title: Growth hormone deficiency and replacement in patients with treated Cushing's Disease, prolactinomas and non-functioning pituitary adenomas: effects on body composition, glucose metabolism, lipid status and bone mineral density.
abstract: OBJECTIVE
  This study was designed to determine whether previous Cushing's disease (CD) or prolactinoma (PRL) could exert adverse effects additional to those of growth hormone (GH) deficiency as a consequence of variable degrees of prior hypogonadism or hypercatabolism. We report the effects of 5 years GH treatment in 124 GH deficiency adults; 42 patients with non-functioning pituitary adenomas (NFPA), 43 with treated PRL and 39 with treated CD.
  
  
  METHODS
  Fasting plasma glucose, HbA(1c), lipoprotein profile, anthropometry and bone mineral density (BMD) were measured at baseline, 6 months and annually up to 5 years.
  
  
  RESULTS
  Mean body mass index remained unchanged in the PRL group and tended to increase in the NFPA group. In contrast, body mass index decreased in the CD group. Decreases in waist and waist/hip ratio were seen in all groups at 6 months. Decreases in total cholesterol and low-density lipoprotein cholesterol were seen in all groups and remained sustained at 5 years. Plasma glucose and HbA(1c) increased at 6 months. Subsequently, plasma glucose returned to baseline values at 5 years; in contrast, HbA(1c )remained unchanged at the end of the study. Baseline lumbar spine and hip BMD were lower in the PRL and CD groups than in the NFPA group, decreased over 1 year in all groups and subsequently increased by 2 years in NFPA with a subsequent increase in lumbar spine BMD in PRL and CD groups delayed to 3-5 years.
  
  
  CONCLUSIONS
  Baseline characteristics and response to GH replacement are qualitatively similar in NFPA, PRL and CD patients. Because improvements in BMD occur later in PRL and CD patients, an extended trial of GH therapy may be indicated in those patients who were commenced on GH therapy as an additional treatment for reduced BMD.
authors.affiliation: Centre for Clinical Endocrinology, St. Bartholomew's Hospital, QMUL, London, UK.
authors.forename: A
authors.initials: A
authors.lastname: Colson
authors.forename: A M
authors.initials: AM
authors.lastname: Brooke
authors.forename: D
authors.initials: D
authors.lastname: Walker
authors.forename: G M
authors.initials: GM
authors.lastname: Besser
authors.forename: S L
authors.initials: SL
authors.lastname: Chew
authors.forename: A B
authors.initials: AB
authors.lastname: Grossman
authors.forename: P J
authors.initials: PJ
authors.lastname: Jenkins
authors.forename: W M
authors.initials: WM
authors.lastname: Drake
authors.forename: J P
authors.initials: JP
authors.lastname: Monson
mesh_terms: D000236:Adenoma / Q000503:physiopathology* / Q000628:therapy*; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D001823:Body Composition / Q000187:drug effects*; D015992:Body Mass Index; D015519:Bone Density / Q000187:drug effects*; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D019382:Human Growth Hormone / Q000172:deficiency* / Q000627:therapeutic use*; D006801:Humans; D050356:Lipid Metabolism / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D047748:Pituitary ACTH Hypersecretion / Q000503:physiopathology* / Q000628:therapy*; D010911:Pituitary Neoplasms / Q000503:physiopathology* / Q000628:therapy*; D015175:Prolactinoma / Q000503:physiopathology* / Q000628:therapy*; D011446:Prospective Studies
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin; D019382:Human Growth Hormone