Tracheobronchopathia Osteoplastica: End Stage of Primary Lung Amyloidosis?

Alroy, G; Lichtig, Chaim; Kaftori, Joseph K.

doi:10.1378/chest.61.5.465

Cited by 63 publications

(21 citation statements)

References 7 publications

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“…It has also been suggested that it aris es as a final evolutive stage of tracheobron chial amyloidosis [4,6,11,12], The disease has also been found associated to ozena [4,5], as observed in one of the cases described in this study. Finally, it has been related to a secretory increase of growth hormone [13].…”

Section: Discussionsupporting

confidence: 62%

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Tracheobronchopathia osteochondroplastica

et al. 1981

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6 cases of tracheobronchopathia osteochondroplastica are discussed. Diagnoses were established ante mortem. Endoscopic examination was performed in 3 patients because of hematic expectoration, in the other 3 cases the indication was given by chronic bronchorrhea, slow-resolving pneumonia and suspected neoplasia, respectively. Calcification and cartilaginous areas were restricted to a small portion of the tracheobronchial tree in 1 of the cases; in 3 cases the disease affected the trachea and both main bronchi, whereas it was found markedly spread throughout the trachea in the last 2 patients. Tracheal tomography and bronchoscopic examination are considered the methods of choice for an ante mortem diagnosis of this disease.

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Section: Discussionsupporting

confidence: 62%

“…The disease is characterized by the presence of scattered cartilaginous and/or bony areas in the submucosa apparently un related to the normal cartilage [2][3][4][5][6][7], The first known case was described by Wilks [8] in 1857. Recently Marlin [9] reviewed 245 cases recorded until 1974.…”

Section: Introductionmentioning

confidence: 99%

Tracheobronchopathia osteochondroplastica

et al. 1981

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“…After local processing (or truncated synthesis de novo, or both), these were deposited as amyloid into the white matter and blood vessels in the vicinity of the neoplastic cells. Incrustations which have been described in local amyloid deposits [27] led to cerebral stones. Spongiformly altered and demyelinated white matter in the vicinity of the amyloid deposits led to unusual symptoms in patient ESI.…”

Section: Discussionmentioning

confidence: 96%

Brain-Restricted Amyloidoma of Immunoglobulin λ-Light Chain Origin Clinically Resembling Multiple Sclerosis

Linke¹,

Gerhard²,

Lottspeich³

1992

Biological Chemistry Hoppe-Seyler

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Cerebral amyloid deposits restricted to the white matter and associated with intracerebral lymphoma were biochemically identified. The patient died at 58 years of age after 37 years of illness with progressive neurological symptoms clinically indicative of multiple sclerosis. Pathomorphologically, spongiform alteration and demyelinization of the white matter in the vicinity of the amyloid deposits was detected and systemic amyloidosis excluded. Immunohistochemically, the amyloid was found to be of immunoglobulin -light chain origin. To establish the nature of this amyloid, its fibrils were extracted and the amyloid fibril proteins isolated by size exclusion chromatography. Immunochemically, the purified amyloid fibril proteins were shown to be of immunoglobulin -light chain origin. This finding was substantiated chemically. Since the N-terminal amino acid was blocked, tryptic peptides were isolated by reversed phase HPLC. The amino-acid sequence of two major peptides revealed homology with the variable region of the immunoglobulinlight chain. This report defines a novel local -amyloid disease restricted to the white matter of the brain. Auf das Gehirnmark beschränkte Amyloidablagerungen vom Immunglobulin-~Leichtketten-Typ mit einem Syndrom ähnlich einer Multiplen SkleroseZusammenfassung: Amyloidablagerungen, die auf das Mark des Großhirns beschränkt und mit einem intrazerebralen Lymphom assoziiert waren, wurden biochemisch identifiziert. Der Patient starb mit 58 Jahren nach 37jähriger Krankheit mit einer progressiven neurologischen Symptomatik, die klinisch an eine Multiple Sklerose erinnerte. Eine generalisierte Amyloidose wurde ausgeschlossen. Die Amyloidablagerungen wurden immunhistochemisch an Formalin-fixierten Gewebeschnitten als vom Immunglobulin-X-Leichtkette-Ursprung erkannt. Zur unzweideutigen Identifizierung der chemischen Natur des Amyloid wurden zunächst die Amyloidfibrillen extrahiert und danach die Amyloidfibrillenproteine durch Gelfiltration isoliert; diese zeigten immunchemisch ebenfalls -Leichtkettennatur. Diese Befunde wurden durch chemische Analyse bewiesen. Da die N-terminale Aminosäure unreaktiv war, wurden tryptische Peptide über RP-HPLC isoliert. Die Aminosäurese-quenzanalyse zweier Peptide zeigt Homologie mit dem variablen Abschnitt einer Immunglobulin--Leichtkette. Diese Befunde definieren ein neues Krankheitsbild, das von lokalen, auf das Gehirnmark beschränkte -Amyloidablagerungen verursacht wird.

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“…An association with amyloidosis [7,8] was suggested, but not confirmed in a large group of patients. Furthermore, its relationship with malignancies is unclear [9,10].…”

Section: Discussionmentioning

confidence: 91%

An unusual cause of recurrent fever

Los¹,

Schramel²,

Harten³

et al. 1997

Eur Respir J

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A 49 year old man was referred to our hospital in 1994, because of intermittent fever and production of mucopurulent sputum. His complaints started at 43 yrs of age. The symptoms were mostly self-limiting, and occurred five times a year. Over the years, periods of bronchitis had increased to 12 times a year. In addition, a sinusitis with Klebsiella ozaenae became apparent, which was treated with antibiotics and intranasal beclomethasone dipropionate. Coughing was most severe during the night, with production of mucopurulent sputum. The patient's exercise tolerance was normal; he had worked for more than 10 years as a shoemaker. He has no smoking history.Physical examination and routine laboratory investigations were normal. Posteroanterior and lateral chest radiography and lung function tests were normal. A fibreoptic bronchoscopy was performed and showed many abnormalities of the trachea and bronchi (figs. 1 and 2). Specimens were taken for microbiological analysis, and biopsies were sampled for histological examination ( fig. 3). Because of the extent of the abnormalities seen during bronchoscopy, computed tomography (CT) of the chest was performed (figs. 4 and 5).

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Tracheobronchopathia Osteoplastica: End Stage of Primary Lung Amyloidosis?

Cited by 63 publications

References 7 publications

Tracheobronchopathia osteochondroplastica

Tracheobronchopathia osteochondroplastica

Brain-Restricted Amyloidoma of Immunoglobulin λ-Light Chain Origin Clinically Resembling Multiple Sclerosis

An unusual cause of recurrent fever

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