To the Editor:
I read with great interest the paper by Henderson, et al1 on shrinking lung syndrome (SLS) as a manifestation of pleuritis.
A decrease in lung compliance in patients with SLS was found. Analysis of the computed tomography images did not show any evidence of parenchymal lung disease. Further, the study subjects with SLS had intact corrected DLCO values. The authors appropriately point out that both of these important observations make interstitial lung disease an unlikely cause of the decreased lung compliance. The authors described that a comparable decrease in lung compliance has been observed in patients who are chronically restricted to lower lung volumes; for example, patients with spinal cord injury or muscular dystrophy. The authors further describe that tissue remodeling with changes in the elasticity of the lung tissue are the proposed underlying pathophysiology. It is important to point out that none of the studies cited as reference for tissue remodeling in the setting of chronically restricted lung volumes show direct evidence of tissue remodeling in the lung.
Conversely, chest wall strapping is an experimental procedure that is used to model the effect of breathing at low lung volumes on pulmonary physiology2,3,4. Restrictions to inspiration by chest wall strapping of normal volunteers lead to an immediate decrease in lung compliance2,3,4. This is fully reversible by relieving the chest wall strapping and allowing again for deep inspirations to total lung capacity. Restriction to 60% to 65% of the normal total lung capacity by chest wall strapping was sufficient to demonstrate the decrease in lung compliance3. These immediate and immediately reversible changes in lung compliance with chest wall strapping strongly suggest that changes in surface forces at the air liquid interface of the lung are the underlying etiology for the lung compliance changes3. Surfactant is the main regulator of surface forces in the lung5. In that context, alterations in surfactant have also been implicated in the pathophysiology of SLS6.
Breathing at lower lung volumes secondary to pleuritis, as described in the study by Henderson, et al1, is conceptually similar to chest wall strapping. It is very likely that changes in surface forces and possibly surfactant play a role in the observed decreased lung compliance in patients with pleuritis.
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