RT Journal Article
SR Electronic
T1 KL‐6 levels are elevated in plasma from patients with acute respiratory distress syndrome
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 142
OP 145
DO 10.1183/09031936.03.00070303
VO 23
IS 1
A1 H. Sato
A1 M.E.J. Callister
A1 S. Mumby
A1 G.J. Quinlan
A1 K.I. Welsh
A1 R.M. duBois
A1 T.W. Evans
YR 2004
UL http://erj.ersjournals.com/content/23/1/142.abstract
AB The acute respiratory distress syndrome (ARDS) is an extreme form of lung injury characterised by disruption to the alveolar epithelium. KL‐6 is a mucin-like glycoprotein expressed on type II pneumocytes. Circulating levels of KL‐6 have diagnostic and prognostic significance in a number of interstitial lung diseases, and when elevated are thought to indicate disruption of the alveolar epithelial lining. In this study, the authors sought to determine whether plasma KL‐6 levels were elevated in patients with ARDS and whether these were associated with aetiology, disease severity, outcome or ventilatory strategy. Plasma samples were collected from 28 patients with ARDS, nine ventilated controls of matched illness severity and 10 healthy individuals. KL‐6 concentrations were measured by enzyme-linked immunosorbent assay. Patients with ARDS had higher plasma levels of KL‐6 (median 537 U·mL−1, interquartile range (IQR) 383–1,119), as compared to ventilated controls (median 255 U·mL−1, IQR 83–338) and normal individuals (median 215 U·mL−1, IQR 149–307). In patients with ARDS, plasma KL-6 levels were higher in nonsurvivors than survivors, and correlated positively with oxygenation index and negatively with arterial oxygen tension:inspiratory oxygen fraction ratio. There were also significant positive correlations with mean and peak airway pressures. Elevated levels of plasma KL‐6 may provide a useful marker for acute respiratory distress syndrome in ventilated patients and have possible prognostic significance. Alveolar epithelial cell damage may be influenced by the nature of mechanical ventilatory support. KL‐6 ELISA kits were kindly provided by Eisai Co. (Tokyo, Japan). H. Sato is supported by a grant from Eisai Co.. M.E.J. Callister is supported by a Wellcome Trust Fellowship. This work was supported partly by the British Lung Foundation and the Dunhill Medical Trust. ¶Joint first authors.