Centrilobular and Panlobular Emphysema in Smokers: Two Distinct Morphologic and Functional Entities
Authors:
- David H. EidelmanDEDavid H. Eidelman
- Jose L. IzquierdoJIJose L. Izquierdo
- Heberto GhezzoHGHeberto Ghezzo
- Marina P. SaettaMSMarina P. Saetta
- Manuel G. CosioMCManuel G. Cosio
- 1 December 1991
- journal article
- Published by Oxford University Press (OUP) in American Review of Respiratory Disease
- Vol. 144 (6) , 1385-1390
Abstract
In order to investigate the hypothesis that different morphologic patterns of disease might correspond to different mechanical properties of the lung in emphysema, pulmonary function tests and lung mechanics were measured in 34 subjects undergoing lung resection for peripheral lung tumors. Using standard microscopic criteria, pure or predominant centrilobular (n = 18) or panlobular (n = 16) emphysema was diagnosed in lungs. The degree of emphysema measured by the mean linear intercept (Lm) was not significantly different between the two groups. However, the coefficient of variation of the interalveolar wall distance (CV) was significantly higher for the same Lm in CLE than in PLE. This indicates that CLE has an uneven pattern of destruction, whereas PLE is more homogeneous. CLE had a higher degree of abnormalities in the small airways (SAD) than did PLE (p < 0.05) mainly because of significantly higher muscle score (p < 0.001) and fibrosis. CLE also had a higher proportion of airways less than 400 µm in diameter than did PLE (p < 0.05). Static compliance, specific compliance, and the exponential constant (K) were significantly lower (p < 0.005, p < 0.001, and p < 0.05, respectively) in CLE than in PLE. FEV1/FVC was significantly correlated with SAD in CLE (r = −0.69, p < 0.01) but not in PLE (r = 0.29 p > 0.05); conversely, FEV1/FVC was significantly correlated with elasticity (K) in PLE (r = −0.72, p < 0.01) but not in CLE (r = 0.08, p > 0.05). We conclude that smokers develop two different kinds of lung destruction with different mechanical behavior probably because of the different patterns of distribution of lung destruction and the different degree of small airways involvement. This suggests that lung abnormalities in smokers may result from different pathogenetic mechanisms.Keywords
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