title: Evaluation of pituitary function after traumatic brain injury in childhood.
abstract: OBJECTIVE
  Post-traumatic hypopituitarism is well described amongst adult traumatic brain injury (TBI) survivors. We aimed to determine the prevalence and clinical significance of pituitary dysfunction after head injury in childhood.
  
  
  METHODS
  Retrospective exploratory study.
  
  
  METHODS
  33 survivors of accidental head injury (27 boys). Mean (range) age at study was 13·4 years (5·4-21·7 years) and median (range) interval since injury 4·3 years (1·4-7·8 years). Functional outcome at study: 15 good recovery, 16 moderate disability, two severe disability.
  
  
  METHODS
  Early morning urine osmolality and basal hormone evaluation were followed by the gonadotrophin releasing hormone (GnRH) and insulin tolerance (n = 25) or glucagon tests (if previous seizures, n = 8). Subjects were not primed. Head injury details were extracted from patient records.
  
  
  RESULTS
  No subject had short stature (mean height SD score +0·50, range -1·57 to +3·00). Suboptimal GH responses (<5 μg/l) occurred in six peri-pubertal boys (one with slow growth on follow-up) and one postpubertal adolescent (peak GH 3·2 μg/l). Median peak cortisol responses to insulin tolerance or glucagon tests were 538 and 562 nm. Nine of twenty-five and two of eight subjects had suboptimal responses, respectively, two with high basal cortisol levels. None required routine glucocorticoid replacement. In three, steroid cover was recommended for moderate/severe illness or injury. One boy was prolactin deficient. Other basal endocrine results and GnRH-stimulated LH and FSH were appropriate for age, sex and pubertal stage. Abnormal endocrine findings were unrelated to the severity or other characteristics of TBI or functional outcome.
  
  
  CONCLUSIONS
  No clinically significant endocrinopathy was identified amongst survivors of accidental childhood TBI, although minor pituitary hormone abnormalities were observed.
authors.affiliation: Section of Child Life & Health, University of Edinburgh Royal Hospital for Sick Children, Edinburgh, UK. s.khadr@ich.ucl.ac.uk
authors.forename: Sophie N
authors.initials: SN
authors.lastname: Khadr
authors.forename: Patricia M
authors.initials: PM
authors.lastname: Crofton
authors.forename: Patricia A
authors.initials: PA
authors.lastname: Jones
authors.forename: Barbara
authors.initials: B
authors.lastname: Wardhaugh
authors.forename: Jennifer
authors.initials: J
authors.lastname: Roach
authors.forename: Amanda J
authors.initials: AJ
authors.lastname: Drake
authors.forename: Robert A
authors.initials: RA
authors.lastname: Minns
authors.forename: Christopher J H
authors.initials: CJ
authors.lastname: Kelnar
mesh_terms: D000293:Adolescent; D001930:Brain Injuries / Q000503:physiopathology*; D002648:Child; D003430:Cross-Sectional Studies; D005260:Female; D005934:Glucagon; D019382:Human Growth Hormone / Q000172:deficiency; D006801:Humans; D006854:Hydrocortisone / Q000172:deficiency; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007328:Insulin; D008297:Male; D010902:Pituitary Gland / Q000503:physiopathology*; D010907:Pituitary Hormones / Q000502:physiology*; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D012189:Retrospective Studies
chemical_list: D007328:Insulin; D010907:Pituitary Hormones; D019382:Human Growth Hormone; D005934:Glucagon; D006854:Hydrocortisone