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Procedures: Bronchology |

Isolated Tracheobronchial Hyperkeratosis FREE TO VIEW

Xiaolei Zhang, MD
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Zhongri Hospital, Bejijing, China


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A425. doi:10.1016/j.chest.2016.02.443
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Published online

SESSION TITLE: Bronchology

SESSION TYPE: Case Report Slide

PRESENTED ON: Sunday, April 17, 2016 at 02:15 PM - 03:45 PM

INTRODUCTION: Airway hyperkeratosis is uncommon and affects upper airway, such as the laryngeal area in most cases. Tracheobronchial involvement is very rarely reported, and here we report a case of isolated tracheobronchial hyperkeratosis.

CASE PRESENTATION: An otherwise healthy 32-year-old man presented with recurrent cough, sputum production and intermittent low-grade fever over three years. He had been treated as bronchitis with antibiotics, and the above symptoms could be relieved temporarily. He had a 5 pack year history of smoking and had quit 3 years ago. He worked in an open-air steel market with heavy ground dust pollution. Physical examination revealed no significant abnormalities. His tuberculin skin test and T-spot. TB blood test were both negative. Pseudomonas aeruginosa were seen in sputum cultures. Spirometry showed mild airflow obstruction. Chest CT scan showed no significant abnormalities. Bronchoscopy revealed diffuse white nodules like paving stone changes in the tracheobronchial mucosa with no laryngeal area involvement (Panel A, B and C). The results of tissue stains and cultures for acid-fast bacilli and fungal organisms were negative. Multiple tracheobronchial mucosa biopsy showed squamous cell metaplasia and hyperkeratosis, with no dysplasia or malignancy (Panel D).

DISCUSSION: Lower airway hyperkeratosis is very rare and isolated tracheobronchial involvement has not been documented before. The cause of airway hyperkeratosis is not clear and maybe related with chronic inflammatory stimulus, air pollution, inhalation of poisonous gases, occupational dust exposure or trace element deficiency. The tracheobronchial hyperkeratosis may occur as a result of smoking and chronic dust exposure in this patient who maybe genetically predisposed to such lesions. The relationship between chronic airway infection and hyperkeratosis has not been determined. Does chronic airway infection serve as an incentive for hyperkeratosis? Or loss of normal clean function of airway secondary to hyperkeratosis, induced recurrent infection. Tracheobronchial hyperkeratosis should be differentially diagnosed from bronchial tuberculosis and fungus infection. There is no specific treatment for airway hyperkeratosis yet. The primary concern for the management of airway hyperkeratosis is the potential for malignant conversion. The risk is increased by the presence of dysplasia, since increasing severity of dysplasia appears to increase the risk of malignant conversion. Hence close follow-up with surveillance bronchoscopy is ongoing for this subject.

CONCLUSIONS: Lower airway hyperkeratosis has no specific clinical characteristics. Broncoscopy with multiple-section histopathological analysis is necessary for accurate diagnosis. Close follow-up is mandatory due to its potential for malignant conversion.

Reference #1: Isenberg et al. Institutional and Comprehensive Review of Laryngeal Leukoplakia. Annals of Ototogy, Rhinology & laryngology. 117(l);74-79.

DISCLOSURE: The following authors have nothing to disclose: Xiaolei Zhang

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