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A case of post-traumatic isolated ACTH deficiency with spontaneous recovery 9 months after the event
  1. N Karavitaki1,
  2. J Wass1,
  3. J D Henderson Slater2,
  4. D Wade2
  1. 1Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK
  2. 2Oxford Centre for Enablement, Nuffield Orthopaedic Centre, Oxford, UK
  1. Correspondence to:
 Professor J A H Wass
 Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Old Road, Headington, Oxford, OX3 7LJ, UK; john.wass{at}noc.anglox.nhs.uk

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Survivors of traumatic brain injury (TBI) often suffer from significant adverse physical, neuropsychological, and social sequelae. TBI may pose significant risks to pituitary function;1–5 untreated hypopituitarism may aggravate these adverse consequences. Studies on the natural history of post-TBI hypopituitarism are lacking, and the reversibility of hormone deficits remains uncertain.

We describe a case of a man who suffered a transient period of secondary hypoadrenalism after a serious TBI. This is the first reported case of reversible isolated adrenocorticotrophic hormone (ACTH) deficiency following head trauma.

CASE REPORT

An 18 year old man was assaulted on 14 September 2003 and immediately admitted to the local accident and emergency unit with a Glasgow Coma Scale (GCS) score of 3/15 and constricted pupils. Brain computed tomography (CT) revealed multiple small bleeds involving the basal ganglia, left cerebellum, and midbrain, and a left maxilla linear fracture. No other serious injuries were found. He was ventilated on admission, supported in the intensive care unit, and 4 days later transferred to a trauma ward with an unaltered brain CT. Over the next 7 weeks, his GCS remained reduced (6–11/15) with a marked improvement after this time. During his acute recovery phase, no hypotensive insults were recorded, but he had episodes of …

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