Fatal Bronchopulmonary Hemorrhage Due to Unrecognized Amyloidosis

Shaheen, Nicolas A.; Salman, Salah D.; Nassar, Victor H.

doi:10.1001/archotol.1975.00780330055014

Cited by 20 publications

(10 citation statements)

References 16 publications

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“…More common forms consist of cutaneous and gastrointestinal tract bleedings [6]. One case of fatal bronchopulmonary haemorage due to unrecognised amyloidosis has been reported [14].…”

Section: Discussionmentioning

confidence: 99%

Idiopathic Systemic Amyloidosis Primarily Affecting the Lungs with Fatal Pulmonary Haemorrhage due to Vascular Involvement

Sterlacci

Veits

Moser

et al. 2008

Pathol. Oncol. Res.

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A patient who presented with dyspnea and suspected interstitial pulmonary fibrosis suffered a fatal pulmonary haemorrhage with no feasible cause for bleeding. Autopsy revealed abundant amyloid deposits in both lungs with a diffuse alveolar septal distribution pattern. Amyloid was also found in the cardiac interstitium and in many vessel walls. Considering the affected organs and the histological characteristics, the deposits were regarded as light chain-type. Amyloidosis, which is generally an uncommon disease, very rarely affects the lung predominantly. Haemorrhagic diathesis is a known complication in amyloidosis patients, although fatal haemorrhage is rare and has not yet been reported solely of pulmonary origin. This report describes an uncommon case of idiopathic systemic amyloidosis mainly manifesting in the lungs. The diagnosis was established after fatal pulmonary haemorrhage caused by vessel impairment due to additional vascular amyloid deposits.

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“…More common forms consist of cutaneous and gastrointestinal tract bleedings [6]. One case of fatal bronchopulmonary haemorage due to unrecognised amyloidosis has been reported [14].…”

Section: Discussionmentioning

confidence: 99%

Idiopathic Systemic Amyloidosis Primarily Affecting the Lungs with Fatal Pulmonary Haemorrhage due to Vascular Involvement

Sterlacci

Veits

Moser

et al. 2008

Pathol. Oncol. Res.

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“…[8] Care should be taken during resection attempts, however, as there has been documented fatal hemorrhage with resection of friable endotracheal and endobronchial amyloid tissue. [9] Advanced local disease may require tracheotomy or laryngectomy to provide a safe airway. [2,5] Treatment with colchicine and systemic glucocorticoids, which have benefit in systemic amyloidosis, have not yielded strong responses in localized TBA.…”

Section: Discussionmentioning

confidence: 99%

Tracheobronchial Amyloidosis: A Case Report and Review of the Literature

Birkeland¹,

McHugh²,

Spector³

2014

Journal of Case Reports in Medicine

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Objectives This is a case report on tracheobronchial amyloidosis. This disease may provide a diagnostic challenge for otolaryngologists due to its rarity and relative lack of literature. Our case highlights presentation and workup of this disease. Methods The index patient's workup included clinical exam, CT of the neck and chest, direct laryngoscopy, bronchoscopy and biopsy. Additional reports of tracheobronchial amyloidosis were identified in a PubMed database search. Results Our index patient presented with dyspnea and hoarseness. Clinic laryngoscopy showed a tracheal mass. Radiology demonstrated an irregular tracheal soft tissue lesion. The patient underwent biopsy, and pathology was consistent with amyloidosis. He had no systemic signs of amyloidosis. He underwent local resection to improve his airway diameter, with no complications. Conclusions Tracheobronchial amyloidosis should be kept in an otolaryngologist's differential diagnosis for patients with nonspecific upper airway symptomatology and radiographic lesions in the trachea or bronchi.

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“…[43][44][45] Hemoptysis can occur with both diffuse and nodular types of pulmonary amyloidosis. 35,46,47 Fatal hemorrhage has occurred after biopsy was performed in cases of unrecognized laryngotracheal amyloidosis 46 or pulmonary parenchymal amyloidosis. 48 Amyloid angiopathy is a defined cause of hemorrhage in the brain but not in the lungs.…”

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confidence: 99%

Case 20-1998

Berk¹,

Mark²

1998

N Engl J Med

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A 53-year-old man with cardiac amyloidosis was admitted to the hospital because of hemoptysis and a pulmonary lesion.The patient had first been seen at this hospital four years earlier because of atrial fibrillation, congestive heart failure, and an embolic stroke. Microscopical examination of a specimen from a right ventricular endomyocardial biopsy showed amyloid believed to be related to transthyretin (prealbumin), a finding indicative of familial amyloidosis. A coronary angiographic study revealed minimal atherosclerosis. There was moderate global and inferior hypokinesis, with severe mitral regurgitation. Symptoms were well controlled with colchicine, furosemide, warfarin, and propranolol.Twenty months before admission, the patient returned to the hospital because of two transient bouts of garbled speech, with numbness and weakness of the right hand. Examination revealed no neurologic abnormality. Noninvasive carotid studies showed minimal bilateral disease. Computed tomographic (CT) and magnetic resonance imaging (MRI) scans of the brain showed normal findings. A cardiac ultrasonographic study showed an increase in the left ventricular ejection fraction from the base-line value of 25 percent to 32 percent. No thrombus was seen, but the enlarged left atrium was not well visualized. The symptoms were ascribed to cerebral emboli. Aspirin was prescribed, and the dosage of warfarin was increased.During the ensuing 19 months, the patient's international normalized ratio (INR) ranged between 1 and 6 because of poor compliance. He had repeated bruising and minor bleeding from the lower gastrointestinal tract. One month before admission, he began to have a dry cough and a slight increase in exertional dyspnea and fatigue, with a loss of 4.5 kg in weight. On the evening before admission, he coughed up moderate amounts of fresh blood. He returned to the hospital the next day.The patient had never smoked and did not drink alcohol. There was no history of lung disease, rheumatic heart disease, recent fever, chills or sweats, chest pain, tuberculosis or tuberculin skin testing, or exposure to toxic materials or dusts. Chest x-ray films obtained one year earlier showed no abnormalities. There was no family history of amyloidosis.The temperature was 37°C, the pulse was 92, and the respirations were 20. The blood pressure was 100/80 mm Hg.On examination, the patient was thin and appeared chronically ill. The jugular venous pressure was 7 to 8 cm. Breath sounds were diminished at the left base, with a few crackles. The heart rhythm was irregular. A grade 2 holosystolic murmur was heard at the apex. The results of a neurologic examination were normal.The urine was orange, with trace-positive tests for protein and bilirubin; the sediment was normal. The results of hematologic laboratory values are shown in Table 1. The conjugated bilirubin level was 0.6 mg per deciliter (10 m mol per liter), and the total bilirubin level was 1.6 mg per deciliter (27 m mol per liter). Other blood chemical and enzyme levels were normal. An elect...

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Fatal Bronchopulmonary Hemorrhage Due to Unrecognized Amyloidosis

Cited by 20 publications

References 16 publications

Idiopathic Systemic Amyloidosis Primarily Affecting the Lungs with Fatal Pulmonary Haemorrhage due to Vascular Involvement

Idiopathic Systemic Amyloidosis Primarily Affecting the Lungs with Fatal Pulmonary Haemorrhage due to Vascular Involvement

Tracheobronchial Amyloidosis: A Case Report and Review of the Literature

Case 20-1998

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