Endocrine Abstracts

Background: Traumatic brain injury (TBI) is a cause of hypopituitarism. Previous reports suggest complete or partial pituitary dysfunction in up to 40% of subjects.

Aim: To investigate the presence of anterior pituitary hormone deficits in TBI patients tested at least 3 months after the injury.

Patients and methods: The patients were recruited from those who have been assessed by the local Rehabilitation Centre over the last 5 years. The endocrine evaluation included short synacthen test, serum FSH, LH, testosterone, oestradiol/menstrual history, TSH, freeT3, freeT4, prolactin, IGF-I and glucagon test. Subjects with peak GH<6 mU/l on glucagon test were further assessed by GHRH+arginine test and were diagnosed as GH deficient if the peak GH was<18 mU/l. The cortisol response was considered adequate if >580 nmol/l on stimulatory tests.

Results: 29 subjects consented to take part [24/5 males/females, median age 46 years (range 19–65.5), median BMI 24 Kg/m² (range 19.6–37)]. The median interval since the TBI [median GCS on admission 5 (range 3–15)] was 35 months (range 3–276). All but four had post-traumatic amnesia of at least 1 week. No patient had FSH/LH or TSH deficiency. Prolactin was normal in all cases. ACTH deficiency was diagnosed in one subject (3.5%), which proved to be transient (diagnosis 4 months and recovery 9 months following TBI). Peak GH<10 mU/l on glucagon test was found in 3 cases (10.3%). Severe GH deficiency was found in one patient (3.4%) (peak GH 3.8 and 17.8 mU/l on glucagon and GHRH+arginine tests, respectively), who however, 3 years following a minor TBI suffered intracerebral haemorrhage.

Conclusions: In this series of patients with TBI tested at least 3 months after head trauma, anterior hypopituitarism was rare. Using strict criteria, it is possible that other series have overestimated the frequency of pituitary dysfunction after TBI.