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Serum Surfactant Protein-A Levels Predict Development of ARDS in At-Risk Patients*

K.E. Greene, MD; S. Ye; R.J. Mason, MD, FCCP; P.E. Parsons, MD
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*From the National Jewish Medical Center and Denver Health Medical Center, Departments of Medicine, Pulmonary, and Critical Care Medicine, Denver, CO.

Correspondence to: K.E. Greene, MD, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, National Jewish Medical and Research Center, 1400 Jackson St, Denver, CO 80206



Chest. 1999;116(suppl_1):90S-91S. doi:10.1378/chest.116.suppl_1.90S
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Extract

Patients with ARDS have significant quantitative and qualitative surfactant abnormalities. We, and others, have shown that patients with established ARDS have decreased BAL surfactant protein (SP)-A levels and increased serum SP-A. We hypothesized that serum SP-A levels reflect epithelial cell injury and would, therefore, predict the development of ARDS in patients at risk for the syndrome. To investigate this, we measured serum SP-A levels in patients who were at risk for developing ARDS from sepsis, trauma, or aspiration of gastric contents and from normal healthy volunteers. Patients were enrolled as part of the ARDS Specialized Center of Research project within 8 h of being identified as being at risk and serum samples were obtained within 12 h. Patients were then followed up to determine if they ultimately developed the syndrome. SP-A levels were measured using a double monoclonal antibody sandwich enzyme-linked immunosorbent assay. SP-A levels were compared using one-way analysis of variance with Tukey-Kramer test for multiple comparisons. Significance was assigned at a p value of < 0.05. Overall, baseline SP-A levels in all at-risk patients who ultimately developed ARDS were significantly higher when compared with those patients who did not develop the syndrome (123 ng/mL, [n = 26] vs 30 ng/mL [n = 25]). Subgroup analysis revealed that baseline serum SP-A levels in patients who developed ARDS from either sepsis or aspiration were significantly higher when compared to patients with the same risk factors who did not develop ARDS (sepsis: 253 ng/mL [n = 6] vs 32 ng/mL [n = 6]; aspiration: 93 ng/mL [n = 4] vs 33 ng/mL [n = 4]). In contrast, SP-A levels in trauma patients who developed ARDS (46 ng/mL [n = 15]) were not different from trauma patients who did not develop ARDS (42 ng/mL [n = 16]), and were identical to normal volunteers (30 ng/mL [n = 16]). In conclusion, baseline serum SP-A levels appear to predict the development of ARDS in patients at risk from sepsis and aspiration, but not trauma. These results are consistent with other studies demonstrating differences in circulating endothelial markers, endotoxin, and tumor necrosis factor-α in patients with sepsis compared to patients with trauma. Our findings suggest that serum SP-A levels may allow for early identification of patients at high risk for developing ARDS and may help in the development of specific targeted therapeutic interventions.


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