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| The first 150 words of the full text of this article appear below. |
The acute respiratory distress syndrome (ARDS) is an acute and severe form of microvascular lung injury which is frequently seen in intensive therapy units. Reductions in mortality have been reported by some centres; however, 40-70% of patients still die from this syndrome.1 2 Treatment at present is largely supportive and, despite our increased understanding of the pathological processes involved, there are no specific treatments of proven benefit.
Interstitial and intra-alveolar fibrosis are hallmarks of the more
advanced stages of ARDS and are characterised by the abnormal and
excessive deposition of extracellular matrix proteins, in particular
collagen.3 4 Histologically and biochemically this is
similar to the fibrosis seen in other more chronic forms of
interstitial lung disease4; however, more is known of the mediators and cellular events that occur in these disorders. The decrease in pulmonary compliance and progressive hypoxia resulting from
fibrotic change leads to ventilator dependence. As a result, progressive
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