SFEBES2014 Poster Presentations Steroids (39 abstracts)
The endocrine response to severe trauma: the Steroids and Immunity from injury to Rehabilitation (SIR) study
Mark Foster 1, , Angela Taylor 1 , Neil Hill 3, , Rob Staruch 2, , Donna O’Neil 1 , Julian Bion 1, , Stephen Young 1 , Mark Midwinter 1, , Janet Lord 1 & Wiebka Arlt 1
1University Of Birmingham, Birmingham, UK; 2University Hospital Birmingham, Birmingham, UK; 3Royal Centre Of Defence Medicine, Birmingham, UK; 4Institute Of Naval Medicine, Gosport, Hants, UK; 5Imperial College London, W12 0NN, London, UK.
There are 1.21 million deaths from road traffic accidents worldwide. In Afghanistan, there have been 2005 battle injuries over 10 years. Advances in military trauma care have improved survival, resulting in more severely injured individuals entering the trauma care pathway. Improved understanding of endocrine-immune changes after severe trauma may facilitate novel interventions to improve outcomes. We prospectively recruited 102 severely injured patients at the Queen Elizabeth Hospital Birmingham; 52 military and 50 civilian patients with a mean injury severity score of 27.2±13.9. Blood and 24-h urine was collected at baseline (injury <24 h) and after 1–6 weeks and 3–6 months. Measurements included serum and urinary steroids by mass spectrometry, neutrophil phagocytic activity, urinary nitrogen excretion and muscle thickness by ultrasound; comparisons were made to 30 healthy controls and 100 military controls under combat stress. Results demonstrated a significant increase in serum cortisol, peaking at 2 weeks, with an increased cortisol:cortisone ratio returning to normal after 4 weeks. Both DHEA and DHEAS were significantly down-regulated (P<0.0001) and while DHEA returned to normal after 2 months, DHEAS remained very low throughout the 6 months of follow-up. Serum testosterone was initially completely suppressed (P<0.0001) but normalised after week 4. Neutrophil phagocytosis was significantly impaired and returned to normal only after 3 months. Urinary protein loss and muscle mass followed a U-shaped curve with an initial steep decrease followed by recovery to normal at months 2 and 3 post-injury, respectively. In conclusion, the acute response to severe injury comprises increased glucocorticoid activation and down-regulation of adrenal and gonadal androgens. The resurgence of testosterone 4 weeks post-injury initiates an anabolic recovery phase, however, neutrophil phagocytosis shows only delayed recovery and serum DHEAS remained suppressed until 6 months post-injury. Delineation of whether the endocrine changes are beneficial or adverse will determine the potential for future intervention studies.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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