Am. J. Respir. Crit. Care Med., Vol 150, No. 4, 10 1994, 1067-1074.
Ultrastructural alterations of the air-blood barrier in sarcoidosis and hypersensitivity pneumonitis and their relation to lung histopathology
C Planes, D Valeyre, A Loiseau, JF Bernaudin and P Soler
INSERM U 82, UFR Xavier Bichat, Paris, France.
To evaluate the incidence of air-blood barrier lesions in the course of
chronic interstitial lung diseases, we studied by electron microscopy open
lung biopsy specimens from patients with sarcoidosis or chronic
hypersensitivity pneumonitis, and compared the distribution of
ultrastructural air-blood barrier lesions (including swelling or
destruction of epithelial and endothelial cells, type II cell hyperplasia,
and basement membrane disruption) with the type of histopathologic
abnormalities present (including inflammation, inflammation and fibrosis,
or fibrosis alone). Ultrastructural lesions of the air-blood barrier were
frequently observed in sarcoidosis as well as hypersensitivity pneumonitis.
Their nature and distribution were highly dependent on the histologic
pattern of lung tissue in which they were present: epithelial and/or
endothelial injury was more frequently observed in inflammatory areas (90
to 100% of all lung specimens displaying inflammation alone), whereas type
II cell hyperplasia was mainly identified in fibrotic tissues (83 to 100%
of all lung specimens displaying fibrosis alone). Strikingly, in lung
tissue considered as normal by light microscopy, air-blood barrier was
frequently found to be damaged (50 to 62% of apparently normal lung
specimens), suggesting that alveolar lesions may constitute an early
phenomenon in the course of pulmonary inflammatory processes. The air-
blood barrier alterations observed in this study may provide an anatomic
basis for the modifications of alveolar permeability described in pulmonary
sarcoidosis and hypersensitivity pneumonitis.
