External Beam Radiation Therapy for Tracheobronchial Amyloidosis

Neben-Wittich, M.A.; Foote, Robert L.; Kalra, Sumit

doi:10.1378/chest.06-3118

Cited by 87 publications

(45 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Two recent reports from Japan demonstrated surgical salvage in patients who were initially medically operable but had refused surgery up-front [8,9]. Our series demonstrates that surgical salvage may also be feasible in selected patients that were initially considered medically inoperable.…”

supporting

confidence: 51%

Tracheobronchial amyloidosis: evidence for local B-cell clonal expansion: Figure 1–

Borie¹,

Danel²,

Molinier‐Frenkel³

et al. 2012

Eur Respir J

View full text Add to dashboard Cite

supporting

confidence: 51%

Tracheobronchial amyloidosis: evidence for local B-cell clonal expansion: Figure 1–

Borie¹,

Danel²,

Molinier‐Frenkel³

et al. 2012

Eur Respir J

View full text Add to dashboard Cite

“…This may be useful for the proximal or mid-airway [16]. Because plasma cells are radiosensitive, low-dose radiation therapy remains the mainstay of treatment for tracheobronchial amyloidosis [17]. High-dose chemotherapy combined with autologous stem cell transplantation confers better prognosis in systemic light chain amyloidosis lesions [18].…”

Section: Resultsmentioning

confidence: 99%

Primary Laryngo-Tracheobronchial Amyloidosis: A Case Report and Literature Review

Jiao¹,

Liu²,

Liu³

et al. 2017

J Clin Case Rep

View full text Add to dashboard Cite

Primary laryngo-tracheobronchial amyloidosis is a rare pulmonary disease for which there is currently no established treatment. Herein, we report a case involving a 51-year-old woman who was admitted to hospital primarily due to intermittent hoarseness. Botryoidal masses were visible at the entrance of the throat. On chest computed tomography, eccentric soft tissue density shadows were apparent in the tracheal bifurcation of the proximal segment of the trachea, and the lumen was narrowed. Electronic bronchoscopy revealed extensive new biological invasive growth from the nasopharynx to the glottis. The glottis and larynx were irregularly shaped with clear characteristics and congestion. New biological growth was also observed in the right upper lobe, right middle bronchus, and right lower lobe mucosa. The patient was ultimately diagnosed with primary laryngo-tracheobronchial amyloidosis via pathological analysis. Although amyloidosis is a benign lesion, to date, there are no curative treatments. The present article briefly highlights the pertinent literature, and discusses the clinical manifestations and progress of treatment in primary laryngo-tracheobronchial amyloidosis.

show abstract

“…Proximal and severe mid airway disease can lead to airway compromise, which is usually treated with laser or forceps debridement, or external beam radiation therapy. 55,61 Recurrence is common after laser or forceps debridement, and approximately 30% of these patients eventually die of the disease. 55 However, external beam radiation therapy may offer better outcomes.…”

Section: Clinical Featuresmentioning

confidence: 99%

Amyloidosis of the Lung

Khoór¹,

Colby²

2017

Archives of Pathology &Amp; Laboratory Medicine

View full text Add to dashboard Cite

Context.—Amyloidosis is a heterogeneous group of diseases characterized by the deposition of congophilic amyloid fibrils in the extracellular matrix of tissues and organs. To date, 31 fibril proteins have been identified in humans, and it is now recommended that amyloidoses be named after these fibril proteins. Based on this classification scheme, the most common forms of amyloidosis include systemic AL (formerly primary), systemic AA (formerly secondary), systemic wild-type ATTR (formerly age-related or senile systemic), and systemic hereditary ATTR amyloidosis (formerly familial amyloid polyneuropathy). Three different clinicopathologic forms of amyloidosis can be seen in the lungs: diffuse alveolar-septal amyloidosis, nodular pulmonary amyloidosis, and tracheobronchial amyloidosis. Objective.—To clarify the relationship between the fibril protein–based amyloidosis classification system and the clinicopathologic forms of pulmonary amyloidosis and to provide a useful guide for diagnosing these entities for the practicing pathologist. Data Sources.—This is a narrative review based on PubMed searches and the authors' own experiences. Conclusions.—Diffuse alveolar-septal amyloidosis is usually caused by systemic AL amyloidosis, whereas nodular pulmonary amyloidosis and tracheobronchial amyloidosis usually represent localized AL amyloidosis. However, these generalized scenarios cannot always be applied to individual cases. Because the treatment options for amyloidosis are dependent on the fibril protein–based classifications and whether the process is systemic or localized, the workup of new clinically relevant cases should include amyloid subtyping (preferably with mass spectrometry–based proteomic analysis) and further clinical investigation.

show abstract

External Beam Radiation Therapy for Tracheobronchial Amyloidosis

Cited by 87 publications

References 15 publications

Tracheobronchial amyloidosis: evidence for local B-cell clonal expansion: Figure 1–

Tracheobronchial amyloidosis: evidence for local B-cell clonal expansion: Figure 1–

Primary Laryngo-Tracheobronchial Amyloidosis: A Case Report and Literature Review

Amyloidosis of the Lung

Contact Info

Product

Resources

About