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Endocrine Abstracts (2014) 34 S5.1 | DOI: 10.1530/endoabs.34.S5.1

1University of Birmingham, Birmingham, UK; 2University Hospital Birmingham, Birmingham, UK; 3Institute of Naval Medicine, Alverstoke, Hants, UK.


Advances in trauma care have improved survival resulting in more severely injured individuals surviving to enter the trauma care pathway. A significant threat to recovery is now the dysregulated immune response to injury. The hyperinflammatory response of the innate immune system (SIRS), combined with immunoparesis, leads to complications such as multi-organ failure and sepsis. Moreover, recovery from trauma is significantly affected by age, which may be due to changes in the immune and endocrine systems with age that modify the ability to respond appropriately to trauma. Increased understanding of endocrine and immune changes in trauma may influence the development of novel interventions for trauma.

We carried out a prospective cohort study in 102 severely injured patients with an injury severity score (ISS) range 4–75, at the Queen Elizabeth Hospital Birmingham. Blood samples and 24-h urines were collected at baseline (<24 h after major trauma), on days 3, 5, 10, 14, 21, 28 and 2, 3, 4, and 6 months post injury. Serum DHEAS post injury was significantly lower than in healthy controls (P<0.0001) and was still lower than controls at 6 months. The cortisol:DHEAS ratio peaked after 20 days and normalised by 6 months. Nitrogen excretion peaked early at 23 gN/day and dropped below 10 gN/day by week 6. Muscle thickness reduced by 31% at 6 weeks and returned to baseline 5 months post injury; this U-shaped curve correlated with the course of nitrogen excretion (P<0.0001). Serum pro-inflammatory (IL6 and IL8) and anti-inflammatory (IL10) cytokine levels were elevated in response to injury returning to normal levels 4–6 weeks post-injury. HMGB1 and mtDNA (P<0.001) in the serum of trauma patients were significantly elevated when compared to healthy controls.

These results provide evidence of the inflammatory and endocrine drivers of trauma-related sarcopenia and suggest that modifying the inflammatory and HPA axis response could reduce sarcopenia.

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