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A case of post-traumatic isolated ACTH deficiency with spontaneous recovery 9 months after the event

¹ Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK
² Oxford Centre for Enablement, Nuffield Orthopaedic Centre, Oxford, UK

Correspondence to:
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@noc.anglox.nhs.uk

Keywords: pituitary gland; hypopituitarism; head injury

The first 150 words of the full text of this article appear below.

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, . . . [Full text of this article]