- •Preface to the First Edition
- •Preface to the Second Edition
- •Contents
- •Diagnostic Challenges
- •Expert Centers
- •Patient Organizations
- •Clinical Trials
- •Research in Orphan Lung Diseases
- •Orphan Drugs
- •Orphanet
- •Empowerment of Patients
- •Conclusions
- •References
- •Introduction
- •Challenges to Overcome in Order to Undertake Quality Clinical Research
- •Lack of Reliable Data on Prevalence
- •Small Number of Patients
- •Identifying Causation/Disease Pathogenesis
- •Disease Complexity
- •Lack of Access to a Correct Diagnosis
- •Delay in Diagnosis
- •Challenges But Not Negativity
- •Some Success Stories
- •The Means to Overcome the Challenges of Clinical Research: Get Bigger Numbers of Well-Characterized Patients
- •The Importance of Patient Organizations
- •National and International Networks
- •End Points for Trials: Getting Them Right When Numbers Are Small and Change Is Modest
- •Orphan Drug Development
- •Importance of Referral Centers
- •Looking at the Future
- •The Arguments for Progress
- •Concluding Remarks
- •References
- •3: Chronic Bronchiolitis in Adults
- •Introduction
- •Cellular Bronchiolitis
- •Follicular Bronchiolitis
- •Respiratory Bronchiolitis
- •Airway-Centered Interstitial Fibrosis
- •Proliferative Bronchiolitis
- •Diagnosis
- •Chest Imaging Studies
- •Pulmonary Function Testing
- •Lung Biopsy
- •Mineral Dusts
- •Organic Dusts
- •Volatile Flavoring Agents
- •Infectious Causes of Bronchiolitis
- •Idiopathic Forms of Bronchiolitis
- •Connective Tissue Diseases
- •Organ Transplantation
- •Hematopoietic Stem Cell Transplantation
- •Drug-Induced Bronchiolitis
- •Treatment
- •Constrictive Bronchiolitis
- •Follicular Bronchiolitis
- •Airway-Centered Interstitial Fibrosis
- •Proliferative Bronchiolitis
- •References
- •Background and Epidemiology
- •Pathophysiology
- •Host Characteristics
- •Clinical Manifestations
- •Symptoms
- •Laboratory Evaluation
- •Skin Testing
- •Serum Precipitins
- •Eosinophil Count
- •Total Serum Immunoglobulin E Levels
- •Recombinant Antigens
- •Radiographic Imaging
- •Pulmonary Function Testing
- •Histology
- •Diagnostic Criteria
- •Historical Diagnostic Criteria
- •Rosenberg and Patterson Diagnostic Criteria
- •ISHAM Diagnostic Criteria
- •Cystic Fibrosis Foundation Diagnostic Criteria
- •General Diagnostic Recommendations
- •Allergic Aspergillus Sinusitis (AAS)
- •Natural History
- •Treatment
- •Corticosteroids
- •Antifungal Therapy
- •Monoclonal Antibodies
- •Monitoring for Treatment Response
- •Conclusions
- •References
- •5: Orphan Tracheopathies
- •Introduction
- •Anatomical Considerations
- •Clinical Presentation
- •Etiological Considerations
- •Idiopathic Subglottic Stenosis
- •Introduction
- •Clinical Features
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Introduction and Clinical Presentation
- •Clinical Features
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Tracheomalacia
- •Introduction
- •Clinical Features
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Tracheobronchomegaly
- •Introduction
- •Clinical Features
- •Pathophysiology
- •Pulmonary Function Studies
- •Imaging Studies
- •Treatment
- •Tracheopathies Associated with Systemic Diseases
- •Relapsing Polychondritis
- •Introduction
- •Clinical Features
- •Laboratory Findings
- •Pulmonary Function and Imaging Studies
- •Treatment
- •Introduction
- •Clinical Features
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Tracheobronchial Amyloidosis
- •Introduction
- •Clinical Features
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Sarcoidosis
- •Introduction
- •Pulmonary Function Studies
- •Imaging Studies
- •Bronchoscopy
- •Treatment
- •Orphan Tracheopathies: Conclusions
- •References
- •6: Amyloidosis and the Lungs and Airways
- •Introduction
- •Diagnosis and Evaluation of Amyloidosis
- •Systemic AA Amyloidosis
- •Systemic AL Amyloidosis
- •Amyloidosis Localised to the Respiratory Tract
- •Laryngeal Amyloidosis
- •Tracheobronchial Amyloidosis
- •Parenchymal Pulmonary Amyloidosis
- •Pulmonary Amyloidosis Associated with Sjögren’s Disease
- •Conclusions
- •References
- •Introduction
- •Pathophysiology
- •Genetic Predisposition
- •Immune Dysregulation
- •Epidemiology
- •Incidence and Prevalence
- •Triggering Factors
- •Clinical Manifestations
- •General Symptoms
- •Pulmonary Manifestations
- •Ear, Nose, and Throat (ENT) Manifestations
- •Neurological Manifestations
- •Skin Manifestations
- •Cardiac Manifestations
- •Gastrointestinal Involvement
- •Renal Manifestations
- •Ophthalmological Manifestations
- •Complementary Investigations
- •Diagnosis
- •Diagnostic Criteria
- •Prognosis and Outcomes
- •Phenotypes According to the ANCA Status
- •Treatment
- •Therapeutic Strategies
- •Remission Induction
- •Maintenance Therapy
- •Other Treatments
- •Prevention of AEs
- •Conclusions
- •References
- •8: Granulomatosis with Polyangiitis
- •A Brief Historical Overview
- •Epidemiology
- •Pathogenesis
- •Clinical Manifestations
- •Constitutional Symptoms
- •Ear, Nose, and Throat (ENT) Manifestations
- •Pulmonary Manifestations
- •Kidney and Urological Manifestations
- •Kidney Manifestations
- •Urological Manifestations
- •Neurological Manifestations
- •Peripheral Nervous System (PNS) Manifestations
- •Central Nervous System (CNS) Manifestations
- •Spinal Cord and Cranial Nerve Involvement
- •Skin and Oral Mucosal Manifestations
- •Eye Manifestations
- •Cardiac Involvement
- •Gastrointestinal Manifestations
- •Gynecological and Obstetric Manifestations
- •Venous Thrombosis and Other Vascular Events
- •Other Manifestations
- •Pediatric GPA
- •Diagnosis
- •Diagnostic Approach
- •Laboratory Investigations
- •Biology
- •Immunology
- •Pathology
- •Treatment
- •Glucocorticoids
- •Cyclophosphamide
- •Rituximab
- •Other Current Induction Approaches
- •Other Treatments in GPA
- •Intravenous Immunoglobulins
- •Plasma Exchange
- •CTLA4-Ig (Abatacept)
- •Cotrimoxazole
- •Other Agents
- •Principles of Treatment for Relapsing and Refractory GPA
- •Outcomes and Prognostic Factors
- •Survival and Causes of Deaths
- •Relapse
- •Damage and Disease Burden on Quality of Life
- •Conclusions
- •References
- •9: Alveolar Hemorrhage
- •Introduction
- •Clinical Presentation
- •Diagnosis (Table 9.1, Fig. 9.3)
- •Pulmonary Capillaritis
- •Histology (Fig. 9.4)
- •Etiologies
- •ANCA-Associated Small Vessel Vasculitis: Granulomatosis with Polyangiitis (GPA)
- •ANCA-Associated Small Vessel Vasculitis: Microscopic Polyangiitis
- •Isolated Pulmonary Capillaritis
- •Systemic Lupus Erythematosus
- •Antiphospholipid Antibody Syndrome
- •Anti-Basement Membrane Antibody Disease (Goodpasture Syndrome)
- •Lung Allograft Rejection
- •Others
- •Bland Pulmonary Hemorrhage (Fig. 9.5)
- •Histology
- •Etiologies
- •Idiopathic Pulmonary Hemosiderosis
- •Drugs and Medications
- •Coagulopathy
- •Valvular Heart Disease and Left Ventricular Dysfunction
- •Other
- •Histology
- •Etiologies
- •Hematopoietic Stem Cell Transplantation (HSCT)
- •Cocaine Inhalation
- •Acute Exacerbation of Interstitial Lung Disease
- •Acute Interstitial Pneumonia
- •Acute Respiratory Distress Syndrome
- •Miscellaneous Causes
- •Etiologies
- •Pulmonary Capillary Hemangiomatosis
- •Treatment
- •Conclusions
- •References
- •Takayasu Arteritis
- •Epidemiology
- •Pathologic Features
- •Pathogenesis
- •Clinical Features
- •Laboratory Findings
- •Imaging Studies
- •Therapeutic Management
- •Prognosis
- •Behçet’s Disease
- •Epidemiology
- •Pathologic Features
- •Pathogenesis
- •Diagnostic Criteria
- •Clinical Features
- •Pulmonary Artery Aneurysm
- •Pulmonary Artery Thrombosis
- •Pulmonary Parenchymal Involvement
- •Laboratory Findings
- •Imaging Studies
- •Therapeutic Management
- •Treatment of PAA
- •Treatment of PAT
- •Prognosis
- •References
- •Introduction
- •Portopulmonary Hypertension (PoPH)
- •Epidemiology and Risk Factors
- •Molecular Pathogenesis
- •PoPH Treatment
- •Hepatopulmonary Syndrome (HPS)
- •Epidemiology and Risk Factors
- •Molecular Pathogenesis
- •HPS Treatment
- •Conclusion
- •References
- •12: Systemic Sclerosis and the Lung
- •Introduction
- •Risk factors for SSc-ILD
- •Genetic Associations
- •Clinical Presentation of SSc-ILD
- •Pulmonary Function Tests (PFTs)
- •Imaging
- •Management
- •References
- •13: Rheumatoid Arthritis and the Lungs
- •Introduction
- •Epidemiology
- •Risk Factors for ILD (Table 13.3)
- •Pathogenesis
- •Clinical Features and Diagnosis
- •Treatments
- •Prognosis
- •Epidemiology
- •Risk Factors
- •Clinical Features, Diagnosis, and Outcome
- •Subtypes or RA-AD
- •Obliterative Bronchiolitis
- •Bronchiectasis
- •COPD
- •Cricoarytenoid Involvement
- •Pleural Disease
- •Conclusion
- •References
- •Introduction
- •Systemic Lupus Erythematosus
- •Epidemiology
- •Pathophysiology
- •Pulmonary Manifestations
- •Pleural Disease
- •Shrinking Lung Syndrome
- •Thrombotic Manifestations
- •Interstitial Lung Disease
- •Other Pulmonary Manifestations
- •Prognosis
- •Sjögren’s Syndrome
- •Epidemiology
- •Pathophysiology
- •Pulmonary Manifestations
- •Airway Disorders
- •Lymphoproliferative Disease
- •Interstitial Lung Disease
- •Prognosis
- •Mixed Connective Tissue Disease
- •Epidemiology
- •Pathophysiology
- •Pulmonary Manifestations
- •Pulmonary Hypertension
- •Interstitial Lung Disease
- •Prognosis
- •Myositis
- •Epidemiology
- •Pathophysiology
- •Pulmonary Manifestations and Treatments
- •Interstitial Lung Disease
- •Respiratory Muscle Weakness
- •Other Pulmonary Manifestations
- •Prognosis
- •Other Therapeutic Options in CTD-ILD
- •Lung Transplantation
- •Conclusion
- •References
- •Introduction
- •Diagnostic Criteria
- •Controversies in the Diagnostic Criteria
- •Typical Clinical Features
- •Disease Progression and Prognosis
- •Summary
- •References
- •Introduction
- •Histiocytes and Dendritic Cells
- •Introduction
- •Cellular and Molecular Pathogenesis
- •Pathology
- •Clinical Presentation
- •Treatment and Prognosis
- •Erdheim-Chester Disease
- •Epidemiology
- •Cellular and Molecular Pathogenesis
- •Histopathology and Immunohistochemistry
- •Clinical Presentation
- •Investigation/Diagnosis
- •Chest Studies
- •Cardiovascular Imaging
- •CNS Imaging
- •Bone Radiography
- •Other Imaging Findings and Considerations
- •Disease Monitoring
- •Pathology
- •Management/Treatment
- •Prognosis
- •Rosai-Dorfman Destombes Disease
- •Epidemiology
- •Etiology/Pathophysiology
- •Histopathology and Immunohistochemistry
- •Clinical Presentation
- •Investigation/Diagnosis
- •Management/Treatment
- •Prognosis
- •Conclusions
- •Diagnostic Criteria for Primary Histiocytic Disorders of the Lung
- •References
- •17: Eosinophilic Pneumonia
- •Introduction
- •Eosinophil Biology
- •Physiologic and Immunologic Role of Eosinophils
- •Release of Mediators
- •Targeting the Eosinophil Cell Lineage
- •Historical Perspective
- •Clinical Presentation
- •Pathology
- •Diagnosis
- •Eosinophilic Lung Disease of Undetermined Cause
- •Idiopathic Chronic Eosinophilic Pneumonia
- •Clinical Features
- •Imaging
- •Laboratory Studies
- •Bronchoalveolar Lavage
- •Lung Function Tests
- •Treatment
- •Outcome and Perspectives
- •Clinical Features
- •Imaging
- •Laboratory Studies
- •Bronchoalveolar Lavage
- •Lung Function Tests
- •Lung Biopsy
- •Treatment and Prognosis
- •Eosinophilic Granulomatosis with Polyangiitis
- •History and Nomenclature
- •Pathology
- •Clinical Features
- •Imaging
- •Laboratory Studies
- •Pathogenesis
- •Diagnosis
- •Treatment and Prognosis
- •Long-Term Outcome
- •Hypereosinophilic Syndrome
- •Pathogenesis
- •Clinical and Imaging Features
- •Laboratory Studies
- •Treatment and Prognosis
- •Eosinophilic Pneumonias of Parasitic Origin
- •Tropical Eosinophilia [191]
- •Ascaris Pneumonia
- •Eosinophilic Pneumonia in Larva Migrans Syndrome
- •Strongyloides Stercoralis Infection
- •Eosinophilic Pneumonias in Other Infections
- •Allergic Bronchopulmonary Aspergillosis
- •Pathogenesis
- •Diagnostic Criteria
- •Biology
- •Imaging
- •Treatment
- •Bronchocentric Granulomatosis
- •Miscellaneous Lung Diseases with Associated Eosinophilia
- •References
- •Introduction
- •Pulmonary Langerhans’ Cell Histiocytosis
- •Epidemiology
- •Pathogenesis
- •Diagnosis
- •Clinical Features
- •Extrathoracic Lesions
- •Pulmonary Function Tests
- •Chest Radiography
- •High-Resolution Computed Tomography (HRCT)
- •Bronchoscopy and Bronchoalveolar Lavage (BAL)
- •Lung Biopsy
- •Pathology
- •Treatment
- •Course and Prognosis
- •Case Report I
- •Introduction
- •Epidemiology
- •Clinical Features
- •Histopathological Findings
- •Radiologic Findings
- •Prognosis and Therapy
- •Desquamative Interstitial Pneumonia
- •Epidemiologic and Clinical Features
- •Histopathological Findings
- •Radiological Findings
- •Prognosis and Therapy
- •Conclusion
- •References
- •19: Lymphangioleiomyomatosis
- •Introduction
- •Pathogenesis
- •Presentation
- •Prognosis
- •Management
- •General Measures
- •Parenchymal Lung Disease
- •Pleural Disease
- •Renal Angiomyolipoma
- •Abdominopelvic Lymphatic Disease
- •Pregnancy
- •Tuberous Sclerosis
- •Drug Treatment
- •Bronchodilators
- •mTOR Inhibitors
- •Anti-Oestrogen Therapy
- •Experimental Therapies
- •Interventions for Advanced Disease
- •Oxygen Therapy
- •Pulmonary Hypertension
- •References
- •20: Diffuse Cystic Lung Disease
- •Introduction
- •Lymphangioleiomyomatosis
- •Pathogenesis
- •Pathologic and Radiographic Characteristics
- •Diagnostic Approach
- •Pulmonary Langerhans Cell Histiocytosis (PLCH)
- •Pathogenesis
- •Pathological and Radiographic Characteristics
- •Diagnostic Approach
- •Birt-Hogg-Dubé Syndrome (BHD)
- •Pathogenesis
- •Pathological and Radiographic Characteristics
- •Diagnostic Approach
- •Lymphoproliferative Disorders
- •Pathogenesis
- •Pathological and Radiographic Characteristics
- •Diagnostic Approach
- •Amyloidosis
- •Light Chain Deposition Disease (LCDD)
- •Conclusion
- •References
- •Introduction
- •Lymphatic Development
- •Clinical Presentation of Lymphatic Disorders
- •Approaches to Diagnosis and Management of Congenital Lymphatic Anomalies
- •Generalized Lymphatic Anomaly
- •Etiopathogenesis
- •Clinical Presentation and Diagnosis
- •Course/Prognosis
- •Management
- •Kaposiform Lymphangiomatosis
- •Etiopathogenesis
- •Clinical Presentation and Diagnosis
- •Management
- •Course/Prognosis
- •Gorham Stout Disease
- •Etiopathogenesis
- •Clinical Presentation and Diagnosis
- •Management
- •Course/Prognosis
- •Channel-Type LM/Central Conducting LM
- •Etiopathogenesis
- •Clinical Presentation and Diagnosis
- •Management
- •Course/Prognosis
- •Yellow Nail Syndrome
- •Etiopathogenesis
- •Clinical Presentation and Diagnosis
- •Management
- •Course/Prognosis
- •Summary
- •References
- •Introduction
- •Historical Note
- •Epidemiology
- •Pathogenesis
- •Surfactant Homeostasis in PAP
- •GM-CSF Signaling Disruption
- •Myeloid Cell Dysfunction
- •GM-CSF Autoantibodies
- •Lymphocytosis
- •Clinical Manifestations
- •Clinical Presentation
- •Secondary Infections
- •Pulmonary Fibrosis
- •Diagnosis
- •Pulmonary Function Testing
- •Radiographic Assessment
- •Bronchoscopy and Bronchoalveolar Lavage
- •Laboratory Studies and Biomarkers
- •GM-CSF Autoantibodies
- •Genetic Testing
- •Lung Pathology
- •Diagnostic Approach to the Patient with PAP
- •Natural History and Prognosis
- •Treatment
- •Whole-Lung Lavage
- •Subcutaneous GM-CSF
- •Inhaled GM-CSF
- •Other Approaches
- •Conclusions and Future Directions
- •References
- •Introduction
- •Epidemiology
- •Gastric Contents
- •Pathobiology of GER/Microaspirate in the Lungs of Patients with IPF
- •GER and the Microbiome
- •Diagnosis
- •Clinical History/Physical Exam
- •Investigations
- •Esophageal Physiology
- •Upper Esophageal Sphincter
- •Esophagus and Peristalsis
- •Lower Esophageal Sphincter and Diaphragm
- •Esophageal pH and Impedance Testing
- •High Resolution Esophageal Manometry
- •Esophagram/Barium Swallow
- •Bronchoalveolar Lavage/Sputum: Biomarkers
- •Treatment
- •Anti-Acid Therapy (PPI/H2 Blocker)
- •GER and Acute Exacerbations of IPF
- •Suggested Approach
- •Summary and Future Directions
- •References
- •Introduction
- •Familial Interstitial Pneumonia
- •Telomere Related Genes
- •Genetic
- •Telomere Length
- •Pulmonary Involvement
- •Interstitial Lung Disease
- •Other Lung Disease
- •Hepatopulmonary Syndrome
- •Emphysema
- •Extrapulmonary Manifestations
- •Mucocutaneous Involvement
- •Hematological Involvement
- •Liver Involvement
- •Other Manifestations
- •Treatment
- •Telomerase Complex Agonists
- •Lung Transplantation
- •Surfactant Pathway
- •Surfactant Protein Genes
- •Pulmonary Involvement
- •Treatment
- •Heritable Forms of Pulmonary Fibrosis with Autoimmune Features
- •TMEM173
- •COPA
- •Pulmonary Alveolar Proteinosis
- •GMCSF Receptor Mutations
- •GATA2
- •MARS
- •Lysinuric Protein Intolerance
- •Lysosomal Diseases
- •Hermansky-Pudlak Syndrome
- •Lysosomal Storage Disorders
- •FAM111B, NDUFAF6, PEPD
- •Conclusion
- •References
- •Introduction
- •Pathophysiology
- •Clinical Presentation
- •Epidemiology
- •Genetic Causes of Bronchiectasis
- •Disorders of Mucociliary Clearance
- •Cystic Fibrosis
- •Primary Ciliary Dyskinesia
- •Other Ciliopathies
- •X-Linked Agammaglobulinemia
- •Chronic Granulomatous Disease and Other Disorders of Neutrophil Function
- •Other Genetic Disorders Predisposing to Bronchiectasis
- •Idiopathic Bronchiectasis
- •Diagnosis of Bronchiectasis
- •Management of Patients with Bronchiectasis
- •Airway Clearance Therapy (ACT)
- •Management of Infections
- •Immune Therapy
- •Surgery
- •Novel Therapies for Managing Cystic Fibrosis
- •Summary
- •References
- •Pulmonary Arteriovenous Malformations
- •Background Pulmonary AVMs
- •Anatomy Pulmonary AVMs
- •Clinical Presentation of Pulmonary AVMs
- •Screening Pulmonary AVMs
- •Treatment Pulmonary AVMs
- •Children with Hereditary Hemorrhagic Telangiectasia
- •Pulmonary Hypertension
- •Pulmonary Hypertension Secondary to Liver Vascular Malformations
- •Pulmonary Arterial Hypertension
- •Background HHT
- •Pathogenesis
- •References
- •27: Pulmonary Alveolar Microlithiasis
- •Introduction
- •Epidemiology
- •Pathogenesis
- •Clinical Features
- •Diagnosis
- •Management
- •Summary
- •References
- •Introduction
- •Hermansky-Pudlak Syndrome
- •Telomerase-Associated Pulmonary Fibrosis
- •Lysosomal Storage Diseases
- •Lysinuric Protein Intolerance
- •Familial Hypocalciuric Hypercalcemia
- •Surfactant Dysfunction Disorders
- •Concluding Remarks
- •References
- •Introduction
- •Background
- •Image Acquisition
- •Key Features of Fibrosis
- •Ancillary Features of Fibrosis
- •Other Imaging Findings in FLD
- •Probable UIP-IPF
- •Indeterminate
- •Alternative Diagnosis
- •UIP in Other Fibrosing Lung Diseases
- •Pleuroparenchymal Fibroelastosis (PPFE)
- •Combined Pulmonary Fibrosis and Emphysema
- •Chronic Hypersensitivity Pneumonitis
- •Other Fibrosing Lung Diseases
- •Fibrosing Sarcoidosis
- •CTD-ILD and Drug-Induced FLD
- •Complications
- •Prognosis
- •Computer Analysis of CT Imaging
- •The Progressive Fibrotic Phenotype
- •Other Imaging Techniques
- •Conclusion
- •References
- •Introduction
- •Bronchoalveolar Lavage (BAL)
- •Technique
- •Interpretation
- •Transbronchial Biopsy (TBB)
- •Transbronchial Lung Cryobiopsy (TLCB)
- •References
- •Introduction
- •Overview of ILD Diagnosis
- •Clinical Assessment
- •Radiological Assessment
- •Laboratory Assessment
- •Integration of Individual Features
- •Multidisciplinary Discussion
- •Diagnostic Ontology
- •Conclusions
- •References
- •Introduction
- •Idiopathic Pulmonary Fibrosis
- •Chronic Hypersensitivity Pneumonitis
- •Connective Tissue Disease
- •Drug-Induced Lung Diseases
- •Radiation Pneumonitis
- •Asbestosis
- •Hermansky-Pudlak Syndrome
- •Risk Factors for Progression
- •Diagnosis
- •Pharmacological Management
- •Conclusions
- •References
- •Historical Perspective
- •Epidemiology and Etiologies
- •Tobacco Smoking and Male Sex
- •Genetic Predisposition
- •Systemic Diseases
- •Other Etiological Contexts
- •Clinical Manifestations
- •Pulmonary Function and Physiology
- •Imaging
- •Computed Tomography Characteristics and Patterns
- •Thick-Walled Large Cysts
- •Imaging Phenotypes
- •Pitfalls
- •Pathology
- •Diagnosis
- •CPFE Is a Syndrome
- •Biology
- •Complications and Outcome
- •Mortality
- •Pulmonary Hypertension
- •Lung Cancer
- •Acute Exacerbation of Pulmonary Fibrosis
- •Other Comorbidities and Complications
- •Management
- •General Measures and Treatment of Emphysema
- •Treatment of Pulmonary Fibrosis
- •Management of Pulmonary Hypertension
- •References
- •Acute Interstitial Pneumonia (AIP)
- •Epidemiology
- •Presentation
- •Diagnostic Evaluation
- •Radiology
- •Histopathology
- •Clinical Course
- •Treatment
- •Epidemiology
- •Presentation
- •Diagnostic Evaluation
- •Radiology
- •Histopathology
- •Clinical Course
- •Desquamative Interstitial Pneumonia (DIP)
- •Presentation
- •Diagnostic Evaluation
- •Radiology
- •Histopathology
- •Clinical Course
- •Treatment
- •Epidemiology
- •Presentation
- •Diagnostic Evaluation
- •Radiology
- •Histopathology
- •Clinical Course
- •Treatment
- •References
- •Organizing Pneumonias
- •Epidemiology
- •Pathogenesis
- •Clinical Features
- •Imaging
- •Multifocal Form
- •Isolated Nodular Form
- •Other Imaging Patterns
- •Histopathological Diagnosis of OP Pattern
- •Etiological Diagnosis of OP
- •Treatment
- •Clinical Course and Outcome
- •Severe Forms of OP with Respiratory Failure
- •Acute Fibrinous and Organizing Pneumonia
- •Granulomatous Organizing Pneumonia
- •Acute Interstitial Pneumonia
- •Epidemiology
- •Clinical Picture
- •Imaging
- •Histopathology
- •Diagnosis
- •Treatment
- •Outcome
- •References
- •36: Pleuroparenchymal Fibroelastosis
- •Introduction
- •Epidemiology
- •Clinical Manifestations
- •Laboratory Findings
- •Respiratory Function
- •Radiologic Features
- •Pathologic Features
- •Diagnosis
- •Treatment
- •Prognosis
- •Conclusions
- •References
- •Introduction
- •Acute Berylliosis
- •Chronic Beryllium Disease
- •Exposure
- •Epidemiology
- •Immunopathogenesis and Pathology
- •Genetics
- •Clinical Description and Natural History
- •Treatment and Monitoring
- •Indium–Tin Oxide-Lung Disease
- •Hard Metal Lung
- •Flock Worker’s Disease
- •Asbestosis
- •Nanoparticle Induced ILD
- •Flavoring-Induced Lung Disease
- •Silica-Induced Interstitial Lung Disease
- •Chronic Silicosis
- •Acute and Accelerated Silicosis
- •Chronic Obstructive Disease in CMDLD
- •Simple CMDLD
- •Complicated CMDLD
- •Conclusion
- •References
- •38: Unclassifiable Interstitial Lung Disease
- •Introduction
- •Diagnostic Scenarios
- •Epidemiology
- •Clinical Presentation
- •Diagnosis
- •Clinical Features
- •Radiology
- •Laboratory Investigations
- •Pathology
- •Conclusion
- •References
- •39: Lymphoproliferative Lung Disorders
- •Introduction
- •Nodular Lymphoid Hyperplasia
- •Lymphocytic Interstitial Pneumonia (LIP)
- •Follicular Bronchitis/Bronchiolitis
- •Castleman Disease
- •Primary Pulmonary Lymphomas
- •Primary Pulmonary MALT B Cell Lymphoma
- •Pulmonary Plasmacytoma
- •Follicular Lymphoma
- •Lymphomatoid Granulomatosis
- •Primary Pulmonary Hodgkin Lymphoma (PPHL)
- •Treatment
- •References
- •Introduction
- •Late-Onset Pulmonary Complications
- •Bronchiolitis Obliterans (BO)
- •Pathophysiology
- •Diagnosis
- •Management of BOS
- •Post-HSCT Organizing Pneumonia
- •Other Late-Onset NonInfectious Pulmonary Complications (LONIPCs)
- •Conclusion
- •References
- •Introduction
- •Pulmonary Hypertension Associated with Sarcoidosis (Group 5.2)
- •PH Associated with Pulmonary Langerhans Cell Histiocytosis (Group 5.2)
- •PH in Combined Pulmonary Fibrosis and Emphysema (Group 3.3)
- •PH Associated with Lymphangioleiomyomatosis (Group 3)
- •Hereditary Hemorrhagic Telangiectasia (Group 1.2)
- •Pulmonary Veno-Occlusive Disease (Group 1.5)
- •Small Patella Syndrome (Group 1.2)
- •Conclusion
- •References
- •Introduction
- •Epidemiology
- •Timing, Chronology, Delay Time
- •Route of Administration
- •Patterns of Involvement [3, 4]
- •Drugs and Agents Fallen Out of Favor
- •Drug-Induced Noncardiac Pulmonary Edema
- •Drug-Induced Cardiogenic Pulmonary Edema
- •The “Chemotherapy Lung”
- •Drug-Induced/Iatrogenic Alveolar Hemorrhage
- •Drugs
- •Superwarfarin Rodenticides
- •Transfusion Reactions: TACO–TRALI
- •Acute Eosinophilic Pneumonia
- •Acute Granulomatous Interstitial Lung Disease
- •Acute Organizing Pneumonia (OP), Bronchiolitis Obliterans Organizing Pneumonia (BOOP), or Acute Fibrinous Organizing Pneumonia (AFOP) Patterns
- •Acute Amiodarone-Induced Pulmonary Toxicity (AIPT)
- •Accelerated Pulmonary Fibrosis
- •Acute Exacerbation of Previously Known (Idiopathic) Pulmonary Fibrosis
- •Anaphylaxis
- •Acute Vasculopathy
- •Drug-Induced/Iatrogenic Airway Emergencies
- •Airway Obstruction as a Manifestation of Anaphylaxis
- •Drug-Induced Angioedema
- •Hematoma Around the Upper Airway
- •The “Pill Aspiration Syndrome”
- •Catastrophic Drug-Induced Bronchospasm
- •Peri-operative Emergencies (Table 42.8)
- •Other Rare Presentations
- •Pulmonary Nodules and Masses
- •Pleuroparenchymal Fibroelastosis
- •Late Radiation-Induced Injury
- •Chest Pain
- •Rebound Phenomenon
- •Recall Pneumonitis
- •Thoracic Bezoars: Gossipybomas
- •Respiratory Diseases Considered Idiopathic That May Be Drug-Induced (Table 42.4)
- •Eye Catchers
- •Conclusion
- •References
- •Cancer Mimics of Organizing Pneumonia
- •Lung Adenocarcinoma/Bronchioloalveolar Carcinoma
- •Primary Pulmonary Lymphoma
- •Cancer Mimics of Interstitial Lung Diseases
- •Lymphangitic Carcinomatosis
- •Epithelioid Hemangio-Endothelioma
- •Lymphomatoid Granulomatosis
- •Cystic Tumors
- •Cavitating Tumors
- •Intrathoracic Pseudotumors
- •Respiratory Papillomatosis
- •Pulmonary Langerhans Cell Histiocytosis
- •References
- •Index
42 Drug-Induced/Iatrogenic Respiratory Disease: With Emphasis on Unusual, Rare, and Emergent Drug-Induced Reactions |
749 |
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Drugs and Agents Fallen Out of Favor
Prescription hexamethonium, mecamylamine, aminorex, l-tryptophan, fenfuramine, dexfenfuramine, phentermine, and benfuorex caused interstitial lung disease, ARDS, eosinophilic tissue damage, or pulmonary hypertension. These drugs are not available anymore. They are still indexed in Pneumotox, because any recalled drug may be obtained from a shelf somewhere, be synthetized in the home, be used experimentally, regain popularity in light of new indications (e.g., thalidomide), or because drug congeners may produce the same or similar adverse reactions (e.g., benfuorex v. fenfuramine). Mitomycin-C is far less used now that it was in the past and mitomycin pulmonary toxicity has become a rare occurrence, though rare cases emerge following instillation of the drug in the urinary bladder to treat bladder carcinoma [66]. The same concerns apply to mitomycin-induced hemolytic and uremic syndrome.
The antirheumatics, gold and penicillamine, have fallen into disuse since the advent of methotrexate, lefunomide, and the newer TNF-alfa and JAK antagonists. Gold-induced pneumonitis and penicillamine-associated obliterative bronchiolitis are for now diseases of the past. Penicillamine was not cited in a recent paper on airway disease in rheumatoid arthritis (RA) [67].
Amphetamine-like anorectics (aminorex in the 1960s, fenfuramine-dexfenfuramine in the 1990s, benfuorex in the 2000s) were recalled due to an epidemiologically signi cant surge of acquired pulmonary hypertension (PHT) and valvular heart disease. In the 1970s, aminorex was shown to cause pulmonary hypertension and plexiform pulmonary arterial changes in young women who used the drug as a weight reducing agent. Death occurred after an average 3.5 years on the drug from right ventricular failure. An epidemic of PHTn and valvular heart disease was also reported with the use of the then newer anorexigens fenfuramine and dextro-isomer dexfenfuramine in the 1980s and 1990s [68]; this resolved with recall of the drugs. Household manufacture of aminorex was responsible for sporadic PHT. Aminorex is a metabolite of levamisole, a veterinary antihelminthic agent widely present as an adulterant added by purveyors in cocaine. Only one case of pulmonary hypertension has been reported following exposure to cocaine-levamisole. Benfuorex, which was marketed as an antidiabetic drug is in fact closely related to fenfuramine. An epidemic of valvular heart disease and PHT developed (mostly in France) following long-term exposure to the drug [69], prior to its recall in 2009.
Several members of the thiazolidinedione (glitazones) family were discontinued in some countries owing to their propensity to cause capillary leak, pleural effusions, and irreversible heart failure.
l-tryptophan once was a popular nutraceutical. The compound produced an epidemic of “eosinophilia-myalgia syn-
drome,” with an increase in blood eosinophils. About half of affected patients presented with small irregular or dense radiographic opacities in the lung and with pleural effusion. An ARDS picture was noted in a few. Minute amounts of contaminants formed during the synthesis of tryptophan at the Showa Denko plant in Japan were blamed as the cause for the syndrome. Incident cases diminished sharply after l-tryptophan was recalled. Only sporadic cases are now being reported.
Dronedarone was designed to supplant amiodarone. Unfortunately, severe liver injury and sporadic ILD cases have prevented this drug from being released [3, 4].
Flavocoxid, a dietary supplement/medical food marketed under the tradename Limbrel® was recalled by the company in 2017–2018 under FDA action following reports of severe ILD.
A thorough history for DIRD must include use of herbal therapies, as many plants have been reported to cause pulmonary in ltrates, ARDS, bronchiolitis obliterans or arrhythmia.
Potentially Life-Threatening Drug-Induced/
Iatrogenic Emergencies (Table 42.6)
Pulmonologists, internal medicine specialists, oncologists, radiologists, anesthesiologists, surgeons, emergency physicians, intensive care and ENT specialists, nurses, dental surgeons may be confronted with unexpected acute life-threatening drug-induced respiratory and/or systemic emergencies. Acute reactions may affect the lung, upper airway, small airways, pulmonary circulation, pleura, pericardium or they can be systemic with associated pulmonary involvement. Clinical presentations include diffuse pulmonary in ltrates, acute airway obstruction, pleural or pericardial effusion, acute pulmonary hypertension. Causality can be straightforward when a reaction occurs during or immediately following administration of the drug. Onset can be within seconds. Some reactions develop electively during the intraor perioperative period, leading to dif cult diagnostic and management challenges. Consideration of drug-induced etiologies is paramount as drug withdrawal can be life-saving.
Acute Drug-Induced/Iatrogenic Emergencies with Di use Pulmonary Infltrates and ARDS (Table 42.7)
The Adult Respiratory Distress Syndrome (ARDS) is de ned by the triad of pulmonary in ltrates in the absence of cardiac failure, and a ratio of partial pressure of oxygen in arterial blood to FiO2 of less than 200. Different underlying pulmonary processes can lead to an ARDS picture including pulmonary edema, diffuse alveolar damage, severe in ltrative
750 |
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P. Bonniaud and P. Camus |
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Table 42.6 Life-threatening drug-induced/iatrogenic respiratory reactions |
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Typical timing to |
Develops |
|
|
Pattern of DI involvement |
onset |
in |
Typical drugs or compoundsa |
Main complications |
Angioedema and UAO |
Immediate-to-late |
min-h |
ACEI, ARB |
UAO, throat closure, locked |
|
|
|
|
airway, asphyxia |
Anaphylaxis |
Immediate |
min |
Drugs, biologics, RCM, latex |
Bronchoconstriction, shock, |
|
|
|
|
pulmonary edema |
Laryngospasm |
Immediate |
sec |
|
Asphyxia, NPPE |
Sudden catastrophic |
Immediate |
min |
β-blockers, NSAID, aspirin, muscle |
Locked airway, ARF, hypoxia, |
bronchospasm |
|
|
relaxants, abused drugs |
brain death |
Acute intraoperative DI |
Intraoperative, |
sec-min |
See speci c table |
Anaphylaxis, acute |
respiratory problem |
immediate |
|
|
bronchospasm, death |
|
|
|
|
|
Flash pulmonary edema |
min |
min |
Adrenaline, abused drugs, chemo, |
Hypoxemia, ARDS |
|
|
|
RCM |
|
Noncardiac pulmonary edema |
min-h (months with |
min-h |
Chemo, hydrochlorothiazide, |
Hypoxemia, ARDS |
|
oral drugs) |
|
salicylate (dose-related) |
|
|
|
|
|
|
ARDS-DAD |
d-y |
h-d |
Amiodarone, bleomycin, blood, |
Hypoxemic ARF |
|
|
|
chemo agents, paraquat |
|
|
|
|
TKI, oxygen, radiation therapy |
May evolve to pulmonary |
|
|
|
|
brosis |
Alveolar hemorrhage |
d-mo |
h-d |
All anticoagulants, platelets |
ARDS, clotting in central airway |
|
|
|
inhibitors, cocaine, PTU |
|
Dense acute interstitial lung |
w-y |
h-d |
Methotrexate |
Hypoxemic ARF/ARDS |
disease |
|
|
|
|
Acute amiodarone pulmonary |
d-y |
h-d |
Amiodarone |
Hypoxemic ARF/ARDS. Late |
toxicity |
|
|
|
pulmonary brosis |
|
|
|
|
|
Acute eosinophilic pneumonia |
d-mo |
h-d |
Minocycline, cocaine, venlafaxine, |
Hypoxemic ARF/ARDS |
|
|
|
tobacco/marijuana smoke |
|
Acute radiation-induced lung |
w |
d-w |
Radiation therapy to the chest |
Hypoxemic ARF/ARDS |
injury |
|
|
|
|
|
|
|
|
|
Catastrophic pulmonary |
Intraoperative, |
min |
Protamine |
Acute RVF, hypoxemia |
hypertension |
immediate |
|
|
|
Acute foreign body embolism |
h-d |
h-d |
Lipids, silicone, hyaluronate, acrylate |
Acute RVF |
|
|
|
cement |
|
|
|
|
|
|
Opportunistic infection |
w-y |
d |
Corticosteroids, immunosuppressants, |
ARF/ARDS (undistinguishable |
|
|
|
anti-TNF |
from DIRD) |
Massive pleural/pericardial |
w-y |
h-d |
Dantrolene, lupus-inducing drugs, all |
Compression/tamponade |
effusion/bleeding |
|
|
anticoagulants |
|
|
|
|
|
|
Acute methemoglobinemia |
h-d |
min-h |
Benzocaine, dapsone, nitrites, |
Tissue hypoxia, pulmonary |
|
|
|
oxidizing/occupational agents |
edema, brain damage |
Ventilatory arrest |
Immediate |
sec |
Opiates, colimycin |
Tissue hypoxia |
Neuromuscular failure |
h-d |
min-h |
Aminosides, curares, dantrolene, |
Hypoxemic ARF |
|
|
|
narcotics |
|
|
|
|
|
|
Acute left ventricular failure |
h-d |
h-d |
Doxorubicin, fuorouracil |
Pulmonary edema |
|
|
|
|
|
Multiple Organ Dysfunction |
w-mo |
d |
Drugs that induce DRESS |
Multi-organ dysfunction/failure |
Syndrome |
|
|
|
|
See Pneumotox
Abbreviations: ACEI: ACE inhibitors ARDS: adult respiratory distress syndrome; ARF: acute respiratory failure; DAD: diffuse alveolar damage; DAH: diffuse alveolar hemorrhage; DI: drug-induced; DIRD: drug-induced respiratory disease; DRESS: drug rash eosinophilia and systemic symptoms; NCPE noncardiac pulmonary edema; NPPE: negative pressure pulmonary edema; NSAID: nonsteroidal anti-infammatory drug; NSIP: nonspeci c interstitial pneumonia; PTU: propylthiouracil; RCM: radiocontrast media; RILI: radiation-induced lung injury; RVF: right ventricular failure; TKI: tyrosine kinase inhibitor; UAO: acute airway obstruction
h: hours, d: days, w: weeks, mo: months, sec: seconds a Complete list of offenders see pneumotox.com
lung disease including cellular NSIP, organizing pneumonia, eosinophilic pneumonia, or alveolar hemorrhage. In practice, lung tissue is rarely available for review. However, certain clinical and gas exchange features are suggestive of particular histopathological pattern-based classi cations
used by pathologists, which has practical implications as regards recognition and management, assessment of drug causality, and treatment. For instance, the majority of ARDS cases de ned clinically show features of diffuse alveolar damage (DAD) on pathological examination [60, 70, 71]. In
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Table 42.7 Drug-induced/Iatrogenic ARDS
|
Clinical pathological |
|
|
|
|
|
|
Imaging (may |
|
|
|
diagnosis |
Subpattern |
Pathology |
Typical drugs/agents |
Time to onset |
Tempo |
BAL |
predominate in LL) |
Diagnosis |
|
|
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1. |
Pulmonary edema |
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Noncardiogenic |
Pulmonary edema |
NCPE—Alveolar |
Chemo, ARA-C, HCT, |
Short |
Acute |
? |
GGO + pleural effusion |
Normal heart, short |
|
|
(NCPE) |
|
fooding |
tocolytic β2 agonists, |
|
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tempo |
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heroin, |
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Flash PE |
NCPE |
Adrenaline, RCM |
Ultrashort |
Hyperacute |
? |
Haze, GGO, lobular |
Tempo, foam at mouth |
|
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<5 min |
|
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thickening |
|
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Transient |
Mild NCPE, DAD, |
Paclitaxel, ATG |
Short |
Acute |
|
Slight haze, GGO, |
Short-lived; relapse on |
|
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|
pulmonary |
vasculitis |
|
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lobular thickening |
rechallenge |
|
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ltratesin |
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|
Pulmonary edema |
NCPE |
Hydrochlorothiazide |
Short |
Acute |
? |
Alveolar shad ± pleural |
Tempo, shock, relapse |
|
|
|
and shock |
|
|
|
Hyperacute |
|
eff. |
on rechallenge |
|
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|
Salicylate |
NCPE, DAD |
Salicylate |
Variable |
Subacute |
? |
Alveolar |
Salicylamide, |
|
|
|
pulmonary edema |
|
|
|
|
|
shadowing ± pleural |
metabolic acidosis, |
|
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eff. |
anion gap |
|
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|
Imaging-related |
NCPE |
Radiocontrast media |
Very short |
Acute, |
? |
|
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|
NCPE |
|
|
|
hyperacute |
|
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Drug addict |
NCPE |
Heroin, methadone |
|
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|
|
|
|
|
|
|
|
TRALI |
Pulmonary edema, |
Hemotherapy, IVIG |
Within 8 h |
Acute |
? |
Bilateral ltratesin or |
Tempo—Relevant |
|
|
|
|
DAD, DAH |
|
|
|
|
whiteout |
antibody in donor |
|
|
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|
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|
|
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|
|
|
|
|
NPPE |
Negative pressure |
Inspiration against a |
Short |
Subacute- |
|
|
Obstructed airway |
|
|
|
|
pulmonary edema |
restricted or closed airway |
|
Acute |
|
|
|
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Cardiogenic PE |
|
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Echocardiography |
|
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(US) |
|
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Fluid overload |
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||
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TACO |
PE |
Hemotherapy |
Short |
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Infusional |
PE |
Overzealous fuids |
Short |
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Cardiotoxicity |
PE |
Cardiotoxic drugs, ICI |
Progressive |
|
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related |
|
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Drug-induced |
PE |
Coronarotoxic drugs 5 FU |
Short |
|
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CAD |
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(continued) |
|
Reactions Induced-Drug Emergent and Rare, Unusual, on Emphasis With Disease: Respiratory Induced/Iatrogenic-Drug 42
751
com/.https://meduniver сайта язык русский на перевода для списке в находится книга Данная
Table 42.7 (continued)
|
|
Clinical pathological |
|
|
|
|
|
|
Imaging (may |
|
|
|
|
diagnosis |
Subpattern |
Pathology |
Typical drugs/agents |
Time to onset |
Tempo |
BAL |
predominate in LL) |
Diagnosis |
|
|
|
|
|
|
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|
2. |
Acute ILD |
|
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Chemotherapy |
Pulmonary edema, |
Chemo agents, ICI |
Days-Weeks |
Acute/ |
N + reactive |
Haze, GGO, |
|
|
|
|
|
lung |
NSIP, DAD, reactive |
|
|
Subacute |
cells |
consolidation, whiteout |
|
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pneumocytes |
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Acute ILD |
Dense NSIP w/wo |
Methotrexate, |
Variable |
cute |
L/N |
Bilateral ltratesin |
Exclusion/BAL: |
|
|
|
|
|
pulmonary edema or |
nitrofurantoin, mTOR |
|
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|
Pathology in selected |
|
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DAD |
inhibitors |
|
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cases |
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Acute |
Acute granulomatous |
BCG, fudarabine, IFN, |
Variable |
Acute |
L |
Bilateral ltratesin |
Pathology |
|
|
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|
granulomatous ILD |
ILD |
MTX |
|
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Acute foreign |
Foreign body |
Talc, crospovidone, |
Subacute |
Subacute |
- |
Bilateral ltratesin |
BAL, pathology |
|
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|
body reaction |
granuloma |
excipients, food |
|
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Acute |
AEP |
Minocycline, daptomycin |
Weeks |
Acute |
E |
Bilateral ltratesin |
Eos blood/BAL |
|
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eosinophilic |
|
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pneumonia |
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Acute OP/AFOP |
OP/AFOP w/wo foam |
Amiodarone, statins, ICI |
Variable |
Acute |
M |
Bilateral ltratesin |
Pathology |
|
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cells |
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Accelerated |
Dense interstitial |
Bleomycin, nitrosoureas, |
Days to |
Subacute |
N |
Bilateral ltratesin |
Pathology |
|
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pulmonary |
brosis |
anti-TNF agents, paraquat |
weeks |
|
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brosis |
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Acute amiodarone |
NSIP w/wo a DIP and/ |
Amiodarone |
Weeks- |
Acute |
M |
Bilateral ltratesin |
BAL/Pathology |
|
|
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lung |
or endogenous lipoid |
|
months |
|
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pneumonia pattern |
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Acute |
DAD + foam cells |
Amiodarone |
Acute |
Acute |
M |
Bilateral ltratesin |
BAL/Pathology |
|
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postoperative APT |
|
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3. |
DAH |
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Bland DAH |
DAH |
All anticoagulants, |
Variable |
Acute |
RBC |
Bilateral ltratesin |
BAL |
|
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|
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antiplatelet |
|
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ANA-related |
DAH |
Hydralazine, PTU, |
Variable |
Acute |
RBC |
Bilateral ltratesin |
BAL + Ab |
|
|
|
|
DAH |
|
anti-TNF |
|
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|
|
|
|
|
|
|
|
|
|
|
ANCA-related |
DAH w/wo capillaritis |
PTU, cocaine levamisole |
Variable |
Acute |
RBC |
Bilateral ltratesin |
BAL + Ab |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Secondary DAH |
DAH and silicone or |
Silicone, hyaluronate |
Short |
Subacute |
RBC |
Bilateral ltratesin |
BAL, silicone, |
|
|
|
|
|
hyaluronate |
|
|
|
|
|
hyaluronate |
|
|
|
|
|
|
|
|
|
|
|
|
|
4. |
Exacerbation of preexisting IPF |
|
|
|
|
|
|
|
|
||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Subacute |
NSIP/OP + brosis |
Any drug causing ILD, |
Variable |
Acute |
L/E/N |
Aggravated bilateral |
? BAL |
|
|
|
|
|
|
COVID19 vaccine |
|
|
|
ltratesin |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Precipitous |
DAD + PF |
Amiodarone, anti TNF, |
Variable |
Acute |
N |
Bilateral ltratesin |
– |
|
|
|
|
|
|
chemo, COVID19 vaccine |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
5.Acute vasculopathy
|
|
Fat embolism |
Fat embolism |
Amphotericin, propofol |
Short |
Acute |
AMa |
Bilateral ltratesin |
BAL |
|
|
syndrome |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Silicone |
Silicone embolism |
Subcutaneous fuid |
hours-days |
Subacute/ |
AMa |
Bilateral ltratesin |
BAL/Pathology |
|
|
embolism sd |
|
silicone injections |
|
Acute |
|
|
|
|
|
|
|
|
|
|
|
|
|
6. RILI |
Outside the |
DAD |
Irradiation (chemo |
Weeks |
Subacute |
L |
Haze, GGO |
BAL, imaging |
|
|
|
radiation eld |
|
aggravate) |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Abbreviations, see text
a AM: macrophages containing foreign body inclusions
752
Camus .P and Bonniaud .P