Biomarkers and mediators of muscle dysfunction in patients with ARDS

• Research type

  Research Study

• Full title

  Biomarkers and mediators of muscle dysfunction in patients with Acute Respiratory Distress Syndrome during their acute illness and recovery period

• IRAS ID

  132751

• Contact name

  Mark J Griffiths

• Contact email

  m.griffiths@imperial.ac.uk

• Sponsor organisation

  Royal Brompton and Harefield NHS Foundation Trust (RB&HFT)

• Duration of Study in the UK

  1 years, 0 months, 1 days

• Research summary

  Acute Respiratory Distress Syndrome (ARDS) is a syndrome of injury to the tissue of the lung with many causes, including infection and even the use of the ventilator that we use to help people breathe on the intensive care unit (ICU). It carries with it a high risk of death and long-term disability in those that survive an ICU admission. Patients with severe ARDS cannot get enough oxygen to their vital organs despite maximal therapy with a ventilator. In some cases, a machine that can take over the function of the lungs may be required. This machine is called ECMO (extracorporeal membrane oxygenation) and is similar to a bypass machine used in cardiac surgery.
  With or without ECMO, patients with severe ARDS are critically unwell for a prolonged period of time. Most will experience a syndrome of weakness and loss of muscle bulk termed Intensive Care Unit Acquired Paresis (ICUAP). ICUAP results in longer ICU admissions, duration of mechanical ventilation and increased risk of death compared to patients without ICUAP. In survivors of ICU, weakness may persist for years and they may never fully recover, reducing their quality of life. The underlying mechanisms leading to ICUAP involve altering the expression of proteins that either positively or negatively regulate muscle growth. However, we do not know how a number of these proteins actually lead to muscle wasting or how they are affected by the inflammatory burden of both ARDS and ECMO. This research aims to investigate these molecular pathways, with the aim of identifying therapeutic targets that could improve patient health by reducing the burden of muscle atrophy in critical illness.

• REC name

  London - Camden & Kings Cross Research Ethics Committee

• REC reference

  14/LO/2208

• Date of REC Opinion

  3 Mar 2015

• REC opinion

  Further Information Favourable Opinion