0
ONLINE EXCLUSIVES
Chest Imaging and Pathology for Clinicians |

Persistent Lobar Atelectasis in a Patient With Chronic Hoarseness FREE TO VIEW

Chris L. Scelsi, DO; Tanya Khasnavis, BS; Nikhil G. Patel, MD; Jayanth H. Keshavamurthy, MD; William B. Davis, MD
Author and Funding Information

aDepartment of Radiology, Augusta University, Augusta, GA

bMedical College of Georgia, Augusta University, Augusta, GA

cDepartment of Pathology, Augusta University, Augusta, GA

dDepartment of Pulmonology and Critical Care, Augusta University, Augusta, GA

CORRESPONDENCE TO: Chris Scelsi, DO, Department of Radiology, Augusta University, 1120 15th St, Augusta, GA 30912


Copyright 2017, American College of Chest Physicians. All Rights Reserved.


Chest. 2017;151(5):e107-e113. doi:10.1016/j.chest.2017.01.029
Text Size: A A A
Published online

A 61-year-old woman presented for outpatient evaluation of a 1-week history of fever and upper respiratory symptoms. She denied tobacco use, weight loss, hemoptysis, chronic cough, or recent travel and was in otherwise good health. Her medical history was insignificant except for her chronic hoarseness from a prior laryngeal disease. She denied any worsening hoarseness or any other vocal changes. She did report a positive family history of squamous cell lung cancer in her father.

Figures in this Article

Her initial workup included a chest radiograph, which demonstrated middle lobe atelectasis. She was prescribed a short course of antibiotics with quick resolution of her symptoms. However, a follow-up radiograph obtained 8 weeks later again demonstrated atelectasis of the middle lobe (Fig 1). A CT scan was subsequently obtained, with the primary concern of an obstructing lesion.

Figure 1
Figure Jump LinkFigure 1 A, Posteroanterior and lateral radiographs of the chest (8 weeks after initial presentation) demonstrate atelectasis of the middle lobe. B, Coronal view contrast-enhanced CT scan demonstrates complete collapse of the middle lobe.Grahic Jump Location

Contrast-enhanced CT imaging of the chest demonstrated atelectasis (Fig 2A, yellow arrow) of the middle lobe with luminal narrowing of the middle lobe bronchus (Fig 2A, black arrow) just distal to its origin from bronchus intermedius (Fig 2A, asterisk). Of further interest, there was diffuse circumferential nodular thickening of the bronchi and trachea (Figs 2B, 2C) with scattered bronchial wall calcifications (Fig 2B, black arrow). Three-dimensional volume rendering of the tracheobronchial tree (Fig 3A) demonstrated nodular irregularity of the trachea with absence of the collapsed middle bronchus (black arrow). CT-generated virtual bronchoscopy images were also obtained and showed diffuse endobronchial nodularity (Fig 3B).

Figure 2
Figure Jump LinkFigure 2 Axial views of contrast-enhanced CT image. A, Lung window demonstrating narrowing of the middle lobe bronchus (black arrow) distal to its origin from the bronchus intermedius (red asterisk). Atelectasis of the middle lobe is also seen here (yellow arrow). B, Intermediate lung-mediastinal window demonstrating nodular irregularity and thickening of the bronchus intermedius and the left main bronchus. Note the focal nodule representing an amyloidoma (yellow arrow) involving the posterior wall of the bronchus intermedius. Wall thickening and calcification of the left main bronchus is also demonstrated (black arrow). C, Mediastinal window demonstrating focal thickening (yellow arrow) of the anterior tracheal wall that causes luminal narrowing.Grahic Jump Location
Figure 3
Figure Jump LinkFigure 3 A, Three-dimensional volume reconstruction of the airway from the CT scan in Figure 2, demonstrating the irregular contour of the trachea. The collapsed middle lobe bronchus is absent (black arrow). B, CT-generated virtual bronchoscopy within the trachea near the level of the carina (asterisk) shows endobronchial nodularity with posterior tracheal membrane involvement.Grahic Jump Location

She was referred to the pulmonology department; pulmonary function testing demonstrated normal spirometric results, lung volume, and diffusion. Bronchoscopy was subsequently performed and revealed extensive narrowing of the airways, with an endobronchial nodular appearance similar to the CT-generated virtual bronchoscopy images. The middle lobe bronchus was nearly occluded, with a “fish mouth” appearance without evidence of an obstructing endobronchial lesion. A similar nodular appearance was also seen involving the larynx. A bronchial biopsy of the carina and brushings of the middle lobe bronchus were sent for histopathologic evaluation.

H&E staining of the bronchial tissue demonstrated waxy-appearing eosinophilic extracellular deposits (Figs 4A, 4B). The eosinophilic material has a “cracked” appearance after tissue processing (Figs 4A, 4B).

Figure 4
Figure Jump LinkFigure 4 H&E staining at (A) ×20 and (B) ×40 magnification of the biopsied bronchial wall demonstrating waxy eosinophilic extracellular deposits. A “cracked” appearance, better seen on B, is due to tissue processing. C, Congo-red staining at ×20 magnification demonstrating apple-green birefringence under polarized light.Grahic Jump Location

What is the diagnosis?

What is your differential diagnosis?

Diagnosis: Tracheobronchial amyloidosis causing persistent middle lobe atelectasis is the diagnosis. Other differential diagnoses that cause tracheobronchial narrowing include granulomatosis with polyangiitis, tuberculosis, sarcoidosis, relapsing polychondritis, tracheobronchopathia osteochondroplastica, and papillomatosis. It should be noted that there is significant overlap in the bronchoscopic appearances, and findings are not limited to a single disease process.

Clinical Discussion

Amyloidosis is a difficult to diagnose spectrum of diseases caused by the extracellular accumulation of misfolded protein in a predominantly β-pleated sheet structure. More than 20 separate amyloidogenic proteins have been described as causing disease in humans, with highly variable organ involvement.,,Table 1, summarizes the four main types of amyloid that demonstrate lung involvement. Regarding the localized AL subtype, three main patterns of pulmonary disease have been described. Tracheobronchial amyloidosis (TBA) is the most common form and is characterized by nodular or diffuse amyloid deposits in the tracheobronchial walls. A second pattern of discrete nodular opacities has been described in which amyloid deposits present as multiple peripheral lung nodules of varying sizes. The third type presents as a diffuse interstitial reticulonodular type of pattern and represents the rarest subtype., Although systemic amyloidosis has been estimated to affect < 200,000 Americans, localized pulmonary involvement is extremely rare, with a reported incidence of about five to 10 cases per million per year.,

Table Graphic Jump Location
Table 1 Summary of Amyloid Types With Lung Involvement

TBA usually presents after the fifth decade of life with a variety of nonspecific respiratory symptoms, such as dyspnea, hemoptysis, or chronic cough. Hoarseness may also be a presenting symptom if laryngeal or vocal cord involvement is present, as with the patient. Due to airway thickening and nodularity, endobronchial collapse and obstruction causes wheezing, stridor, atelectasis, and recurrent infection. These patients are frequently misdiagnosed as having asthma, chronic bronchitis, or a neoplastic process, given their propensity to experience atelectasis and postobstructive pneumonia.

Diagnostic clues can be seen on spirometry, as the tracheal infiltration and narrowing worsens with disease progression. Blunting of the peak expiratory and inspiratory flow loops can be seen, and if the tracheal involvement is primarily proximal, the flow-volume loop demonstrates a pattern consistent with fixed upper airway obstruction., Serial spirometry is valuable, as it is the most sensitive noninvasive diagnostic test to measure the progression of amyloid deposition. Serum and urine protein electrophoresis with immunofixation can be used as a screening test for suspected AL amyloidosis. Subsequent subcutaneous fat or a rectal tissue biopsy can confirm the presence of systemic amyloidosis. Chest imaging obviously plays a key role, but histopathologic and immunohistochemical analysis ultimately confirms the diagnosis in most cases. Both of these modalities are discussed in the subsequent sections.

Currently, the main treatment options rely on endobronchial techniques and Nd:YAG laser ablation to remove symptomatic lesions causing luminal obstruction. Rigid bronchoscopy, with endobronchial debulking, cryotherapy, or stent placement (or a combination), has been shown to provide significant clinical improvement., Treatment with external-beam radiation has also been reported to produce improvements in functional status and pulmonary function testing, with decreased local recurrences. In addition, one recent case report described the use of colchicine in a patient with advanced diffuse TBA, whose disease progression was significantly slowed, and this patient remained asymptomatic for 4 years. Other more specific treatment options also include bypass tracheostomy and airway stenting, depending on the location of the obstruction.

The prognosis varies based on the location and extent and whether systemic disease is present. With primary TBA, long periods of disease stability have been reported and managed only with observation. However, as the deposited amyloid burden worsens, obstruction can lead to recurrent infection and ultimately respiratory failure. Reported survival rates vary in the literature. One study reported a 70% survival after 7 to 12 years, whereas others reported survival rates of 31% and 43% after 4 and 6 years, respectively. Another study reported an estimated 5-year survival rate of the diffuse TBA subtype to be about 30% to 50%.,,

Radiologic Discussion

TBA has been divided into distal, mid, and proximal involvement. Proximal disease causes symptoms of upper airway obstructions, whereas distal disease causes lower airway symptoms. Plain films are highly insensitive, but indirect signs, such as recurrent atelectasis, suggest an underlying pathologic condition.

On CT imaging, submucosal amyloid deposits cause the characteristic bronchial wall thickening, luminal irregularities, wall calcifications, and focal nodularity (amyloidoma). All of these characteristic findings were demonstrated in the patient (Fig 2). Identification of posterior tracheal membrane involvement (Figs 2B, 2C) is also an important distinction from other airway diseases such as relapsing polychondritis and tracheobronchopathia osteochondroplastica. Both of these disorders spare the posterior tracheal membrane and are limited to the cartilaginous rings. Other differential diagnoses are outlined in Table 2 and include Coccidioides infection, tuberculosis, granulomatosis with polyangiitis, sarcoidosis, Crohn disease, and papillomatosis that can involve the entire tracheal wall.,

Table Graphic Jump Location
Table 2 Differential Diagnosis of Nonneoplastic Causes of Tracheobronchial Narrowing

Other imaging modalities such as MRI are uncommon and rarely discussed in case reports except when cardiac amyloidosis is suspected.123I-labeled serum amyloid P scintigraphy has been used in the evaluation of visceral amyloid involvement; however, its role in TBA is not well defined in the current literature. However, 99mTc-hydroxymethylene diphosphonate uptake by amyloid lesions in TBA has been described and is likely related to the high calcium content within the deposits. Fluorodeoxyglucose (FDG)-PET/CT is another modality that has been described in case reports of pulmonary amyloid nodules and TBA. Soussan et al presented one case of TBA that showed intense tracheobronchial uptake and postulated that histiocytic infiltration within the amyloid deposit may explain the FDG uptake. Glaudemans et al also described FDG uptake in localized amyloidosis by the amyloid site. The role of FDG-PET/CT is still not fully defined but may help with early detection of disease.

Pathologic Discussion

Amyloid is deposited as β-pleated sheets of fibrils in collagenous layers. In TBA, this typically occurs in the basal membranes of the bronchial mucosa. On H&E staining, this appears as a waxy accumulation of eosinophilic extracellular material that may have a “cracked” appearance due to tissue processing (Figs 4A, 4B). Commonly seen are calcifications, peripheral plasma cells, and multinucleated giant cells associated with the inflammatory response. Important differential considerations should include hyaline scar/fibrosis, light-chain deposition disease, and plasmacytoma.,

Classically, demonstration of apple-green birefringence with Congo-red staining (Fig 4C) under polarized microscopy has been the gold standard. Other stains such as Thioflavin T and crystal violet, which rely on changes in fluorescence and metachromasia when bound to amyloid fibrils, are also commonly used. Immunohistochemical analysis with serum amyloid A protein, which is found in all amyloid subtypes, can be used for confirmation. However, identifying the presence of disease is typically not an issue; determining the subtype of amyloid usually presents a much bigger challenge. Using antibodies to the major amyloid proteins, immunohistochemical fluorescence is routinely used to differentiate between subtypes but has multiple limitations, especially because of high background staining. Novel techniques such as laser microdissection of amyloid deposits with subsequent mass spectrometry-based proteomic analysis have been shown to have incredible accuracy and may ultimately supersede immunohistochemical analysis to identify amyloid subtypes.

The patient in our study presented with an extremely rare case of TBA with persistent middle lobe atelectasis. After further review, she was found to have a known history of prior laryngeal disease and hoarseness that was due to biopsy-proven localized AL laryngeal amyloidosis, which helped narrow the differential diagnosis. CT findings demonstrated circumferential wall thickening, nodularity, and calcification. Biopsies were performed through bronchoscopy and demonstrated apple-green birefringence with Congo-red staining and ultimately confirmed the diagnosis. She is currently being managed with yearly follow-up with pulmonology, chest radiography, and pulmonary function tests. Currently, she remains asymptomatic without a decline in pulmonary function testing parameters. She has had no frequent infections or functional limitation for > 6 years after her initial diagnosis. Her yearly chest radiograph still demonstrates atelectasis of the middle lobe.

Financial/nonfinancial disclosures: None declared.

Prince J.S. .Duhamel D.R. .Levin D.L. .Harrell J.H. .Friedman P.J. . Nonneoplastic lesions of the tracheobronchial wall: radiologic findings with bronchoscopic correlation. Radiographics. 2002;22:S215-S230 [PubMed]journal. [CrossRef] [PubMed]
 
Wang Q. .Chen H. .Wang S. . Laryngo-tracheobronchial amyloidosis: a case report and review of literature. Int J Clin Exp Pathol. 2014;7:7088-7093 [PubMed]journal. [PubMed]
 
Pepys M.B. . Amyloidosis. Annu Rev Med. 2006;57:223-241 [PubMed]journal. [CrossRef] [PubMed]
 
Baker K.R. .Rice L. . The amyloidoses: clinical features, diagnosis and treatment. Methodist DeBakey Cardiovasc J. 2012;8:3-7 [PubMed]journal
 
Gertz M.A. . How to manage primary amyloidosis. Leukemia. 2012;26:191-198 [PubMed]journal. [CrossRef] [PubMed]
 
Gilmore J.D. .Hawkins P.N. . Amyloidosis and the respiratory tract. Thorax. 1999;54:444-451 [PubMed]journal. [CrossRef] [PubMed]
 
Berk J.L. .O’Regan A. .Skinner M. . Pulmonary and tracheobronchial amyloidosis. Semin Respir Crit Care Med. 2002;23:144-165 [PubMed]journal
 
Berraondo J. .Novella L. .Sanz F. .Lluch R. .de Casimiro E. .Lloret T. . Management of tracheobronchial amyloidosis with therapeutic bronchoscopic techniques. Arch Bronconeumol. 2013;49:207-209 [PubMed]journal. [PubMed]
 
Morrison J. .Butnor K. .Davis G.S. . A bronchoscopic oddity: recurrent pneumonias secondary to nodular tracheobronchial amyloidosis. Chest. 2009;136:- [PubMed]journal
 
Karkhanis V.S. .Desai U. .Joshi J.M. . Flow volume loop as a diagnostic marker. Lung India. 2013;30:166-168 [PubMed]journal. [CrossRef] [PubMed]
 
Madden B.P. .Lee M. .Paruchuru P. . Successful treatment of endobronchial amyloidosis using Nd:YAG laser therapy as an alternative to lobectomy. Monaldi Arch Chest Dis. 2001;56:27-29 [PubMed]journal. [PubMed]
 
Alloubi I. .Thumerel M. .Begueret H. .Baste J. .Velly J. .Jougon J. . Outcomes after bronchoscopic procedures for primary tracheobronchial amyloidosis: retrospective study of 6 cases. Pulm Med. 2012;2012:1-4 [PubMed]journal
 
Morales A. .Pari M. .López-Lisbona R. .Cubero N. .Dorca J. .Rosell A. . Colchicine treatment for tracheobronchial amyloidosis. Respiration. 2016;91:251-255 [PubMed]journal. [CrossRef] [PubMed]
 
Chatkin G. .Pipkin M. .Pinto J.A.F. .da Silva V.D. .Chatkin J.M. . Primary tracheobronchial amyloidosis. J Bras Pneumol. 2008;34:528-531 [PubMed]journal. [PubMed]
 
Birkeland A.C. .McHugh J.B. .Spector M.E. . Tracheobronchial amyloidosis: a case report and review of the literature. J Case Rep Med. 2014;3:235859- [PubMed]journal. [PubMed]
 
Daniels J.T. .Cury J.D. .Diaz J. . An unusual case of postobstructive pneumonia. Chest. 2007;131:930-933 [PubMed]journal. [CrossRef] [PubMed]
 
Czeyda-Pommersheim F. .Hwang M. .Chen S.S. .Strollo D. .Fuhrman C. .Bhalla S. . Amyloidosis: modern cross sectional imaging. Radiographics. 2015;35:1381-1392 [PubMed]journal. [CrossRef] [PubMed]
 
Prince J.S. .Duhammel D.R. .Levin D.L. .Harrell J.H. .Friedman P.J. . Nonneoplastic lesions of the tracheobronchial wall: radiologic findings with bronchoscopic correlation. Radiographics. 2002;22:S215-S230 [PubMed]journal. [CrossRef] [PubMed]
 
Sachchithanantham S. .Wechalekar A.D. . Imaging in systemic amyloidosis. Br Med Bull. 2013;107:41-56 [PubMed]journal. [CrossRef] [PubMed]
 
Yoshida S. .Suematsu T. .Koizumi T. .et al Demonstration of primary tracheobronchial amyloidosis by 99mTc-HDMP bone SPECT. Ann Nucl Med. 1993;7:269-272 [PubMed]journal. [CrossRef] [PubMed]
 
Soussan M. .Ouvrier M.J. .Pop G. .Galas J.L. .Neuman A. .Weinmann P. . Tracheobronchial FDG uptake in primary amyloidosis detected by PET/CT. Clin Nucl Med. 2011;36:723-724 [PubMed]journal. [CrossRef] [PubMed]
 
Glaudemans A.W. .Slart R.H. .Noordzij W. .Dierckx R.A. .Hazenberg B.P. . Utility of 18F-FDG PET(/CT) in patients with systemic and localized amyloidosis. Eur J Nucl Med Mol Imaging. 2013;40:1095-1101 [PubMed]journal. [CrossRef] [PubMed]
 
Kayser K. . Analytical Lung Pathology.  1992;:48-49 [PubMed] Springer Berlin, Germanyjournal
 
Fletcher C.D.M. . Diagnostic Histopathology of Tumors.  2013;:196-197 [PubMed] Churchill Livingstone London, UKjournal
 
Biancalana M. .Koide S. . Molecular mechanism of Thioflavin-T binding to amyloid fibrils. Biochim Biophys Acta. 2010;1804:1405-1412 [PubMed]journal. [CrossRef] [PubMed]
 
Jerzykowska S. .Cymerys M. .Gil L.A. . Primary systemic amyloidosis as a real diagnostic challenge—case study. Cent Eur J Immunol. 2014;39:61-66 [PubMed]journal. [PubMed]
 
Vrana J.A. .Gamez J.D. .Madden B.J. .Theis J.D. .Bergen R.H. III.Dogan A. . Classification of amyloidosis by laser microdissection and mass spectrometry-based proteomic analysis in clinical biopsy specimens. Blood. 2009;114:4957-4959 [PubMed]journal. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1 A, Posteroanterior and lateral radiographs of the chest (8 weeks after initial presentation) demonstrate atelectasis of the middle lobe. B, Coronal view contrast-enhanced CT scan demonstrates complete collapse of the middle lobe.Grahic Jump Location
Figure Jump LinkFigure 2 Axial views of contrast-enhanced CT image. A, Lung window demonstrating narrowing of the middle lobe bronchus (black arrow) distal to its origin from the bronchus intermedius (red asterisk). Atelectasis of the middle lobe is also seen here (yellow arrow). B, Intermediate lung-mediastinal window demonstrating nodular irregularity and thickening of the bronchus intermedius and the left main bronchus. Note the focal nodule representing an amyloidoma (yellow arrow) involving the posterior wall of the bronchus intermedius. Wall thickening and calcification of the left main bronchus is also demonstrated (black arrow). C, Mediastinal window demonstrating focal thickening (yellow arrow) of the anterior tracheal wall that causes luminal narrowing.Grahic Jump Location
Figure Jump LinkFigure 3 A, Three-dimensional volume reconstruction of the airway from the CT scan in Figure 2, demonstrating the irregular contour of the trachea. The collapsed middle lobe bronchus is absent (black arrow). B, CT-generated virtual bronchoscopy within the trachea near the level of the carina (asterisk) shows endobronchial nodularity with posterior tracheal membrane involvement.Grahic Jump Location
Figure Jump LinkFigure 4 H&E staining at (A) ×20 and (B) ×40 magnification of the biopsied bronchial wall demonstrating waxy eosinophilic extracellular deposits. A “cracked” appearance, better seen on B, is due to tissue processing. C, Congo-red staining at ×20 magnification demonstrating apple-green birefringence under polarized light.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 Summary of Amyloid Types With Lung Involvement
Table Graphic Jump Location
Table 2 Differential Diagnosis of Nonneoplastic Causes of Tracheobronchial Narrowing

References

Prince J.S. .Duhamel D.R. .Levin D.L. .Harrell J.H. .Friedman P.J. . Nonneoplastic lesions of the tracheobronchial wall: radiologic findings with bronchoscopic correlation. Radiographics. 2002;22:S215-S230 [PubMed]journal. [CrossRef] [PubMed]
 
Wang Q. .Chen H. .Wang S. . Laryngo-tracheobronchial amyloidosis: a case report and review of literature. Int J Clin Exp Pathol. 2014;7:7088-7093 [PubMed]journal. [PubMed]
 
Pepys M.B. . Amyloidosis. Annu Rev Med. 2006;57:223-241 [PubMed]journal. [CrossRef] [PubMed]
 
Baker K.R. .Rice L. . The amyloidoses: clinical features, diagnosis and treatment. Methodist DeBakey Cardiovasc J. 2012;8:3-7 [PubMed]journal
 
Gertz M.A. . How to manage primary amyloidosis. Leukemia. 2012;26:191-198 [PubMed]journal. [CrossRef] [PubMed]
 
Gilmore J.D. .Hawkins P.N. . Amyloidosis and the respiratory tract. Thorax. 1999;54:444-451 [PubMed]journal. [CrossRef] [PubMed]
 
Berk J.L. .O’Regan A. .Skinner M. . Pulmonary and tracheobronchial amyloidosis. Semin Respir Crit Care Med. 2002;23:144-165 [PubMed]journal
 
Berraondo J. .Novella L. .Sanz F. .Lluch R. .de Casimiro E. .Lloret T. . Management of tracheobronchial amyloidosis with therapeutic bronchoscopic techniques. Arch Bronconeumol. 2013;49:207-209 [PubMed]journal. [PubMed]
 
Morrison J. .Butnor K. .Davis G.S. . A bronchoscopic oddity: recurrent pneumonias secondary to nodular tracheobronchial amyloidosis. Chest. 2009;136:- [PubMed]journal
 
Karkhanis V.S. .Desai U. .Joshi J.M. . Flow volume loop as a diagnostic marker. Lung India. 2013;30:166-168 [PubMed]journal. [CrossRef] [PubMed]
 
Madden B.P. .Lee M. .Paruchuru P. . Successful treatment of endobronchial amyloidosis using Nd:YAG laser therapy as an alternative to lobectomy. Monaldi Arch Chest Dis. 2001;56:27-29 [PubMed]journal. [PubMed]
 
Alloubi I. .Thumerel M. .Begueret H. .Baste J. .Velly J. .Jougon J. . Outcomes after bronchoscopic procedures for primary tracheobronchial amyloidosis: retrospective study of 6 cases. Pulm Med. 2012;2012:1-4 [PubMed]journal
 
Morales A. .Pari M. .López-Lisbona R. .Cubero N. .Dorca J. .Rosell A. . Colchicine treatment for tracheobronchial amyloidosis. Respiration. 2016;91:251-255 [PubMed]journal. [CrossRef] [PubMed]
 
Chatkin G. .Pipkin M. .Pinto J.A.F. .da Silva V.D. .Chatkin J.M. . Primary tracheobronchial amyloidosis. J Bras Pneumol. 2008;34:528-531 [PubMed]journal. [PubMed]
 
Birkeland A.C. .McHugh J.B. .Spector M.E. . Tracheobronchial amyloidosis: a case report and review of the literature. J Case Rep Med. 2014;3:235859- [PubMed]journal. [PubMed]
 
Daniels J.T. .Cury J.D. .Diaz J. . An unusual case of postobstructive pneumonia. Chest. 2007;131:930-933 [PubMed]journal. [CrossRef] [PubMed]
 
Czeyda-Pommersheim F. .Hwang M. .Chen S.S. .Strollo D. .Fuhrman C. .Bhalla S. . Amyloidosis: modern cross sectional imaging. Radiographics. 2015;35:1381-1392 [PubMed]journal. [CrossRef] [PubMed]
 
Prince J.S. .Duhammel D.R. .Levin D.L. .Harrell J.H. .Friedman P.J. . Nonneoplastic lesions of the tracheobronchial wall: radiologic findings with bronchoscopic correlation. Radiographics. 2002;22:S215-S230 [PubMed]journal. [CrossRef] [PubMed]
 
Sachchithanantham S. .Wechalekar A.D. . Imaging in systemic amyloidosis. Br Med Bull. 2013;107:41-56 [PubMed]journal. [CrossRef] [PubMed]
 
Yoshida S. .Suematsu T. .Koizumi T. .et al Demonstration of primary tracheobronchial amyloidosis by 99mTc-HDMP bone SPECT. Ann Nucl Med. 1993;7:269-272 [PubMed]journal. [CrossRef] [PubMed]
 
Soussan M. .Ouvrier M.J. .Pop G. .Galas J.L. .Neuman A. .Weinmann P. . Tracheobronchial FDG uptake in primary amyloidosis detected by PET/CT. Clin Nucl Med. 2011;36:723-724 [PubMed]journal. [CrossRef] [PubMed]
 
Glaudemans A.W. .Slart R.H. .Noordzij W. .Dierckx R.A. .Hazenberg B.P. . Utility of 18F-FDG PET(/CT) in patients with systemic and localized amyloidosis. Eur J Nucl Med Mol Imaging. 2013;40:1095-1101 [PubMed]journal. [CrossRef] [PubMed]
 
Kayser K. . Analytical Lung Pathology.  1992;:48-49 [PubMed] Springer Berlin, Germanyjournal
 
Fletcher C.D.M. . Diagnostic Histopathology of Tumors.  2013;:196-197 [PubMed] Churchill Livingstone London, UKjournal
 
Biancalana M. .Koide S. . Molecular mechanism of Thioflavin-T binding to amyloid fibrils. Biochim Biophys Acta. 2010;1804:1405-1412 [PubMed]journal. [CrossRef] [PubMed]
 
Jerzykowska S. .Cymerys M. .Gil L.A. . Primary systemic amyloidosis as a real diagnostic challenge—case study. Cent Eur J Immunol. 2014;39:61-66 [PubMed]journal. [PubMed]
 
Vrana J.A. .Gamez J.D. .Madden B.J. .Theis J.D. .Bergen R.H. III.Dogan A. . Classification of amyloidosis by laser microdissection and mass spectrometry-based proteomic analysis in clinical biopsy specimens. Blood. 2009;114:4957-4959 [PubMed]journal. [CrossRef] [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543