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Inhalation of activated protein C: A possible new adjunctive intervention in acute respiratory distress syndrome

Authors Lars Heslet, Jakob Steen Andersen, Henrik Sengeløv, Björn Dahlbäck, Jorgen Dalsgaard-Nielsen

Published 15 February 2008 Volume 2007:1(4) Pages 465—472

Lars Heslet1, Jakob Steen Andersen1, Henrik Sengeløv2, Björn Dahlbäck3, Jorgen Dalsgaard-Nielsen4

1Department of Intensive Care ITA 4131; 2Department of Hematology L, University Hospital of Copenhagen, Rigshospitalet, Denmark; 3Department of Laboratory Medicin, Clinical Chemistry, Lund University, University Hospital, Malmö, Sweden; 4Department of Clinical Biochemistry, Gentofte University Hospital, Hellerup, Denmark

Abstract: Acute respiratory distress syndrome (ARDS) is a potential lethal disease. At present time no evidence based intervention reduces mortality. The pathophysiology of ARDS include intraalveolar fibrin deposition, hyperinflammation and reduced cellular host defense in the airspace. The normal lung activates protein C (PC) to activated protein C (APC), in contrast to the ARDS lung where the PC-APC axis is disrupted. The lungs have targets for inhaled APC as illustrated by a patient case with ARDS, unresponsive to conventional therapy. After inhalation of 190 µg/kg of APC (Drotrecogin alpha activated) three times a day for seven days, a clear reduction in infiltrates on chest X-ray and a 138% increase in oxygenation capacity as reflected by the PaO2/FiO2 ratio was brought about. The patient, however, died later after cardiac arrest after suspected recurrence of the T-cell lymphoma. No local or systemic adverse effects was found related to the iAPC, during, after or at the time of death. It is suggested based on existing studies and the presented case that inhaled APC is a new treatment option in patients with ARDS – a hypothesis which should be substantiated in a larger series of ARDS patients.

Keywords: ARDS, activated protein C inhalation, pulmonary hemostasis, pulmonary host defense

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