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Correspondence |

Surfactant Replacement Therapy in ARDS FREE TO VIEW

Matt P. Wise, DPhil; Anton G. Saayman, EDIC; Paul J. Frost, MBChB
Author and Funding Information

University Hospital of Wales Cardiff, UK

Correspondence to: Matt P. Wise, DPhil, Adult Critical Care, University Hospital of Wales, Heath Park, Cardiff, CF14 4XW, UK; e-mail: mattwise@doctors.org.uk


Dr. Saayman has received honoraria from Eli Lilly, Pulsion, Lidco, and GlaxoSmithKline. Drs. Wise and Frost have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;136(1):321. doi:10.1378/chest.08-2672
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Published online

To the Editor:

We read with interest the report in CHEST (October 2008) by Taut et al,1 in which a pooled analysis of five studies was performed where recombinant surfactant protein (SP)-C surfactant (Venticute; Nycomed; Roskilde, Denmark) was administered to patients with ARDS. No metaanalysis has demonstrated a survival benefit for surfactant administration in ARDS patients, but the reported studies had confounders such as dissimilar preparations, routes of administration, and doses. Many of these confounders were obviated by focusing on a single surfactant preparation that had been used with a similar protocol. The SP-C surfactant improved indexes of oxygenation, like many ARDS therapies, without altering mortality. However, in a post hoc analysis patients with direct ARDS caused by pneumonia or aspiration demonstrated a survival benefit.1

In contrast to adult and pediatric patients with ARDS, surfactant therapy is a valuable therapy in infants with respiratory distress syndrome.2 In infants, early treatment is more effective than later rescue therapy at reducing mortality.2 Taut et al,1 suggested (perhaps incorrectly3,4) that SP-C surfactant therapy was beneficial in patients with direct ARDS because more surfactant might be inactivated than in individuals with indirect ARDS. However, it would be important to know whether the apparent benefit in patients with direct ARDS was the result of lead-time bias. The very nature of patients with direct lung injury may have meant that they were recruited into studies at an earlier time point in their critical illness than those with indirect ARDS, but this does not appear to have been considered in the analysis.

It is clear that perturbations of surfactant quantity and function persist for many days in ARDS patients,3 and this appears to be worse in those with indirect ARDS.4 Moreover, in individuals with direct ARDS the failure to recover surfactant function was associated with death.3 All patients who were analyzed who had received SP-C surfactant treatment received only 24 h of therapy,1 and this may have greatly diminished the potential of this treatment to alter outcome.

Finally, one must recall that the protein fraction of surfactant comprises four molecules, two of which (SP-B and SP-C) reduce surface tension, while SP-A and SP-D have important immunomodulatory functions. These latter two proteins are members of the collectin family of host defense molecules, which bind microorganisms and modulate inflammatory cell function through chemotaxis and cytokine production. SP-D has been demonstrated to profoundly modulate inflammation in a hyperoxic model of acute lung injury.5 We would suggest that the best strategy for the application of exogenous surfactant in ARDS patients would be the early and prolonged use of a preparation containing more than one SP.

Taut FJ, Rippin G, Schenk P, et al. A search for subgroups of patients with ARDS who may benefit from surfactant replacement therapy: a pooled analysis of five studies with recombinant surfactant protein-C surfactant (Venticute). Chest. 2008;134:724-732. [PubMed] [CrossRef]
 
Stevens TP, Sinkin RA. Surfactant replacement therapy. Chest. 2007;131:1577-1582. [PubMed]
 
Schmidt R, Markart P, Ruppert C, et al. Time-dependent changes in pulmonary surfactant function and composition in acute respiratory distress syndrome due to pneumonia or aspiration. Respir Res. 2007;8:55. [PubMed]
 
Pison U, Seeger W, Buchhorn R, et al. Surfactant abnormalities patients with respiratory failure after multiple trauma. Am Rev Respir Dis. 1989;140:1033-1039. [PubMed]
 
Jain D, Atochina-Vasserman EN, Tomer Y, et al. Surfactant protein D protects against acute hyperoxic lung injury. Am J Respir Crit Care Med. 2008;178:805-813. [PubMed]
 

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References

Taut FJ, Rippin G, Schenk P, et al. A search for subgroups of patients with ARDS who may benefit from surfactant replacement therapy: a pooled analysis of five studies with recombinant surfactant protein-C surfactant (Venticute). Chest. 2008;134:724-732. [PubMed] [CrossRef]
 
Stevens TP, Sinkin RA. Surfactant replacement therapy. Chest. 2007;131:1577-1582. [PubMed]
 
Schmidt R, Markart P, Ruppert C, et al. Time-dependent changes in pulmonary surfactant function and composition in acute respiratory distress syndrome due to pneumonia or aspiration. Respir Res. 2007;8:55. [PubMed]
 
Pison U, Seeger W, Buchhorn R, et al. Surfactant abnormalities patients with respiratory failure after multiple trauma. Am Rev Respir Dis. 1989;140:1033-1039. [PubMed]
 
Jain D, Atochina-Vasserman EN, Tomer Y, et al. Surfactant protein D protects against acute hyperoxic lung injury. Am J Respir Crit Care Med. 2008;178:805-813. [PubMed]
 
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