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Original Research: COPD |

Assessment of Regional Progression of Pulmonary Emphysema With CT Densitometry

M. Els Bakker, PhD; Hein Putter, PhD; Jan Stolk, MD, PhD; Saher B. Shaker, MD; Eeva Piitulainen, MD; Erich W. Russi, MD, FCCP; Berend C. Stoel, PhD
Author and Funding Information

*From the Division of Image Processing, Department of Radiology (Drs. Bakker and Stoel), Department of Medical Statistics (Dr. Putter), and Department of Pulmonology (Dr. Stolk), Leiden University Medical Center, Leiden, the Netherlands; Department of Respiratory Medicine (Dr. Shaker), Gentofte University Hospital, Hellerup, Denmark; Department of Pulmonary Medicine and Allergology (Dr. Piitulainen), Malmö University Hospital, Malmö, Sweden; and Pulmonology Division (Dr. Russi), University Hospital Zurich, Zurich, Switzerland.

Correspondence to: M. Els Bakker, PhD, Division of Image Processing, Department of Radiology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, the Netherlands; e-mail: m.e.Bakker@lumc.nl


This study is an extension of the SPREAD project (Software Performance and Reproducibility in Emphysema Assessment: Demonstration) that has been funded by the Fifth Framework Programme of the European Commission (project No. QLG1-2000-01752; www.lkeb.nl/spread.htm).

Dr. Stoel acts as a consultant for Hoffman La Roche, Talecris Biopharmaceuticals, CLS Behring, and BioImaging Technologies Inc., and has received supplementary grant money from Hoffman La Roche and Talecris Biopharmaceuticals. The other authors have no personal or financial conflicts of interest to disclose.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(5):931-937. doi:10.1378/chest.08-0512
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Background:  Lung densitometry is an effective method to assess overall progression of emphysema, but generally the location of the progression is not estimated. We hypothesized that progression of emphysema is the result of extension from affected areas toward less affected areas in the lung. To test this hypothesis, a method was developed to assess emphysema severity at different levels in the lungs in order to estimate regional changes.

Methods:  Fifty subjects with emphysema due to α1-antitrypsin deficiency (AATD) [AATD deficiency of phenotype PiZZ (PiZ) group] and 16 subjects with general emphysema (general emphysema without phenotype PiZZ [non-PiZ] group) were scanned with CT at baseline and after 30 months. Densitometry was performed in 12 axial partitions of equal volumes. To indicate predominant location, craniocaudal locality was defined as the slope in the plot of densities against partitions. Regional progression of emphysema was calculated after volume correction, and its slope identifies the area of predominant progression. The hypothesis was tested by investigating the correlation between predominant location and predominant progression.

Results:  As expected, the PiZ patients showed more basal emphysema than the non-PiZ group (craniocaudal locality, − 40.0 g/L vs − 6.2 g/L). Overall progression rate in PiZ patients was lower than in non-PiZ subjects. A significant correlation was found between craniocaudal locality and progression slope in PiZ subjects (R = 0.566, p < 0.001). In the non-PiZ group, no correlation was found.

Conclusions:  In the PiZ group, the more emphysema is distributed basally, the more progression was found in the basal area. This finding suggests that emphysema due to AATD spreads out from affected areas.

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