Aspirated Almond Masquerading as an Obstructing Endobronchial Mass Suspicious for Lung Cancer.

Foreign body aspiration is relatively rare in adults compared to children. In adults with delayed presentation, a history of choking is often absent, resulting in delayed diagnosis and significant morbidity. Common presenting features in adults include nonresolving cough with or without fever, hemoptysis, or wheezing and may mimic infectious, inflammatory, or neoplastic disorders. We present a case of a 64-year-old man with 80-pack-year smoking history who had a nonresolving left lower lobe infiltrate on chest radiograph after treatment for community-acquired pneumonia. His insidious-onset symptoms included cough, decreased exercise tolerance, and localized wheezing. Computed tomography of the chest showed a left lower lobe consolidation, with narrowing of the bronchus. Flexible bronchoscopy revealed a fleshy endobronchial mass, prompting endobronchial needle aspiration and biopsies, all of which revealed acute inflammation on rapid onsite evaluation. After multiple biopsies, a white pearly object with a detached brown cover was revealed; the object was found to be an aspirated almond. The almond and its peel were retrieved. The patient acknowledged that he had frequently eaten almonds in the supine position while recovering from a previous injury. His symptoms completely resolved at 3-month follow up, and he has ceased smoking and no longer consumes food while supine.

Accumulation of Ubiquitin and Sequestosome-1 Implicate Protein Damage in Diacetyl-Induced Cytotoxicity.

Inhaled diacetyl vapors are associated with flavorings-related lung disease, a potentially fatal airway disease. The reactive α-dicarbonyl group in diacetyl causes protein damage in vitro. Dicarbonyl/l-xylulose reductase (DCXR) metabolizes diacetyl into acetoin, which lacks this α-dicarbonyl group. To investigate the hypothesis that flavorings-related lung disease is caused by in vivo protein damage, we correlated diacetyl-induced airway damage in mice with immunofluorescence for markers of protein turnover and autophagy. Western immunoblots identified shifts in ubiquitin pools. Diacetyl inhalation caused dose-dependent increases in bronchial epithelial cells with puncta of both total ubiquitin and K63-ubiquitin, central mediators of protein turnover. This response was greater in Dcxr-knockout mice than in wild-type controls inhaling 200 ppm diacetyl, further implicating the α-dicarbonyl group in protein damage. Western immunoblots demonstrated decreased free ubiquitin in airway-enriched fractions. Transmission electron microscopy and colocalization of ubiquitin-positive puncta with lysosomal-associated membrane proteins 1 and 2 and with the multifunctional scaffolding protein sequestosome-1 (SQSTM1/p62) confirmed autophagy. Surprisingly, immunoreactive SQSTM1 also accumulated in the olfactory bulb of the brain. Olfactory bulb SQSTM1 often congregated in activated microglial cells that also contained olfactory marker protein, indicating neuronophagia within the olfactory bulb. This suggests the possibility that SQSTM1 or damaged proteins may be transported from the nose to the brain. Together, these findings strongly implicate widespread protein damage in the etiology of flavorings-related lung disease.