMDR404
To appear in:
Current Problems in Diagnostic Radiology
Cite this article as: Amy C. Taylor MD, Nupur Verma MD, Roberta Slater MD, Tan-Lucien H. Mohammed MD, FCCP, Bad for Breathing: A Pictorial of Drug Induced Pulmonary Disease, Current Problems in Diagnostic Radiology, http://dx. doi.org/10.1067/j.cpradiol.2015.10.002 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
1
Bad for Breathing: A Pictorial of Drug Induced Pulmonary Disease Amy C. Taylor, MDa Nupur Verma, MDa Roberta Slater, MDa Tan-Lucien H. Mohammed, MD, FCCPa a
Department of Radiology University of Florida – College of Medicine Post Office Box 100374 Gainesville, Florida United States of America Corresponding author: Tan-Lucien H. Mohammed, MD, FCCP College of Medicine – University of Florida Department of Radiology Post Office Box 100374 Gainesville, Florida United States of America Phone: 352-265-0291 E-mail: [email protected]
Abstract: Drug-induced lung disease has been described with over three hundred different agents, some of which are asymptomatic and may first present on imaging. These pulmonary diseases may present with variable imaging manifestations, and often overlap with other etiologies such as rejection, lymphoproliferative disorders, and infection which may be suspected in this patient population. However, there are several drugs which have classic imaging appearances, and, in the proper clinical context, the radiologist should include their toxicity in the differential diagnosis, potentially expediting withdrawal of the drug and avoiding irreversible lung injury such as fibrosis. Keywords: Drug toxicity; Ritalin; Cocaine; Interstitial Lung Disease; CT; Amiodarone; Pneumoconiosis Cocaine: The term “crack lung” refers to an acute pulmonary syndrome that occurs after the inhalation of free-base cocaine and is secondary to prolonged inflammatory pulmonary injury. Cocaine inhalation is associated with fever, hypoxemia, hemoptysis, respiratory failure, and diffuse alveolar opacities.1 Lung tissue specimens obtained in affected patients reveal diffuse alveolar damage, alveolar hemorrhage, eosinophilic interstitial and alveolar cell infiltration, and deposition of IgE.1 Chest radiographs demonstrate multifocal airspace disease.1 Computer tomographic (CT) imaging demonstrates
2 predominantly lower lobar multifocal ground glass attenuation with subpleural sparing, as would be expected in diffuse alveolar hemorrhage (Fig. 1).2 Recurrent episodes of hemorrhage may lead to eventual subpleural reticulation and honeycombing.2 Methylphenidate (Ritalin): Intravenous use of methylphenidate has been associated with the development of lower lobe panlobular emphysema, akin to that seen with alpha-1-antitrypsin deficiency. Microscopic talc granulomata may be seen, relating to the injection base.3,4 Chest radiographs show hyperinflation with lower lobe lucency of diffuse panlobular emphysema and CT demonstrates diffuse areas of low attenuation throughout the lungs with a paucity of vessels. (Fig. 2).5 Amiodarone: Amiodarone is a commonly used antiarrhythmic, making this a toxicity most often associated with cardiac patients. Toxicity occurs in 5-10% of patients and can present with both pulmonary and hepatic manifestations. Risk factors for developing toxicity include a daily dose greater than 400 mg and elderly status of the patient.6 Pulmonary imaging classically demonstrates distinctive focal high attenuation consolidations, which are most commonly peripheral in distribution (Fig. 3). However, non-specific interstitial pneumonia (NSIP) is the most commonly encountered manifestation.6 Due to the high iodine content and metabolism of amiodarone in the liver, this organ may also have high attenuation. The combination of high attenuation in the lung, liver, and spleen is characteristic of amiodarone toxicity. Treatment is cessation of amiodarone and administration of corticosteroids.7 Heavy Metals (benzenes): Heavy metal pneumoconiosis results from inhalational exposure to tungsten carbide, cobalt, or diamond-cobalt. The histopathological finding of giant cell interstitial pneumonia (GIP) is pathognomonic for this disorder.8,9 CT imaging often demonstrates patchy ground-glass attenuation and consolidation in the mid and lower lungs (Fig. 4). With long term exposure, fibrosis with architectural distortion, traction bronchiectasis, and honeycombing can occur (Fig. 5).9,10 Prognosis is favorable with early recognition of the patient’s occupational exposure, and removal of the offending environment. Nitrofurantoin: Nitrofurantoin is an antibiotic commonly used to treat urinary tract infections. Pulmonary toxicity is uncommon with its use and occurs in less than 1% of patients; however, when toxicity occurs, it may be either acute or chronic.11 Acute toxicity is more common, usually occurring within two weeks of drug initiation. Imaging demonstrates diffuse bilateral basilar-predominant heterogeneous opacities and pleural effusions. Laboratory assessment may show peripheral eosinophilia.6 Chronic toxicity is less common and often occurs after months or years of continuous use. Imaging in chronic toxicity typically demonstrates an NSIP pattern with bilateral, predominantly basilar, reticular opacities (Fig. 6).11
3 Methotrexate: Methotrexate is a common chemotherapeutic agent used in the treatment of malignancies, as well as for the treatment of severe rheumatoid arthritis and psoriatic arthritis. Pulmonary toxicity occurs in 5-10% of patients and usually develops within months of starting therapy. The most common imaging manifestation is an NSIP pattern (Fig. 7), followed by an organizing pneumonia pattern.6 Respiratory symptoms are often accompanied by fever and peripheral eosinophilia.12 Prognosis is generally favorable with discontinuation of therapy, and treatment with methotrexate can be reintroduced in the future without increased predilection for recurrent toxicity.13 Cyclophosphamide: Cyclophosphamide is a cytotoxic agent used to treat a variety of malignant and nonmalignant conditions. Cyclophosphamide toxicity can occur within weeks to years of use, and there is no relationship between the drug dosage or between the duration of therapy and the development of lung injury. The most common manifestation of toxicity is diffuse alveolar damage (DAD). CT imaging in DAD demonstrates scattered or diffuse ground glass opacities in the early phase, with rapid progression to fibrosis, which usually develops within two weeks. This may present as bronchiectasis, marked architectural distortion, and honeycombing (Fig. 8).12 Prognosis is generally good after therapy has been discontinued; however, the fibrotic lung disease does not change. Bleomycin: Bleomycin is a common chemotherapeutic agent used to treat squamous cell carcinoma, testicular carcinoma, and Hodgkin’s lymphoma. Risk factors for developing bleomycin-induced lung disease include a total cumulative dose greater than 450 units, advanced age, concominant oxygen use, and prior thoracic radiation. The prognosis is poor, and many patients die within 3 months of developing symptoms.6 The most common manifestation of lung injury is DAD, but it may also present as cryptogenic organizing pneumonia (COP), with unilateral or bilateral patchy airspace consolidation in a subpleural and peribronchial distribution (Fig. 9).13 Gemcitabine: Gemcitabine is one of the newer chemotherapeutic cytotoxic agents and is used to treat solid malignancies, including neoplasms of the breast, lung, pancreas, and ovaries. It is generally well tolerated but life-threatening pulmonary toxicity can occur. CT imaging typically demonstrates diffuse ground-glass attenuation with smooth interlobular septal thickening and reticular opacities, which may progress to acute respiratory distress syndrome (ARDS) and death (Fig. 10).12,13 Conclusion: There are innumerable pulmonary drug toxicities, several of which are encountered more frequently given the widespread use of these medications, with a few having classic radiographic findings. Considering drug related lung disease and having knowledge of the most common imaging manifestations allows the radiologist to include potential toxicity in the differential though it may not be suspected clinically. As many of these toxicities may result in loss of pulmonary function or be life-
4 threatening, but are potentially treatable when diagnosed early, allowing the exposure to be removed, the radiologist plays an integral role in expediting the patient’s care and improving prognosis. References 1. Restrepo CS, Carrill JA, Martínez S, et al. Pulmonary Complications from Cocaine and Cocainebased Substances: Imaging Manifestations. Radiographics 2007;27:941-956. 2. Park MS. Diffuse Alveolar Hemorrhage. Tuberc Respir Dis (Seoul) 2013;74(4):151-162. 3. Gotwa MB, Marde SR, Hanks DK, et al. Thoracic Complications of Illicit Drug Use: An Organ System Approach. Radiographics 2002;22:S119-S135. 4. Stern EJ, Frank MS, Schmutz JF, et al. Panlobular Pulmonary Emphysema Caused by IV Injection of Methylphenidate (Ritalin): Findings on Chest Radiographs and CT Scans. Am J Roentgenol 1994;162(3):555-560. 5. Webb WR. Radiology of Obstructive Pulmonary Disease. Am J Roentgenol 1997;169(3):637-647. 6. Rossi SE, Erasmus JJ, McAdam HP, Sporn TA, et al. Pulmonary Drug Toxicity: Radiologic and Pathologic Manifestations. Radiographics 2000;20:1245-1259. 7. Wolkove N, Baltzan M. Amiodarone Pulmonary Toxicity. Can Respir J 2009;16(2):43-48. 8. Kim KI, Kim CW, Lee MK, et al. Imaging of Occupational Lung Disease. Radiographics 2001;21:1371-1391. 9. Choi JW, Lee KS, Chung MP, et al. Giant Cell Interstitial Pneumonia: High-Resolution CT and Pathologic Findings in Four Adult Patients. Am J Roentgenol 2005;184(1):268-272. 10. Akira M. Uncommon Pneumoconioses: CT and Pathologic Findings. Radiology 1995;197(2):403409. 11. Ellis SJ, Cleverley JR, Müller NL. Drug-induced Lung disease: High-Resolution CT Findings. Am J Roentgenol 2000;175:1019-1024. 12. Torrisi, JM, Schwartz LH, Gollub MJ, et al. CT Findings of Chemotherapy-induced Toxicity: What Radiologists Need to Know about the Clinical and Radiologic Manifestations of Chemotherapy Toxicity. Radiology 2011;258:41-56. 13. Boiselle PM, Morrin MM, Huberman MS. Gemcitabine Pulmonary Toxicity: CT Features. J Comput Assis Tomogr 2000;24(6):977-980.
Figure Captions: Figure 1: Cocaine Hemorrhage. Axial CT in lung window in a patient with recent cocaine abuse shows pulmonary hemorrhage shows centrilobular ground glass attenuation (curved arrow). Note the subpleural sparing (straight arrows), which is a hallmark of pulmonary hemorrhage.
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Figure 2: Methylphenidate (Ritalin) abuse. Axial CT in lung window shows emphysema with diffuse areas of low attenuation throughout the lungs with a paucity of vessels (arrows). Figure 3: Amiodarone toxicity. Axial CT in lung window shows bilateral ground glass opacities and interstitial disease (arrows). Note cardiomegaly in the setting of long standing cardiac disease. Figure 4: Heavy metal poisoning – Tungsten. Axial HRCT in a 66 year old male shows multifocal basilar predominant ground glass with associated traction bronchiectasis (curved arrows) and subpleural fibrosis (straight arrow). Figure 5: Heavy metal pneumoconiosis – Benzene. Axial CT in lung window shows multifocal areas of ground glass attenuation (arrows). There is also traction bronchiectasis (curved arrow) which can be seen with long standing exposure. Figure 6: Nitrofurantoin toxicity. Axial CT in chronic toxicity shows an NSIP pattern with bilateral reticular opacities with few areas of bronchiolectasis (arrows) without honeycombing. Figure 7: Methothrexate toxicity. Axial CT in lung windows in a 39 year old female shows peripheral parenchymal opacifications (arrow). Figure 8: Cyclophosphamide toxicity. Axial CT in lung window shows short interval development of fibrosis with architectural distortion and honeycombing (arrows). Figure 9: Bleomycin toxicity. Axial CT shows small bilateral pleural effusions with multifocal patchy basilar consolidation (arrows). Note the lack of airway thickening, bronchiectasis, and honeycombing. Figure 10: Gemcitabine toxicity. Axial CT in lung window shows ground glass attenuation and smoothly thickened interlobular septae (arrows).
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Bad for Breathing: A Pictorial of Drug Induced Pulmonary Disease Amy C. Taylor MD, Nupur Verma MD, Roberta Slater MD, Tan-Lucien H. Mohammed MD, FCCP
www.cpdrjournal.com
PII: DOI: Reference:
S0363-0188(15)30005-0 http://dx.doi.org/10.1067/j.cpradiol.2015.10.002 YMDR404
To appear in:
Current Problems in Diagnostic Radiology
Cite this article as: Amy C. Taylor MD, Nupur Verma MD, Roberta Slater MD, Tan-Lucien H. Mohammed MD, FCCP, Bad for Breathing: A Pictorial of Drug Induced Pulmonary Disease, Current Problems in Diagnostic Radiology, http://dx. doi.org/10.1067/j.cpradiol.2015.10.002 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
1
Bad for Breathing: A Pictorial of Drug Induced Pulmonary Disease Amy C. Taylor, MDa Nupur Verma, MDa Roberta Slater, MDa Tan-Lucien H. Mohammed, MD, FCCPa a
Department of Radiology University of Florida – College of Medicine Post Office Box 100374 Gainesville, Florida United States of America Corresponding author: Tan-Lucien H. Mohammed, MD, FCCP College of Medicine – University of Florida Department of Radiology Post Office Box 100374 Gainesville, Florida United States of America Phone: 352-265-0291 E-mail: [email protected]
Abstract: Drug-induced lung disease has been described with over three hundred different agents, some of which are asymptomatic and may first present on imaging. These pulmonary diseases may present with variable imaging manifestations, and often overlap with other etiologies such as rejection, lymphoproliferative disorders, and infection which may be suspected in this patient population. However, there are several drugs which have classic imaging appearances, and, in the proper clinical context, the radiologist should include their toxicity in the differential diagnosis, potentially expediting withdrawal of the drug and avoiding irreversible lung injury such as fibrosis. Keywords: Drug toxicity; Ritalin; Cocaine; Interstitial Lung Disease; CT; Amiodarone; Pneumoconiosis Cocaine: The term “crack lung” refers to an acute pulmonary syndrome that occurs after the inhalation of free-base cocaine and is secondary to prolonged inflammatory pulmonary injury. Cocaine inhalation is associated with fever, hypoxemia, hemoptysis, respiratory failure, and diffuse alveolar opacities.1 Lung tissue specimens obtained in affected patients reveal diffuse alveolar damage, alveolar hemorrhage, eosinophilic interstitial and alveolar cell infiltration, and deposition of IgE.1 Chest radiographs demonstrate multifocal airspace disease.1 Computer tomographic (CT) imaging demonstrates
2 predominantly lower lobar multifocal ground glass attenuation with subpleural sparing, as would be expected in diffuse alveolar hemorrhage (Fig. 1).2 Recurrent episodes of hemorrhage may lead to eventual subpleural reticulation and honeycombing.2 Methylphenidate (Ritalin): Intravenous use of methylphenidate has been associated with the development of lower lobe panlobular emphysema, akin to that seen with alpha-1-antitrypsin deficiency. Microscopic talc granulomata may be seen, relating to the injection base.3,4 Chest radiographs show hyperinflation with lower lobe lucency of diffuse panlobular emphysema and CT demonstrates diffuse areas of low attenuation throughout the lungs with a paucity of vessels. (Fig. 2).5 Amiodarone: Amiodarone is a commonly used antiarrhythmic, making this a toxicity most often associated with cardiac patients. Toxicity occurs in 5-10% of patients and can present with both pulmonary and hepatic manifestations. Risk factors for developing toxicity include a daily dose greater than 400 mg and elderly status of the patient.6 Pulmonary imaging classically demonstrates distinctive focal high attenuation consolidations, which are most commonly peripheral in distribution (Fig. 3). However, non-specific interstitial pneumonia (NSIP) is the most commonly encountered manifestation.6 Due to the high iodine content and metabolism of amiodarone in the liver, this organ may also have high attenuation. The combination of high attenuation in the lung, liver, and spleen is characteristic of amiodarone toxicity. Treatment is cessation of amiodarone and administration of corticosteroids.7 Heavy Metals (benzenes): Heavy metal pneumoconiosis results from inhalational exposure to tungsten carbide, cobalt, or diamond-cobalt. The histopathological finding of giant cell interstitial pneumonia (GIP) is pathognomonic for this disorder.8,9 CT imaging often demonstrates patchy ground-glass attenuation and consolidation in the mid and lower lungs (Fig. 4). With long term exposure, fibrosis with architectural distortion, traction bronchiectasis, and honeycombing can occur (Fig. 5).9,10 Prognosis is favorable with early recognition of the patient’s occupational exposure, and removal of the offending environment. Nitrofurantoin: Nitrofurantoin is an antibiotic commonly used to treat urinary tract infections. Pulmonary toxicity is uncommon with its use and occurs in less than 1% of patients; however, when toxicity occurs, it may be either acute or chronic.11 Acute toxicity is more common, usually occurring within two weeks of drug initiation. Imaging demonstrates diffuse bilateral basilar-predominant heterogeneous opacities and pleural effusions. Laboratory assessment may show peripheral eosinophilia.6 Chronic toxicity is less common and often occurs after months or years of continuous use. Imaging in chronic toxicity typically demonstrates an NSIP pattern with bilateral, predominantly basilar, reticular opacities (Fig. 6).11
3 Methotrexate: Methotrexate is a common chemotherapeutic agent used in the treatment of malignancies, as well as for the treatment of severe rheumatoid arthritis and psoriatic arthritis. Pulmonary toxicity occurs in 5-10% of patients and usually develops within months of starting therapy. The most common imaging manifestation is an NSIP pattern (Fig. 7), followed by an organizing pneumonia pattern.6 Respiratory symptoms are often accompanied by fever and peripheral eosinophilia.12 Prognosis is generally favorable with discontinuation of therapy, and treatment with methotrexate can be reintroduced in the future without increased predilection for recurrent toxicity.13 Cyclophosphamide: Cyclophosphamide is a cytotoxic agent used to treat a variety of malignant and nonmalignant conditions. Cyclophosphamide toxicity can occur within weeks to years of use, and there is no relationship between the drug dosage or between the duration of therapy and the development of lung injury. The most common manifestation of toxicity is diffuse alveolar damage (DAD). CT imaging in DAD demonstrates scattered or diffuse ground glass opacities in the early phase, with rapid progression to fibrosis, which usually develops within two weeks. This may present as bronchiectasis, marked architectural distortion, and honeycombing (Fig. 8).12 Prognosis is generally good after therapy has been discontinued; however, the fibrotic lung disease does not change. Bleomycin: Bleomycin is a common chemotherapeutic agent used to treat squamous cell carcinoma, testicular carcinoma, and Hodgkin’s lymphoma. Risk factors for developing bleomycin-induced lung disease include a total cumulative dose greater than 450 units, advanced age, concominant oxygen use, and prior thoracic radiation. The prognosis is poor, and many patients die within 3 months of developing symptoms.6 The most common manifestation of lung injury is DAD, but it may also present as cryptogenic organizing pneumonia (COP), with unilateral or bilateral patchy airspace consolidation in a subpleural and peribronchial distribution (Fig. 9).13 Gemcitabine: Gemcitabine is one of the newer chemotherapeutic cytotoxic agents and is used to treat solid malignancies, including neoplasms of the breast, lung, pancreas, and ovaries. It is generally well tolerated but life-threatening pulmonary toxicity can occur. CT imaging typically demonstrates diffuse ground-glass attenuation with smooth interlobular septal thickening and reticular opacities, which may progress to acute respiratory distress syndrome (ARDS) and death (Fig. 10).12,13 Conclusion: There are innumerable pulmonary drug toxicities, several of which are encountered more frequently given the widespread use of these medications, with a few having classic radiographic findings. Considering drug related lung disease and having knowledge of the most common imaging manifestations allows the radiologist to include potential toxicity in the differential though it may not be suspected clinically. As many of these toxicities may result in loss of pulmonary function or be life-
4 threatening, but are potentially treatable when diagnosed early, allowing the exposure to be removed, the radiologist plays an integral role in expediting the patient’s care and improving prognosis. References 1. Restrepo CS, Carrill JA, Martínez S, et al. Pulmonary Complications from Cocaine and Cocainebased Substances: Imaging Manifestations. Radiographics 2007;27:941-956. 2. Park MS. Diffuse Alveolar Hemorrhage. Tuberc Respir Dis (Seoul) 2013;74(4):151-162. 3. Gotwa MB, Marde SR, Hanks DK, et al. Thoracic Complications of Illicit Drug Use: An Organ System Approach. Radiographics 2002;22:S119-S135. 4. Stern EJ, Frank MS, Schmutz JF, et al. Panlobular Pulmonary Emphysema Caused by IV Injection of Methylphenidate (Ritalin): Findings on Chest Radiographs and CT Scans. Am J Roentgenol 1994;162(3):555-560. 5. Webb WR. Radiology of Obstructive Pulmonary Disease. Am J Roentgenol 1997;169(3):637-647. 6. Rossi SE, Erasmus JJ, McAdam HP, Sporn TA, et al. Pulmonary Drug Toxicity: Radiologic and Pathologic Manifestations. Radiographics 2000;20:1245-1259. 7. Wolkove N, Baltzan M. Amiodarone Pulmonary Toxicity. Can Respir J 2009;16(2):43-48. 8. Kim KI, Kim CW, Lee MK, et al. Imaging of Occupational Lung Disease. Radiographics 2001;21:1371-1391. 9. Choi JW, Lee KS, Chung MP, et al. Giant Cell Interstitial Pneumonia: High-Resolution CT and Pathologic Findings in Four Adult Patients. Am J Roentgenol 2005;184(1):268-272. 10. Akira M. Uncommon Pneumoconioses: CT and Pathologic Findings. Radiology 1995;197(2):403409. 11. Ellis SJ, Cleverley JR, Müller NL. Drug-induced Lung disease: High-Resolution CT Findings. Am J Roentgenol 2000;175:1019-1024. 12. Torrisi, JM, Schwartz LH, Gollub MJ, et al. CT Findings of Chemotherapy-induced Toxicity: What Radiologists Need to Know about the Clinical and Radiologic Manifestations of Chemotherapy Toxicity. Radiology 2011;258:41-56. 13. Boiselle PM, Morrin MM, Huberman MS. Gemcitabine Pulmonary Toxicity: CT Features. J Comput Assis Tomogr 2000;24(6):977-980.
Figure Captions: Figure 1: Cocaine Hemorrhage. Axial CT in lung window in a patient with recent cocaine abuse shows pulmonary hemorrhage shows centrilobular ground glass attenuation (curved arrow). Note the subpleural sparing (straight arrows), which is a hallmark of pulmonary hemorrhage.
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Figure 2: Methylphenidate (Ritalin) abuse. Axial CT in lung window shows emphysema with diffuse areas of low attenuation throughout the lungs with a paucity of vessels (arrows). Figure 3: Amiodarone toxicity. Axial CT in lung window shows bilateral ground glass opacities and interstitial disease (arrows). Note cardiomegaly in the setting of long standing cardiac disease. Figure 4: Heavy metal poisoning – Tungsten. Axial HRCT in a 66 year old male shows multifocal basilar predominant ground glass with associated traction bronchiectasis (curved arrows) and subpleural fibrosis (straight arrow). Figure 5: Heavy metal pneumoconiosis – Benzene. Axial CT in lung window shows multifocal areas of ground glass attenuation (arrows). There is also traction bronchiectasis (curved arrow) which can be seen with long standing exposure. Figure 6: Nitrofurantoin toxicity. Axial CT in chronic toxicity shows an NSIP pattern with bilateral reticular opacities with few areas of bronchiolectasis (arrows) without honeycombing. Figure 7: Methothrexate toxicity. Axial CT in lung windows in a 39 year old female shows peripheral parenchymal opacifications (arrow). Figure 8: Cyclophosphamide toxicity. Axial CT in lung window shows short interval development of fibrosis with architectural distortion and honeycombing (arrows). Figure 9: Bleomycin toxicity. Axial CT shows small bilateral pleural effusions with multifocal patchy basilar consolidation (arrows). Note the lack of airway thickening, bronchiectasis, and honeycombing. Figure 10: Gemcitabine toxicity. Axial CT in lung window shows ground glass attenuation and smoothly thickened interlobular septae (arrows).
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