title: Recombinant GH replacement in hypopituitary adults improves endothelial cell function and reduces calculated absolute and relative coronary risk.
abstract: OBJECTIVE
  Adult GH deficiency (GHD) is linked to endothelial dysfunction and vascular disease. We examined the effect of 12 months of GH therapy on endothelial function, C-reactive protein (CRP) and coronary risk.
  
  
  METHODS
  Open-design intervention study.
  
  
  METHODS
  Fourteen GH-deficient patients (nonsmokers, without diabetes, hypertension or vascular disease) studied before, 6 months and 12 months after GH therapy.
  
  
  METHODS
  Flow-mediated dilatation (FMD), carotid intima-media thickness (IMT) thrombomodulin (TM), E-selectin, CRP, lipid profile, blood pressure and anthropometric data were recorded. We used the Framingham equation to calculate coronary risk.
  
  
  RESULTS
  FMD improved (7.5 +/- 1.62 vs. 11.93 +/- 1.52, P = 0.038). Overall there was no change in IMT, TM, E-selectin or CRP. The correlation between TM and FMD showed a trend for statistical significance (r = -0.54, P = 0.056). Changes in CRP correlated with change in IGF-1 (r = -0.67, P = 0.012); E-selectin correlated with high density lipoprotein (HDL)-cholesterol (r = -0.60, P = 0.028), triglycerides (r = 0.68, P = 0.01) and waist-to-hip ratio (WHR) (r = 0.71, P = 0.006). Systolic (127.36 +/- 4.47 vs. 120.36 +/- 3.50, P = 0.017) and diastolic (84.71 +/- 2.73 vs. 76.93 +/- 2.03, P = 0.005) blood pressure decreased. HDL-cholesterol increased (0.70 +/- 0.05 vs. 0.93 +/- 0.06, P = 0.001). WHR decreased (0.90 +/- 0.02 to 0.88 +/- 0.02, P = 0.043) without changes in weight or body mass index (BMI). Ten-year absolute (P = 0.009) and relative (P = 0.002) cardiac risk decreased.
  
  
  CONCLUSIONS
  Biophysical test of endothelial function (FMD) improved after 12 months of GH therapy but there was no significant change in biochemical endothelial or inflammatory markers. Calculated coronary risk decreased mainly due to reduction in systolic and diastolic blood pressure and increase in HDL-cholesterol.
authors.affiliation: Department of Medicine, School of Postgraduate Medicine, Keele University, UK.
authors.forename: T A M
authors.initials: TA
authors.lastname: Abdu
authors.forename: T A
authors.initials: TA
authors.lastname: Elhadd
authors.forename: H
authors.initials: H
authors.lastname: Buch
authors.forename: D
authors.initials: D
authors.lastname: Barton
authors.forename: R
authors.initials: R
authors.lastname: Neary
authors.forename: R N
authors.initials: RN
authors.lastname: Clayton
mesh_terms: D000328:Adult; D001916:Brachial Artery / Q000000981:diagnostic imaging; D002097:C-Reactive Protein / Q000032:analysis; D002339:Carotid Arteries; D008076:Cholesterol, HDL / Q000097:blood; D003327:Coronary Disease / Q000517:prevention & control; D004334:Drug Administration Schedule; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D013006:Growth Hormone / Q000172:deficiency; D020249:Hormone Replacement Therapy; D019382:Human Growth Hormone / Q000008:administration & dosage*; D006801:Humans; D007018:Hypopituitarism / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011994:Recombinant Proteins / Q000008:administration & dosage*; D012039:Regional Blood Flow; D018570:Risk Assessment; D018709:Statistics, Nonparametric; D017539:Tunica Intima / Q000000981:diagnostic imaging; D014463:Ultrasonography; D014664:Vasodilation
chemical_list: D008076:Cholesterol, HDL; D011994:Recombinant Proteins; D019382:Human Growth Hormone; D013006:Growth Hormone; D002097:C-Reactive Protein