Endogenous Cortisol Delivery Following Spinal Cord Injury: Clinical Implications
1Clark J, 1Nenke M, 2David S, 1Marshall R, 3Dunlop S, 4Galea M, 1Torpy D
1ROYAL ADELAIDE HOSPITAL, ADELAIDE, South aust, Australia; 2UNIVERSITY OF ADELAIDE, ADELAIDE, South aust, Australia; 3UNIVERSITY OF WESTERN AUSTRALIA, PERTH, Western au, Australia; 4UNIVERSITY OF MELBOURNE, MELBOURNE, Victoria, Australia
Introduction: Trauma elicits a stress response, activating the hypothalamic-pituitary-adrenal (HPA) axis (cortisol, transported by corticosteroid-binding globulin (CBG)), SNS - sympathoneural (noradrenaline) and sympathoadrenal (adrenaline) systems. We hypothesised that spinal cord injury may lead to suboptimal responses of immunomodulatory cortisol-CBG.
Methods: Four spinal units in Australia and New Zealand participated in this multi-site, assessor-blinded, randomised controlled trial (ACTRN12611001079932). Participants had sustained a traumatic SCI ASIA Impairment Scale [AIS] A, B or C, T12 or above, less than 4 weeks previously. Participants were randomised to passive or FES-assisted cycle ergometry four sessions per week for 12 weeks. Blood samples (visits 0, 1, 2, 3,4, 8, 12) were obtained for the analysis of total and free cortisol, CBG determined as total, high-(ha), low-(la) affinity %, and neutrophil elastase (ELA).
Results: 24 subjects participated (38.4 ±15.6 years, 23 male, 11 tetraplegic, 14 AIS A; 4 B. Circulating total and free cortisol levels were comparable to historic controls without injury : baseline (15.5 ±days) 438 ±110 units, and 45.5 ±16.4 nmol/L-1 respectively, and week-12 349 ±189, 32.6 ± 20.4. Baseline total, la-, haCBG and ELA levels were: 487 ±97; 197 ±78; 290 ±56 nmol.L-1; and 169±198 ng.ml -1.
Discussion: The lack of the expected centrally mediated cortisol rise and CBG depletion from neutrophil elastase may lead to a lack of cortisol’s action in protecting viable peri-injury tissue, potentially exacerbating the effects of spinal injury.
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