title: Clinical implications of residual growth hormone (GH) response to provocative testing in adults with severe GH deficiency.
abstract: BACKGROUND
  The diagnosis of GH deficiency (GHD) in adults is based on provocative tests of GH release, all influenced by clinical factors. It is unknown whether the amount of residual GH reserve under the cutoff value has any physiological implication.
  
  
  OBJECTIVE
  We used a large pharmacoepidemiological database of adult GHD (KIMS) and tested the impact of confounding factors on GH release of no greater than 3 microg/liter after an insulin tolerance test (ITT) and evaluated its potential physiological role.
  
  
  METHODS
  A total of 1098 patients fulfilled the criteria of having a GH peak of no greater than 3 microg/liter during ITT as well as documented IGF-I levels.
  
  
  RESULTS
  The impact of underlying hypothalamic-pituitary disease, age, gender, body weight, as well as treatment modalities such as irradiation on peak GH level to ITT was evaluated, and the correlations between GH peak and targets of GH action were analyzed.
  
  
  RESULTS
  The GH response to ITT was regulated by gender, age, and the number of additional pituitary deficiencies. In a multivariate evaluation, the extent of hypothalamic-pituitary dysfunction was the most important single predictor of GH peak in ITT. GH peaks in ITT were positively related to IGF-I levels and high-density lipoprotein-cholesterol, as well as inversely to triglycerides.
  
  
  CONCLUSIONS
  Even in adult severe GHD, GH release appears to be regulated by factors defined to play an important role in normal GH secretion. The impact of very low GH release on IGF-I and lipid parameters indicates a persistent physiological role of low GH concentrations in severely affected patients with GHD.
authors.affiliation: Department of Endocrinology, Christie Hospital, Wilmslow Road, Manchester M20 4BX, United Kingdom. georg.brabant@manchester.ac.uk
authors.forename: Georg
authors.initials: G
authors.lastname: Brabant
authors.forename: Ase
authors.initials: A
authors.lastname: Krogh Rasmussen
authors.forename: Beverly M K
authors.initials: BM
authors.lastname: Biller
authors.forename: Michael
authors.initials: M
authors.lastname: Buchfelder
authors.forename: Ulla
authors.initials: U
authors.lastname: Feldt-Rasmussen
authors.forename: Kristin
authors.initials: K
authors.lastname: Forssmann
authors.forename: Bjorn
authors.initials: B
authors.lastname: Jonsson
authors.forename: Maria
authors.initials: M
authors.lastname: Koltowska-Haggstrom
authors.forename: Dominique
authors.initials: D
authors.lastname: Maiter
authors.forename: Bernhard
authors.initials: B
authors.lastname: Saller
authors.forename: Andy
authors.initials: A
authors.lastname: Toogood
mesh_terms: D000328:Adult; D016208:Databases, Factual; D005260:Female; D019382:Human Growth Hormone / Q000172:deficiency* / Q000627:therapeutic use; D006801:Humans; D007018:Hypopituitarism / Q000175:diagnosis* / Q000188:drug therapy / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D050356:Lipid Metabolism; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index
chemical_list: D007328:Insulin; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I