Cargando…

Alpha-1-antitrypsin deficient man presenting with lung function decline associated with dust exposure: a case report

INTRODUCTION: People with α(1)-antitrypsin deficiency are at increased risk for the development of chronic obstructive pulmonary disease. Previous retrospective epidemiologic studies have found that exposure to occupational dust among those with α(1)-antitrypsin deficiency is a risk factor at the gr...

Descripción completa

Detalles Bibliográficos
Autores principales: Zutler, Moshe, Quinlan, Patricia J, Blanc, Paul D
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110131/
https://www.ncbi.nlm.nih.gov/pubmed/21504560
http://dx.doi.org/10.1186/1752-1947-5-154
Descripción
Sumario:INTRODUCTION: People with α(1)-antitrypsin deficiency are at increased risk for the development of chronic obstructive pulmonary disease. Previous retrospective epidemiologic studies have found that exposure to occupational dust among those with α(1)-antitrypsin deficiency is a risk factor at the group level for poorer lung function, but on an individual clinical basis, a causal attribution can be difficult to establish. CASE PRESENTATION: We describe the case of a 68-year-old Caucasian man with a 25 pack-year smoking history who presented with new-onset dyspnea on exertion in the setting of workplace dust exposure. During his evaluation, he was found to have α(1)-antitrypsin deficiency with evidence of development of pulmonary emphysema. Workplace spirometric monitoring over 10 years of surveillance for an on-the-job respirator fit program demonstrated a sharp downward slope in forced expiratory volume in one second, or FEV(1), during his periods of most significant dust exposure, which was attenuated after discontinuation of his workplace exposure. CONCLUSION: Patients with α(1)-antitrypsin disease should be assessed for occupational exposures and closely monitored for work-accelerated progression of lung function decline. More generally, this case report supports the biological plausibility of occupationally associated chronic obstructive pulmonary disease, underscoring that work-associated pulmonary disease can be multi-factorial.