Abstract Introduction Amyloidosis is a rare diagnosis with a wide range of presentations, and pulmonary amyloidosis is often an underrecognized manifestation of amyloidosis. This is because it can often be found incidentally on imaging or autopsy. There are three main presentations of pulmonary amyloidosis. These include diffuse alveolar-septal amyloidosis, tracheobronchial amyloidosis, and pulmonary amyloidomas. Diffuse alveolar septal amyloidosis is most commonly due to systemic amyloidosis where amyloid accumulates in the alveolar septal wall and blood vessels. Tracheobronchial Amyloidosis, caused by amyloid deposits in the tracheobronchial tree, is more commonly symptomatic due to airway stenosis. Finally, amyloidomas are deposits of amyloid in the lung parenchyma presenting as distinct masses. This form is more commonly associated with localized amyloidosis, and the nodules are more commonly found incidentally. In this case we describe an amyloidoma found on imaging. Case A 77-year-old male with past medical history of a 12.5-year pack history and exposure to asbestos presented to lung mass clinic after having a new right lower lobe lung nodule seen on chest imaging during a workup for new onset dyspnea. He noted dyspnea after 2-3 blocks and had a calculated Duke Activity Status Index of 36. He was then ordered for CT Thorax without contrast which showed a right lower lobe 2.1 x 1.7 cm nodule with irregular borders. Patient then underwent PET scan which showed increased uptake from the RLL nodule with a SUV of 11.76 and possible uptake in the hilar lymph nodes. Patient then underwent navigational bronchoscopy for biopsy of the mass which showed waxy deposits in alveolar and vessel walls that were Congo red positive with apple green birefringence consistent with an amyloid deposit. Patient then had a urine protein electrophoresis with no M spike. Serum immunofixation showed a normal pattern, and a Kappa/Lambda ratio within normal limits. Bone marrow biopsy showed no signs of amyloid. Discussion This case highlights asbestos as a possible risk factor for amyloidomas. There have been multiple case reports in the literature linking asbestos exposure to amyloidomas, and this case adds another example to the literature. The proposed mechanism is that apoptosis, chronic immune response, and autoantibody generation from asbestos exposure can promote an environment for amyloid deposition. While this linkage has not been well established, it is an area for future research. This abstract is funded by: None
Kovats et al. (Fri,) studied this question.