title: Cardiovascular risk in patients with growth hormone deficiency: effects of growth hormone substitution.
abstract: OBJECTIVE
  To review the literature on the increased cardiovascular risk in patients with growth hormone (GH) deficiency and the positive effects of GH replacement.
  
  
  METHODS
  We analyze the factors that contribute to cardiovascular risk in GH deficiency, including body composition and lipid profile, and summarize GH treatment strategies and results described in the literature.
  
  
  RESULTS
  The prominent clinical finding in patients with GH deficiency is the increased abdominal fat, even in patients with normal weight. Cardiac ejection volume tends to be decreased, and arterial distensibility is diminished. The lipid status is also worsened, accompanied by increased inflammatory markers, such as highly sensitive C-reactive protein. Typically, GH treatment reduces visceral fat and increases muscle mass, changes that diminish cardiovascular risk. Because of direct effects as well as increased hemodynamic performance and increased blood volume, cardiac performance is improved. With GH therapy, total cholesterol and low-density lipoprotein levels decrease by 10% to 20%, and inflammatory markers such as C-reactive protein decline. Carbohydrate metabolism during moderate to long-term treatment is minimally affected, although obese patients with GH deficiency on rare occasion may have hyperglycemia or even diabetes.
  
  
  CONCLUSIONS
  The relevance of the beneficial effects of GH on the cardiovascular system is strongly suggested but not fully proved. The results in a large cohort of GH-treated patients (the KIMS or Pharmacia and Upjohn International Metabolic Surveillance database) demonstrated no difference in cardiovascular risk in comparison with that in a control population after a mean of 3 years of treatment.
authors.affiliation: Department of Medicine, University of Geneva, Cologny (Geneva), Switzerland.
authors.forename: Albert G
authors.initials: AG
authors.lastname: Burger
authors.forename: John P
authors.initials: JP
authors.lastname: Monson
authors.forename: Anna M
authors.initials: AM
authors.lastname: Colao
authors.forename: Anne
authors.initials: A
authors.lastname: Klibanski
mesh_terms: D000273:Adipose Tissue / Q000502:physiology; D000596:Amino Acids / Q000378:metabolism; D001783:Blood Flow Velocity; D050218:Body Fat Distribution; D050260:Carbohydrate Metabolism; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D017536:Carotid Artery, Common / Q000473:pathology; D016893:Carotid Stenosis / Q000473:pathology; D004334:Drug Administration Schedule; D004393:Dwarfism, Pituitary / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy*; D006321:Heart / Q000502:physiology; D020249:Hormone Replacement Therapy; D019382:Human Growth Hormone / Q000627:therapeutic use*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D008055:Lipids / Q000097:blood; D012307:Risk Factors
chemical_list: D000596:Amino Acids; D018836:Inflammation Mediators; D008055:Lipids; D019382:Human Growth Hormone