ULTRASTRUCTURAL ALTERATIONS OF THE AIR-BLOOD BARRIER IN SARCOIDOSIS AND HYPERSENSITIVITY PNEUMONITIS AND THEIR RELATION TO LUNG HISTOPATHOLOGY

Citation
C. Planes et al., ULTRASTRUCTURAL ALTERATIONS OF THE AIR-BLOOD BARRIER IN SARCOIDOSIS AND HYPERSENSITIVITY PNEUMONITIS AND THEIR RELATION TO LUNG HISTOPATHOLOGY, American journal of respiratory and critical care medicine, 150(4), 1994, pp. 1067-1074
Citations number
20
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
ISSN journal
1073449X
Volume
150
Issue
4
Year of publication
1994
Pages
1067 - 1074
Database
ISI
SICI code
1073-449X(1994)150:4<1067:UAOTAB>2.0.ZU;2-R
Abstract
To evaluate the incidence of air-blood barrier lesions in the course o f chronic interstitial lung diseases, we studied by electron microscop y open lung biopsy specimens from patients with sarcoidosis or chronic hypersensitivity pneumonitis, and compared the distribution of ultras tructural air-blood barrier lesions (including swelling or destruction of epithelial and endothelial cells, type II cell hyperplasia, and ba sement membrane disruption) with the type of histopathologic abnormali ties present (including inflammation, inflammation and fibrosis, or fi brosis alone). Ultrastructural lesions of the air-blood barrier were f requently observed in sarcoidosis as well as hypersensitivity pneumoni tis. Their nature and distribution were highly dependent on the histol ogic pattern of lung tissue in which they were present: epithelial and /or endothelial injury was more frequently observed in inflammatory ar eas (90 to 100% of all lung specimens displaying inflammation alone), whereas type II cell hyperplasia was mainly identified in fibrotic tis sues (83 to 100% of all lung specimens displaying fibrosis alone). Str ikingly, in lung tissue considered as normal by light microscopy, air- blood barrier was frequently found to be damaged (50 to 62% of apparen tly normal lung specimens), suggesting that alveolar lesions may const itute an early phenomenon in the course of pulmonary inflammatory proc esses. The air-blood barrier alterations observed in this study may pr ovide an anatomic basis for the modifications of alveolar permeability described in pulmonary sarcoidosis and hypersensitivity pneumonitis.