Biological therapies in the acute respiratory distress syndrome

Abstract

Introduction: The acute respiratory distress syndrome (ARDS) is characterised by life-threatening respiratory failure requiring mechanical ventilation, and multiple organ failure. It has a mortality of up to 30 – 45% and causes a long-term reduction in quality of life for survivors, with only approximately 50% of survivors able to return to work 12 months after hospital discharge.

Areas covered: In this review we discuss the complex pathophysiology of ARDS, describe the mechanistic pathways implicated in the development of ARDS and how these are currently being targeted with novel biological therapies. These include therapies targeted against inflammatory cytokines, mechanisms mediating increased alveolar permeability and disordered coagulation, as well as the potential of growth factors, gene therapy and mesenchymal stem cells.

Expert opinion: Although understanding of the pathophysiology of ARDS has improved, to date there are no effective pharmacological interventions that target a specific mechanism, with the only potentially effective therapies to date aiming to limit ventilator-associated lung injury. However, we believe that through this improved mechanistic insight and better clinical trial design, there is cautious optimism for the future of biological therapies in ARDS, and expect current and future biological compounds to provide treatment options to clinicians managing this devastating condition.

Keywords::

• acute hypoxaemic respiratory failure
• acute lung injury
• acute respiratory distress syndrome
• biological therapies

Declaration of interest

D McAuley has performed paid consultancy work and has been a member of advisory boards on ARDS for GlaxoSmithKline. This author's institution has been paid for the author to undertake bronchoscopy as part of a clinical trial funded by GlaxoSmithKline. He has also received fees for lecturing for AstraZenica, and has a patent submitted for a novel treatment for ARDS (unrelated to the work described in this review). D McAuley has received funding from the Northern Ireland Public Health Agency Research and Development Division Translational Research Group for Critical Care. The authors have no other relevant affiliations or financial involvement with any organisation or entity with a financial interest in or financial conflict with the subject matter of materials discussed in the manuscript apart from those disclosed.

Notes

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